2014 Meeting Program

Transcription

48th Annual Meeting of the
PANCREAS
CLUB
MAY 2-3, 2014
WESTIN LOMBARD • CHICAGO, IL
WELCOME!
Welcome to the 48th Annual Meeting of the Pancreas Club at
the Westin Lombard in Chicago. The Mission of the Pancreas
Club, since its founding in 1966, is to promote the interchange
of ideas between pancreatologists throughout the world and
to maintain an informal “club” atmosphere.
For the first time, the Pancreas Club is pleased to introduce
an expanded two full-day program with the annual dinner
taking place on Friday evening. Once again, we received
over 200 abstracts which were reviewed by the Program
Committee. We know that you will be fully engaged in both
listening to the excellent presentations and in the discussions
which follow. Posters of Distinctions will be presented by
authors and addressed by leading faculty during the Poster
Rounds with Professors. Authors will also be available
posterside during the several Poster Sessions.
PA N C R E A S
C LU B
D I R EC TO R S
L. William Traverso, MD
This meeting will offer continuing medical education credits
through a joint sponsorship with the American College of
Surgeons. We thank them for their support of this important
meeting. We hope this provides a benefit to your CME needs
and appreciate you support of this meeting
The abstracts selected for oral and poster presentation are
included in this program book and are also available on our
website.
DEAR MEMBERS AND GUESTS,
Allow me to add my welcome to the 48th Annual Meeting
of the Pancreas Club at The Westin Lombard Yorktown
Center. The scientific program promises to be robust and
stimulating. For those not attending the scientific sessions,
there is much to do in the city of Lombard. Also known as
Lilac Village, Lombard is famous for Lilacia Park which is
an 8.5 acre horticultural showcase featuring 800 lilcas and
25,000 tulips. Lilac time runs from May 3 through May 18.
For those that love to shop, the Westin Lombard is just steps
from Yorktown Shopping Center where you can shop in
such stores as Von Maur, JC Penney and Carson Pirie Scott.
Further east is the second largest shopping center in the
Chicago area, Oak Brook Center, located at the junction of
22nd Street and Route 83 in Oak Brook, Illinois and is home
to Nordstrom, Lord & Taylor, Macy’s and Neiman Marcus,
along with another 150+ stores. In addition to shopping,
Lombard and Oak Brook offer many restaurants rated as
Illinois best restaurants providing a wide variety of foods,
such as, American, Asian, Bistro, Chinese, French, Italian,
Mexican, sea food and vegetarian – so there is much to do in
the short time you will be in town.
William H. Nealon, MD
Michael Farnell, MD
LOCAL
ARRANGEMENTS
CHAIR
If moving on to downtown Chicago after the meeting, may
I encourage you to take advantage of purchasing through
registration a shuttle reservation for Saturday evening. We
look forward to seeing all of you at the 48th Annual Meeting
of the Pancreas Club for two days of science and fellowship.
Sincerely,
Gerard V. Aranha, MD, FRCSC, (C), FACS
Gerard Aranha, MD
TABLE OF CONTENTS
General Information2
Accreditation & Disclosure Information3
Schedule-at-a-Glance6
2014 Annual Dinner Honoree: L. William Traverso, MD
8
Supporters & Exhibitors9
Hotel Floorplan & Area Map10
Scientific Program11
Poster Listings20
Oral Abstracts37
2014 Membership Roster108
Past & Future Meetings151
1
GENERAL INFORMATION
MEETING LOCATION
The Westin Lombard Yorktown Center
70 Yorktown Shopping Center
Lombard, IL 60148
PHONE: 630-719-8000
MEETING HOURS
REGISTRATION
Grand Ballroom Foyer
Thursday, May 1, 2014 • 6:00 pm – 8:00 pm
Friday, May 2, 2014 • 6:30 am – 5:30 pm
Saturday, May 3, 2014 • 6:45 am – 5:00 pm
SCIENTIFIC SESSIONS
Grand Ballroom A-E with Posters in Grand Ballroom F-J
Friday, May 2, 2014 • 7:45 am – 5:30 pm
Saturday, May 3, 2014 • 8:00 am – 4:45 pm
EXHIBITS
Grand Ballroom F-J
Friday, May 2, 2014
9:30 am – 3:30 pm
9:30 am – 9:50 am
3:10 pm – 3:25 pm
Exhibits Open
Refreshment Break in Exhibit Area
Saturday, May 3, 2014
9:30 am – 6:00 pm
9:45 am – 10:00 am
3:15 pm – 3:30 pm
4:45 pm – 6:00 pm
Exhibits Open
Wine & Cheese Awards Reception
GENERAL BUSINESS MEETING
Grand Ballroom A-E
Friday, May 2, 2014 • 5:30 pm – 6:00 pm
ANNUAL DINNER/RECEPTION
Junior Ballroom
Friday, May 2, 2014 • 6:00 pm – 10:00 pm
AWARDS RECEPTION
Grand Ballroom F-J
Saturday, May 3, 2014 • 4:45 pm – 6:00 pm
TABLE OF CONTENTS
2
General Information
ACCREDITATION & DISCLOSURE INFORMATION
CONTINUING MEDICAL EDUCATION
MEETING/LEARNING OBJECTIVES
At the conclusion of this meeting, participants will be able to:
• Address the challenges of the management of all of the complexities of pancreatic
diseases with considerably greater insight and evidence-based decision making.
• Understand the role of total pancreatectomy and islet autotransplant in
management of chronic pancreatitis.
• Understand the methods for best practice in drain management following
pancreatectomy based upon prospective data.
• Articulate the role of fine needle aspirate of neuroendocrine neoplasms of the
pancreas.
• Understand the algorithm for management of postpancreatectomy
hemorrhage.
• Understand the unique tumor biology of pancreatic carcinoma metastatic to
the lungs.
• List additional/different treatment options for patients based on evidence
provided in abstract presentations.
ACCREDITATION STATEMENT
American College of Surgeons
Division of Education
This activity has been planned and implemented in
accordance with the Essential Areas and Policies
of the Accreditation Council for Continuing Medical
Education through the joint sponsorship of the
American College of Surgeons and the Pancreas Club.
The American College of Surgeons is accredited by
the ACCME to provide continuing medical education
for physicians.
AMA PRA CATEGORY 1 CREDITS™
The American College of Surgeons designates this live activity for a maximum
of 15.25 AMA PRA Category 1 Credits™. Physicians should claim only the credit
commensurate with the extent of their participation in the activity.
PROGRAM COMMITTEE MEMBERS
William Nealon, MD, Chair
Gerard Aranha, MD
Michael Farnell, MD
Jason Fleming, MD
Nipun Merchant, MD
James Moser, MD
Accreditation & Disclosure Information
William Traverso, MD
Mark Truty, MD
Christopher Wolfgang, MD
Victor Zaydfudim, MD
Nicholas Zyromski, MD
TABLE OF CONTENTS
3
DISCLOSURE INFORMATION
In accordance with the ACCME Accreditation Criteria, the American College of
Surgeons, as the accredited provider of this activity, must ensure that anyone in a
position to control the content of the educational activity has disclosed all relevant
financial relationships with any commercial interest. Therefore, it is mandatory
that both the program planning committee and speakers complete disclosure
forms. Members of the program committee were required to disclose all financial
relationships and speakers were required to disclose any financial relationship as
it pertains to the content of the presentations. The ACCME defines a ‘commercial
interest’ as “any entity producing, marketing, re-selling, or distributing health
care goods or services consumed by, or used on, patients”. It does not consider
providers of clinical service directly to patients to be commercial interests. The
ACCME considers “relevant” financial relationships as financial transactions (in any
amount) that may create a conflict of interest and occur within the 12 months
preceding the time that the individual is being asked to assume a role controlling
content of the educational activity.
ACS is also required, through our joint sponsorship partners, to manage any
reported conflict and eliminate the potential for bias during the activity. All program
committee members and speakers were contacted and the conflicts listed below
have been managed to our satisfaction. However, if you perceive a bias during a
session, please report the circumstances on the session evaluation form.
Please note we have advised the speakers that it is their responsibility to
disclose at the start of their presentation if they will be describing the use of
a device, product, or drug that is not FDA approved or the off-label use of an
approved device, product, or drug or unapproved usage.
The requirement for disclosure is not intended to imply any impropriety of such
relationships, but simply to identify such relationships through full disclosure and
to allow the audience to form its own judgments regarding the presentation.
TABLE OF CONTENTS
4
Accreditation
& Disclosure Information
DISCLOSURES
SPEAKERS/MODERATORS/
CHAIRS/DISCUSSANTS
NOTHING TO
DISCLOSE
Ashok Saluja
DISCLOSURE As it pertains to
the content of the presentation
Minneamrita - Stock options/
Partial ownership; Consulting
Carlos Fernandez del Castillo
X
Charles Vollmer
X
Charles Yeo
X
Claudio Bassi
X
David Adams
X
Douglas Evans
X
Elisa Giovannetti
X
Hiroki Yamaue
X
Horacio Asbun
X
Kyoichi Takaori
X
Mark Talamonti
X
Marshall Baker
X
Matthew Katz
X
Michael Kendrick
X
Roberto Coppola
X
Syed Ahmad
X
Shuji Isaji
X
Ugo Boggi
X
PLANNING
COMMITTEE
NOTHING TO
DISCLOSE
Christopher Wolfgang
X
Gerard Aranha *
X
Michael Farnell *
X
Jason Fleming *
X
Nicholas Zyromski *
X
Nipun B. Merchant
X
James Moser *
DISCLOSURE
All commercial relationships
Abbvie - Honorarium;
Speaker/ panel
Mark Truty
X
Victor Zaydfudim *
X
William Nealon *
X
William Traverso
X
Accreditation & Disclosure Information
*Indicates also moderator/faculty
TABLE OF CONTENTS
5
SCHEDULE-AT-A-GLANCE
MEETING ROOMS
SCIENTIFIC SESSIONS: Grand Ballroom A-E
POSTERS: Grand Ballroom F-J
REGISTRATION: Grand Ballroom Foyer
EXHIBITS: Grand Ballroom F-J
THURSDAY, MAY 1, 2014
6:00 pm – 8:00 pm Exhibits/Poster Setup
6:00 pm – 8:00 pm Registration
Grand Ballroom F-J
6:30 pm – 8:00 pm Advisory Committee Meeting/Dinner
Cypress B
FRIDAY, MAY 2, 2014
6:30 am – 5:30 pm Registration
7:00 am – 7:45 am Continental Breakfast
Grand Ballroom F-J
7:45 am – 8:00 am Welcome and Introductory Remarks Grand Ballroom A-E
8:00 am – 9:35 am SCIENTIFIC SESSION I
Grand Ballroom A-E
8:00 am
TOPIC: Borderline Resectable Pancreatic Cancer
8:35 am
TOPIC: Neo-adjuvant Chemo Therapy/Radiation Therapy
9:30 am – 3:30 pm Exhibits Open
9:30 am – 9:50 am Grand Ballroom F-J
Break with Exhibitors & Poster Viewing Grand Ballroom F-J
9:50 am – 11:00 am SCIENTIFIC SESSION II
Grand Ballroom A-E
TOPIC: Minimally Invasive Techniques/Screening for Cancer
11:00 am – 12:00 pm Poster Rounds with Professors
Grand Ballroom F-J
12:00 pm – 1:00 pm Lunch Lilac Room
1:00 pm – 2:00 pm How I Do It Session Grand Ballroom A-E
Borderline Resectable Adenocarcinoma
of the Pancreas: Definitions and Management
2:00 pm – 3:10 pm SCIENTIFIC SESSION III
TOPIC: Translational Studies
Grand Ballroom A-E
3:10 pm – 3:25 pm Break with Exhibitors & View Posters Grand Ballroom F-J
3:25 pm – 5:30 pm
3:25 pm 4:45 pm SCIENTIFIC SESSION IV
TOPIC: Pancreatitis
TOPIC: Neuroendocrine Tumors
Grand Ballroom A-E
5:30 pm – 6:00 pm Pancreas Club Brief Business Meeting Grand Ballroom A-E
6:00 pm – 10:00 pm Pancreas Club Annual Dinner/Reception
Junior Ballroom
TABLE OF CONTENTS
6
Schedule-at-a-Glance
SCHEDULE-AT-A-GLANCE
SATURDAY, MAY 3, 2014
6:45 am – 5:00 pm Registration
Grand Ballroom F-J
8:00 am – 9:45 am SCIENTIFIC SESSION V
TOPIC: IPMN
Grand Ballroom A-E
Grand Ballroom F-J
9:45 am – 10:00 am Break with Exhibitors & Poster Viewing Grand Ballroom F-J
10:00 am – 11:00 am SCIENTIFIC SESSION VI
TOPIC: Cancer Basic
12:00 pm – 1:00 pm Lunch Grand Ballroom A-E
Grand Ballroom F-J
Lilac Room
1:00 pm – 3:15 pm 1:00 pm 2:15 pm SCIENTIFIC SESSION VII
Grand Ballroom A-E
TOPIC: Early Complications After
Pancreatico-Duodenectomy/Drains & Fistulas
TOPIC: Quality/Predictors/Regionalization
3:30 pm – 4:45 pm SCIENTIFIC SESSION VIII Grand Ballroom A-E
3:30 pm TOPIC: Quality/Predictors/Regionalization (continues)
4:10 pm TOPIC: Late Postoperative Issues
4:45 pm – 6:00 pm Wine & Cheese Awards Reception
Grand Ballroom F-J
AWARDS
The Pancreas Club will recognize three outstanding presentations.
They will be awarded during the closing, Saturday afternoon, reception:
• PANCAN RESEARCH AWARD: $1,000 for the best oral presentation
of pancreatic cancer research by a resident or fellow. This award is
generously funded by the Pancreatic Cancer Action Network.
• KENNETH WARREN/PANCREAS CLUB RESEARCH AWARD: $1,000 for
the best oral presentation of clinical or basic science pancreatitis by a
resident or fellow. This award is generously funded by the Pancreas Club
and the Kenneth Warren Foundation.
• JOHN HOWARD RESEARCH AWARD: $1,000 for the best presentation
from young junior faculty, who is within 5 years of their end of residency.
This award is generously funded by the Arpa Foundation.
Schedule-at-a-Glance
TABLE OF CONTENTS
7
2014 ANNUAL DINNER HONOREE
L. WILLIAM TRAVERSO, MD
PRESENTED BY: Richard Kozarek, MD, Virginia Mason Medical Center, Seattle, WA
Bill Traverso has been a member of the Pancreas Club since
1978 and a Director since 1999. His undergraduate degree
was received at the University of Nevada, while his M.D.
degree and residency training were both completed at the
UCLA School of Medicine, Los Angeles. His interest in the
pancreas was fostered by his mentors at UCLA: William
Longmire and Ron Tompkins. The first pylorus-preserving
pancreatoduodenectomy was performed on February 28,
1977 for a patient with chronic pancreatitis. To this day, the procedure is commonly
known as the Traverso-Longmire operation.
Dr. Traverso’s primary interest has been surgical management of pancreatic
disease. He has published over 260 peer-reviewed articles or book chapters
and has made over 300 national and international podium presentations. Dr.
Traverso has served as President of the Society of American Gastrointestinal
and Endoscopic Surgeons, the Society for Surgery of the Alimentary Tract,
the North Pacific Surgical Association and the American College of Surgeons
Washington Chapter. Since 1997, he has been a director for the Japanese Society
of Hepatobiliary and Pancreatic Surgery Observership.
Dr. Traverso has organized a number of international symposia on pancreatic
cancer beginning first in 2001 in Seattle, followed by meetings in Pisa, Rome,
Kyoto and an upcoming meeting in July 2014 in Verona, Italy. He has fostered
relationships with pancreatophiles across the world as evidenced by the strong
international representation at the annual Pancreas Club meeting. Bill helped build
a center of excellence for hepatobiliary and pancreatic disease in his long career
at Virginia Mason Medical Center from 1984-2010. He continues as a leader in
pancreatic surgery in his current position at St. Luke’s Health System, Center for
Pancreatic and Liver Disease, Boise, Idaho. The growth and vitality of the Pancreas
Club has been in no small measure due to his efforts. Please join us as we honor
Bill at the Pancreas Club annual dinner.
PAST ANNUAL DINNER HONOREES
2012
2011
2010
2009
2008
2007
2005
2004
Howard Reber, MD
Edward Bradley, III, MD
Hans Beger
Prof. Seiki Matsuno
Andy Warshaw, MD
Charles Frederick Frey, MD
John M. Howard, MD
John Cameron, MD and Fujio Hanyu, MD
TABLE OF CONTENTS
8
2014 Annual Dinner Honoree
SUPPORTERS & EXHIBITORS
The Pancreas Club gratefully acknowledges support for the 48th Annual
Pancreas Club Meeting from the following:
EDUCATIONAL GRANT SUPPORT
PLATINUM
SILVER
BRONZE
EXHIBITORS
AbbVie
Medtronic Advanced Energy
Celgene Corporation
RedPath Integrated Pathology, Inc.
Ethicon
Vector Surgical, LLC
Forest Pharmaceuticals, Inc.
AWARDS SUPPORT
• Pancreatic Cancer Action Network
In support of PanCan Research Award
• Kenneth Warren Foundation
In support of Kenneth Warren/Pancreas Club Research Award
• The Pancreas Club
In support of Kenneth Warren/Pancreas Club Research Award
• Arpa Foundation
In support of John Howard Research Award
Supporters & Exhibitors
TABLE OF CONTENTS
9
HOTEL FLOORPLAN & AREA MAP
THE WESTIN LOMBARD YORKTOWN CENTER
AREA MAP & LOCAL TRANSPORTATION
The Westin Lombard is located 26 miles from downtown Chicago (DDW hotels). For
your convenience, you have an option of purchasing shuttle reservation for Saturday
evening, after the PC meeting to downtown Chicago. Please stop by the registration
desk to purchase your ticket by 3:00 pm on Friday. Hurry, space is limited!
Chicago O’Hare
International
Airport
290
90
294
19
MIL
ES
41
12
Westin Lombard
Yorktown Center
290
Chicago
26 MILES
TABLE OF CONTENTS
10
Hotel Floorplan & Area Map
SCIENTIFIC PROGRAM
FRIDAY, MAY 2, 2014
6:30 am – 5:30 pm Registration Grand Ballroom Foyer
Grand Ballroom F-J
7:45 am – 8:00 am Welcome and Introductory Remarks Grand Ballroom A-E
William H. Nealon, MD, Vanderbilt University, Nashville, TN
William Traverso, MD, St. Luke’s Hospital, Boise, ID
Michael Farnell, MD, Mayo Clinic, Rochester, MN
8:00 am – 9:35 am SCIENTIFIC SESSION I
Grand Ballroom A-E
MODERATORS: Douglas Evans, MD & Shuji Isaji, MD
TOPIC: Borderline Resectable Pancreatic Cancer
8:00 am
S001 DIAGNOSTIC LAPAROSCOPY TO DETECT OCCULT
8:15 am
S002 RISK OF VENOUS THROMBOEMBOLISM DURING
8:30 am
S003 IMPACT OF SURGICAL RESECTION AFTER
METASTATIC DISEASE PRIOR TO NEOADJUVANT
CHEMORADIATION IN BORDERLINE RESECTABLE PANCREATIC
DUCTAL ADENOCARCINOMA – A COST ANALYSIS –June S. Peng
(Long)
NEOADJUVANT THERAPY FOR RESECTABLE AND BORDERLINE
RESECTABLE (BLR) PANCREATIC ADENOCARCINOMA (PC) –A. N.
Krepline (Long)
CHEMORADIOTHERAPY FOR LOCALLY ADVANCED
UNRESECTABLE PANCREATIC DUCTAL ADENOCARCINOMA –
Masashi Kishiwada, PhD, MD (Short)
TOPIC: Neo-adjuvant Chemo Therapy/Radiation Therapy
8:35 am
S004 A COMPREHENSIVE ASSESSMENT OF NEOADJUVANT
8:50 am
S005 DOES THE USE OF NEOADJUVANT THERAPY FOR
9:05 am
S006 NEOADJUVANT CHEMORADIATION VERSUS
THERAPY FOR PANCREATIC ADENOCARCINOMA: RESULTS
FROM THE NATIONAL CANCER DATABASE (NCDB) –Russell S.
Lewis, BS (Long)
PANCREATIC ADENOCARCINOMA INCREASE POSTOPERATIVE
MORBIDITY AND MORTALITY RATES? –Amanda B. Cooper, MD
(Long)
NEOADJUVANT CHEMOTHERAPY PRIOR TO
PANCREATICODUODENECTOMY FOR PANCREATIC CANCER –
Pragatheeshwar Thirunavukarasu, MD (Long)
Scientific Program
TABLE OF CONTENTS
11
SCIENTIFIC PROGRAM
9:20 am
S007 CHANGES IN BODY COMPOSITION DURING PREOPERATIVE
9:25 am
S008 PROSPECTIVE RANDOMIZED CONTROLLED STUDY
9:30 am
S009 MICROSCOPIC RESIDUAL TUMOR AFTER
THERAPY FOR RESECTABLE PANCREATIC CANCER: DO THEY
MATTER? – Amanda B. Cooper, MD (Short)
COMPARING OUTCOME BETWEEN STANDARD RESECTION AND
AN EXTENDED RESECTION THAT INCLUDED DISSECTION OF THE
NERVE PLEXUS AND VARIOUS LYMPH NODES IN PATIENTS WITH
PANCREATIC HEAD CANCER –Jin-Young Jang (Short)
PANCREATICODUODENECTOMY FOR CANCER. PRELIMINARY
RESULTS OF A MULTICENTRIC PROSPECTIVE RANDOMIZED
TRIAL –Roberto Coppola, MD, FACS (Short)
9:35 am – 9:50 am Grand Ballroom F-J
Break with Exhibitors & Poster Viewing Grand Ballroom F-J
9:50 am – 11:00 am SCIENTIFIC SESSION II
Grand Ballroom A-E
MODERATORS: Horacio Asbun, MD & Ugo Boggi, MD
TOPIC: Minimally Invasive Techniques/Screening for Cancer
9:50 am
S010 MINIMALLY INVASIVE PANCREATODUODENECTOMY: IS THE
LEARNING CURVE SURMOUNTABLE? –Attila Nakeeb, MD (Long)
10:05 am S011 TOTAL LAPAROSCOPIC PANCREATICODUODENECTOMY
FOR PANCREATIC DUCTAL ADENOCARCINOMA: ONCOLOGIC
ADVANTAGES OVER OPEN APPROACHES? –Kristopher P.
Croome, MD, MS (Long)
10:20 am S012 PRELIMINARY RESULTS OF A SWEDISH, MR BASED,
SCREENING PROGRAM FOR INDIVIDUALS AT RISK FOR
PANCREAS CANCER –Marco Del Chiaro, MD, PhD (Long)
10:35 am
S013 EARLY DETECTION OF PANCREATIC INTRAEPITHELIAL
NEOPLASIA USING NON-INVASIVE IMAGING TO LOCALIZE AND
GRADE PROTEASE ACTIVITY – Dana A. Dominguez, BS (Long)
Grand Ballroom F-J
PROFESSORS: Michael Kendrick, MD & Nicholas Zyromski, MD
See page 20 for list of posters. First 10 Posters marked with
★: Authors will be by their posters to discuss their research
poster presentations and Professor will lead short Q&A.
TABLE OF CONTENTS
12
Scientific Program
SCIENTIFIC PROGRAM
12:00 pm – 1:00 pm Lunch Lilac Room
1:00 pm – 2:00 pm HOW I DO IT SESSION Grand Ballroom A-E
Borderline Resectable Adenocarcinoma of the Pancreas:
Definitions and Management
MODERATORS: Jason Fleming, MD & Mark Talamonti, MD
This session is directed at practitioners who take care of patients with
pancreatic cancer. In it we will discuss the management options for patients
with pancreatic cancer who may or may not be suitable for surgical resection.
At the conclusion of this session, the attendees will be able to:
• Interpret diagnostic imaging results in patients with pancreatic cancer.
• Choose management approaches for patients with pancreatic cancer.
• Employ evidence-based principles of management in patient with pancreatic
cancer.
Outline:
• Initial surgical resection of a PC patient with superior mesenteric vein
involvement – Charles Vollmer, MD (8 min.)
• Preoperative therapy of a PC patient with superior mesenteric vein
involvement – Syed Ahmad, MD (8 min.)
• Initial surgical resection of a frail PC patient with a resectable primary tumor
– Charles Yeo, MD (8 min.)
• Preoperative therapy of a frail PC patient with a resectable primary tumor –
Matthew HG Katz, MD (8 min.)
• Discussion (28 min.)
2:00 pm – 3:10 pm SCIENTIFIC SESSION III Grand Ballroom A-E
MODERATORS: Ashok Saluja, MD & Kyoichi Takaori, MD
TOPIC: Translational Studies
2:00 pm
S014 ROLE OF CYB5A IN PANCREATIC CANCER:
2:15 pm
S015 CA 19-9 RESPONSE TO NEOADJUVANT THERAPY PREDICTS
CORRELATION WITH CLINICAL OUTCOME AND FUNCTIONAL
CHARACTERIZATION IN THE MODULATION OF AUTOPHAGY AND
ONCOGENIC PHENOTYPES –Elisa Giovannetti, MD, PhD (Long)
OUTCOME IN PANCREATIC ADENOCARCINOMA –Brian A. Boone,
MD (Long)
Scientific Program
TABLE OF CONTENTS
13
SCIENTIFIC PROGRAM
2:30 pm
S016 DETECTION OF CLINICALLY RELEVANT GENETIC
2:45 pm
S017 NEW PLATFORMS FOR PDAC PRECLINICAL STUDIES: 3D
3:00 pm
S018 BIOLUMINESCENT ORTHOTOPIC PANCREATIC-DUCTAL-
3:05 pm
S019 COUNTERACTING CANCER CELL SURVIVAL STRATEGY:
ALTERATIONS IN FINE NEEDLE ASPIRATES OF PANCREATIC
CANCER IS POSSIBLE USING NEXT-GENERATION SEQUENCING
–Vicente Valero III, MD (Long)
TISSUE-ENGINEERED MODELS BASED ON PRIMARY CANCER
CELLS AND SYNTHETIC SCAFFOLDS – Claudio Ricci, PhD (Long)
ADENOCARCINOMA (PDAC) MOUSE MODELS DERIVED FROM
PRIMARY PDAC CELLS AS A PLATFORM FOR THERAPEUTIC
DISCOVERY –Niccola Funel, PhD (Short)
SENSITIZATION OF PANCREATIC CANCER CELLS TO TRAIL
INDUCED CELL DEATH BY JAK2/STAT3 PATHWAY INHIBITION BY
PREVENTING DEATH RECEPTOR DOWNREGULATION –Kaustav
Majumder, MD (Short)
3:25 pm – 5:30 pm
SCIENTIFIC SESSION IV
Grand Ballroom A-E
MODERATORS: Gerard Aranha, MD & David Adams, MD
TOPIC: Pancreatitis
3:25 pm
S020 TOTAL PANCREATECTOMY WITH ISLET
3:40 pm
S021 COST-EFFECTIVENESS OF TOTAL PANCREATECTOMY WITH
3:55 pm
S022 HIGH READMISSION RATES FOLLOWING SURGERY FOR
4:10 pm
S023 PANCREATICODUODENECTOMY FOR CHRONIC
4:15 pm
S024 RISK OF RECURRENT PANCREATITIS AND PROGRESSION
AUTOTRANSPLANTATION FOR CHRONIC PANCREATITIS: THE
PRICE PATIENTS PAY FOR IMPROVEMENTS IN QUALITY OF LIFE
–Katherine Morgan, MD (Long)
ISLET CELL AUTOTRANSPLANTATION FOR THE TREATMENT OF
SMALL DUCT CHRONIC PANCREATITIS –Daniel E. Abbott, MD
(Long)
CHRONIC PANCREATITIS –A. V. Fisher (Long)
PANCREATITIS: A LONG-TERM FOLLOW-UP –Kristopher P.
Croome, MD (Short)
TO CHRONIC PANCREATITIS AFTER ACUTE PANCREATITIS –
Usama Ahmed Ali, MD, MSc (Long)
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14
Scientific Program
SCIENTIFIC PROGRAM
4:30 pm
S025 SEVERE ACUTE PANCREATITIS: USING A
MULTIDISCIPLINARY PERCUTANEOUS DRAINAGE PROTOCOL THE
MAIN PREDICTOR OF HOSPITAL LENGTH OF STAY IS AMYLASE
OR BACTERIA IN THE PERCUTANEOUS ASPIRATE – M. Sugimoto,
MD (Long)
TOPIC: Neuroendocrine Tumors
4:45 pm
S026 SURGICAL RESECTION PROVIDES A SIGNIFICANT OVERALL
5:00 pm
S027 RISK OF MALIGNANCY IN RESECTED NONFUNCTIONING
5:15 pm
S028 AN INVESTIGATION OF THE UTILITY OF KI-67 EXPRESSION
5:20 pm
S029 THE GASTRINOMA TRIANGLE REVISITED: DUODENAL
5:25 pm
S030 PATTERNS OF PRACTICE AND SURVIVALamONG PATIENTS
SURVIVAL BENEFIT FOR PATIENTS WITH SMALL PANCREATIC
NEUROENDOCRINE TUMORS –Susan M Sharpe, MD (Long)
PANCREATIC NEUROENDOCRINE TUMORS –Michael J. Ferrara,
MS (Long)
IN PANCREATIC NEUROENDOCRINE TUMOUR FINE NEEDLE
ASPIRATION SAMPLES –Nigel B. Jamieson, MD, PhD (Short)
WALL GASTRINOMA AND PANCREATIC GASTRINOMA
LOCATIONS PREDICT BIOLOGICAL BEHAVIOR AND LONGEVITY
–Sam G. Pappas, MD (Short)
WITH NON-METASTATIC PANCREATIC NEUROENDOCRINE
TUMORS UNDER 2 CM –Jan Franko, MD, PhD (Short)
5:30 pm – 6:00 pm Pancreas Club Brief Business Meeting Grand Ballroom A-E
6:00 pm – 10:00 pm Pancreas Club Annual Dinner/Reception Junior Ballroom
DINNER HONOREE: L. William Traverso, MD
See page 8 for details.
Scientific Program
TABLE OF CONTENTS
15
SCIENTIFIC PROGRAM
6:45 am – 5:00 pm Registration 7:00 am – 8:00 am Continental Breakfast
Grand Ballroom F-J
8:00 am – 9:45 am SCIENTIFIC SESSION V
Grand Ballroom A-E
MODERATORS: Carlos Fernandez del Castillo, MD
& Claudio Bassi, MD
TOPIC: IPMN
8:00 am
S031 RE-CLASSIFICATION OF COMBINED-TYPE IPMNS ALLOWS
8:15 am
S032 CLINICAL VALIDATION OF NEW INTERNATIONAL
8:30 am
S033 INTRADUCTAL PAPILLARY MUCINOUS NEOPLASM OF
8:45 am
S034 THE BIOLOGY OF SMALL IPMN CANCERS (< 20 MM
9:00 am
S035 A NATIONAL PERSPECTIVE OF INVASIVE INTRADUCTAL
9:15 am
S036 CHARACTERIZATION OF PANCREATIC STROMAL
9:20 am
S037 CURRENT INDICATIONS FOR SURGERY OF IPMN’S MAY
9:25 am
S038 MAIN PANCREATIC DUCT SIZE AND RISK OF MALIGNANCY
9:30 am
S039 DOES EUS IMPROVE OUTCOME IN SURVEILLANCE OF NON-
FOR A BETTER DEFINITION OF TWO DISEASE ENTITIES –
Giovanni Marchegiani, MD (Long)
CONSENSUS GUIDELINES FOR THE RESECTION OF BRANCH
DUCT TYPE INTRADUCTAL PAPILLARY MUCINOUS NEOPLASMS
(BD-IPMN) –Jin-Young Jang (Long)
THE PANCREAS, ONE MANIFESTATION OF A MORE SYSTEMIC
DISEASE? –Alexandra M. Roch, MD (Long)
INVASIVE COMPONENT): A MULTI-INSTITUTIONAL ANALYSIS –
Jordan M. Winter, MD (Long)
PAPILLARY MUCINOUS NEOPLASM (IPMN) –Russell S. Lewis, BS
(Long)
CELLS ISOLATED FROM PANCREATITIS AND PANCREATIC
ADENOCARCINOMA SURGICAL SPECIMENS –Daniel Delitto, MD
(Short)
OVERLOOK SOME PATIENTS WITH CANCER: RECOMMENDATIONS
FOR CHANGE –Andrew H. Nguyen (Short)
IN INTRADUCTAL PAPILLARY MUCINOUS NEOPLASM –Neda
Rezaee, MD (Short)
RESECTED PRESUMED BRANCH-DUCT INTRADUCTAL PAPILLARY
MUCINOUS NEOPLASMS? –Anna C. Evans, MD (Short)
TABLE OF CONTENTS
16
Scientific Program
SCIENTIFIC PROGRAM
9:35 am
S040 RESECTED PANCREATIC ADENOCARCINOMAS WITH
9:40 am
S041 THE INDOLENT NATURE OF PULMONARY METASTASES
RECURRENCE LIMITED IN LUNG HAVE A SIGNIFICANTLY BETTER
PROGNOSIS THAN THOSE WITH OTHER RECURRENCE PATTERNS
–Lei Zheng, MD, PhD (Short)
FROM PANCREATIC CANCER –Stephanie Downs-Canner, MD (Short)
Grand Ballroom F-J
9:45 am – 10:00 am Break with Exhibitors & Poster Viewing Grand Ballroom F-J
10:00 am – 11:00 am SCIENTIFIC SESSION VI
Grand Ballroom A-E
MODERATORS: James Moser, MD & Elisa Giovannetti, MD
TOPIC: Cancer Basic
10:00 am S042 PANCREATIC STELLATE CELL SECRETED IL-6 MEDIATES
STAT3 DEPENDENT CANCER CELL INVASION –Jason A.
Castellanos, MD (Long)
10:15 am
S043 NEUTROPHIL EXTRACELLULAR TRAPS (NETS) ARE
UPREGULATED IN PANCREATIC CANCER AS A RESULT OF
AUTOPHAGY AND CONTRIBUTE TO HYPERCOAGULABILITY –
Brian A. Boone, MD (Long)
10:30 am S044 ISOLATION AND CHARACTERIZATION OF DCLK1+ TUMOR
CELLS OF PANCREATIC ADENOCARCINOMA PATIENTS –Jeremy
L. Irvan, MD (Long)
10:45 am
S045 SEQUENCE ALTERATIONS IN THE WEE1 NON-CODING
REGION IS A FACILITATOR AND MARKER FOR PANCREATIC
TUMORIGENESIS –Jordan M. Winter, MD (Short)
10:50 am S046 CHEMOTHERAPY RESISTANT PANCREATIC CANCER
TUMOR-ASSOCIATED FIBROBLASTS ARE PROTUMORIGENIC –
Paul A. Toste, MD (Short)
10:55 am
S047 PTK6 INCREASES APOPTOSIS WITH GEMCITABINE
TREATMENT IN PANCREATIC CANCER CELLS BY ENHANCING
DNA DAMAGE –Hiroaki Ono, MD, PhD (Short)
Grand Ballroom F-J
PROFESSORS: Marshall Baker, MD & Victor Zaydfudim, MD
See page page 29 for list of posters. First 10 Posters
marked with ★ : Authors will be by their posters to discuss
their research poster presentations and Professor will lead
short Q&A.
Scientific Program
TABLE OF CONTENTS
17
SCIENTIFIC PROGRAM
12:00 pm – 1:00 pm Lunch 1:00 pm – 3:15 pm Lilac Room
SCIENTIFIC SESSION VII
Grand Ballroom A-E
MODERATORS: Michael Farnell, MD & Hiroki Yamaue, MD
TOPIC: Early Complications After Pancreatico-duodenectomy/Drains & Fistulas
1:00 pm
S048 THE VALUE OF DRAINS AS A FISTULA MITIGATION
1:15 pm
S049 A RANDOMIZED PROSPECTIVE MULTICENTER TRIAL OF
1:30 pm
S050 RISK-ADJUSTED OUTCOMES OF CLINICALLY-
1:45 pm
S051 HIGH PERFORMING WHIPPLE PATIENTS: FACTORS
2:00 pm
S052 THE ASSOCIATION BETWEEN PANCREATIC FISTULA
2:05 pm
S053 DOES DRAIN FLUIDamYLASE ACCURATELY PREDICT
2:10 pm
S054 EARLY DRAIN REMOVAL: THE MIDDLE GROUND
STRATEGY FOR PANCREATODUODENECTOMY: SOMETHING FOR
EVERYONE? RESULTS OF A RANDOMIZED PROSPECTIVE MULTIINSTITUTIONAL STUDY –Matthew T. McMillan, BA (Long)
PANCREATICODUODENECTOMY WITH AND WITHOUT ROUTINE
INTRAPERITONEAL DRAINAGE –George Van Buren, II, MD (Long)
RELEVANT POSTOPERATIVE FISTULA FOLLOWING
PANCREATODUODENECTOMY: A MODEL FOR PERFORMANCE
EVALUATION –Charles M Vollmer, MD (Long)
ASSOCIATED WITH SHORT LENGTH OF STAY AFTER OPEN
PANCREATICODUODENECTOMY –Grace C Lee, BS (Long)
GRADE C AND SURVIVAL AFTER PANCREATIC RESECTION FOR
PANCREATIC CANCER –Manabu Kawai, MD, PhD (Short)
PANCREATIC FISTULA? –Christina W. Lee, MD (Short)
BETWEEN THE DRAIN VERSUS NO DRAIN DEBATE IN PATIENTS
UNDERGOING PANCREATICODUODENECTOMY. A PROSPECTIVE
VALIDATION STUDY –Zhi Ven Fong, MD (Short)
TOPIC: Quality/Predictors/Regionalization
2:15 pm
S055 THE HYSLAR TRIAL: A PROSPECTIVE RANDOMIZED
2:30 pm
S056 CURRENT MANAGEMENT OF DELAYED BLEEDING AFTER
TRIAL ON THE USE OF A RESTRICTIVE FLUID REGIMEN WITH 3%
HYPERTONIC SALINE (HS) VERSUS LACTATED RINGERS (LR) IN
PATIENTS UNDERGOING PANCREATICODUODENECTOMY (PD) –
Harish Lavu, MD (Long)
PANCREATICODUODENECTOMY –Young Joon Ahn, PhD (Long)
TABLE OF CONTENTS
18
Scientific Program
SCIENTIFIC PROGRAM
2:45 pm
S057 BILE-CULTURE BASED ANTIMICROBIAL PROPHYLAXIS
3:00 pm
S058 IT IS QUALITY AND QUANTITY: A SINGLE INSTITUTION’S
REDUCES SURGICAL SITE INFECTIONS (SSIS) IN PANCREATIC
SURGERY –Alessandro Zerbi, MD (Long)
EXPERIENCE IN QUALITY MEASURES OF PANCREATIC CANCER
CARE –Melanie Ongchin, MD (Long)
3:30 pm – 4:45 pm SCIENTIFIC SESSION VIII
Grand Ballroom A-E
MODERATORS: William Nealon, MD & Roberto Coppola, MD
TOPIC: Quality/Predictors/Regionalization (continues)
3:30 pm
S059 MOBILE RISK CALCULATOR APP FOR OPERATIVE
3:35 pm
S060 PREDICTORS OF EARLY READMISSION AFTER
3:40 pm
S061 HIGH-VOLUME SURGEONS VERSUS HIGH-VOLUME
3:55 pm
S062 WHAT ARE THE FINANCIAL IMPLICATIONS OF CENTERS
AND ONCOLOGIC OUTCOMES IN PATIENTS CONSIDERING
PANCREADICODUODENECTOMY FOR PANCREATIC
ADENOCARCINOMA –Steven Nurkin, MD (Short)
PANCREATECTOMY –Caitlin W Hicks, MD, MS (Short)
HOSPITALS: ARE BEST OUTCOMES MORE DUE TO WHO OR
WHERE? –Prashant B. Sukharamwala, MD (Long)
FOR REGIONAL HEALTHCARE? –Alexander S. Rosemurgy, MD
(Long)
TOPIC: Late Postoperative Issues
4:10 pm
S063 THE INCIDENCE OF PANCREATOGENIC DIABETES AFTER
4:20 pm
S064 EFFECT OF HIGH-DOSE PANCREATIC ENZYME
MAJOR PARTIAL PANCREATIC RESECTION MAY BE GREATER
THAN YOU THINK –Richard A. Burkhart, MD (Long)
REPLACEMENT THERAPY ON THE DEVELOPMENT
OF NON-ALCOHOLIC FATTY LIVER DISEASE AFTER
PANCREATICODUODENECTOMY, PAYING ATTENTION TO
ETIOLOGY OF DISEASES AND THE REMNANT PANCREATIC
VOLUME –Rie Sato (Short)
4:45 pm – 6:00 pm Scientific Program
Wine & Cheese Awards Reception
Presentation of three $1,000 awards
(2 for resident/fellow; 1 for junior faculty)
Closing Remarks
Grand Ballroom F-J
TABLE OF CONTENTS
19
POSTER LISTINGS
All posters located in Grand Ballroom F-J.
The ★ symbol indicates Poster of Distinction and they will be identified on the
poster board by GOLD dot. Authors will be available for short oral presentations
during the Poster Rounds with Professors.
Complete Poster Abstract descriptions are available online at www.pancreasclub.com.
FRIDAY, MAY 2, 2014
★P001 THE CLINICAL VALUE OF PERITONEAL CYTOLOGY IN 984 PATIENTS
WITH PANCREATIC CANCER WHO UNDERWENT CURATIVE RESECTION Sohei
Satoi, MD, FACS, Fuyuhiko Motoi, MD, Kenichiro Uemura, MD, Manabu Kawai, MD,
Masanao Kurata, MD, Masayuki Sho, MD, FACS, Ippei Matsumoto, MD, Hiroaki
Yanagimoto, MD, Michiaki Unno, MD, Hiroki Yamaue, MD, Goro Honda, MD,
FACS, Yoshiyuki Nakajima, MD, Makoto Shinzeki, MD, A-Hon Kwon, MD, Yoshiaki
Murakami, MD, Multicenter Study Group of Pancreatobiliary Surgery in Japan,
Osaka, JP
★P002 A 30-YEARS CELEBRATION OF FIRST DESCRIPTION OF CENTRAL
PANCREATECTOMY (THE DAGRADI-SERIO-IACONO OPERATION): HISTORICAL
OUTLINE AND SURGICAL OUTCOME Calogero Iacono, MD, Andrea Ruzzenente,
MD, PhD, Simone Conci, MD, PhD, Claudio Bacchelli, MD, Tommaso Campagnaro,
MD, Alessandro Valdegamberi, MD, Corrado Pedrazzani, MD, Francesca Bertuzzo,
MD, Alfredo Guglielmi, MD, Department of Surgery - Division of General Surgery
A - Unit of Hepato-Pancreatico-Biliary-Surgery - University of Verona Medical
School, Verona, Italy., Verona, IT
★P003 MORBIDITY AND MORTALITY OF PANCREATICODUODENECTOMY FOR
PREMALIGNANT PANCREATIC NEOPLASMS T
imothy E Newhook, MD, Damien J
LaPar, MD, MSc, James M Lindberg, MD, Todd W Bauer, MD, Reid B Adams, MD,
Victor M Zaydfudim, MD, MPH, University of Virginia, Charlottesville, US
★P004 PANCREATICODUODENECTOMY IN FLORIDA: DO 20 YEAR TRENDS
DOCUMENT SALUTARY BENEFITS OF CENTRALIZATION OF CARE? T
homas W
Wood, MD, Sharona B Ross, MD, Amanda E Smart, Carrie E Ryan, MS, Prashant B
Sukharamwala, MD, Alexander S Rosemurgy, MD, Florida Hospital Tampa, Tampa, US
★P005 DEFINING TREATMENT AND OUTCOMES OF HEPATICOJEJUNOSTOMY
FAILURE FOLLOWING PANCREATICODUODENECTOMY R
ichard A Burkhart,
MD, Daniel Relles, MD, Danielle M Pineda, MD, Patricia K Sauter, Ernest L Rosato,
MD, Harish Lavu, MD, Charles J Yeo, MD, Jordan M Winter, MD, Department of
Surgery, Jefferson Pancreas, Biliary, and Related Cancer Center, Thomas Jefferson
University, Philadelphia, PA, Philadelphia, US
★P006 A SERVICE BASED MID LEVEL PROVIDER UTILIZING PERI-OPERATIVE
PATHWAYS CAN REDUCE LENGTH OF STAY AND HOSPITAL COSTS RELATED TO
PANCREATICODUODENECTOMY PATIENTS W
Conway, MD, J Bolton, MD, Ochsner
Medical Center, New Orleans, US
TABLE OF CONTENTS
20
Poster Listings
POSTER LISTINGS
★P007 NEOADJUVANT FOLFIRINOX IN BORDERLINE RESECTABLE PANCREATIC
ADENOCARCINOMA Alessandro Paniccia, MD, Barish H Edil, MD, Richard D
Schulick, MD, MBA, Csaba Gajdos, MD, Joshua T Byers, MS, Cheryl Meguid, DNP,
ACNP, Martin D McCarter, MD, Department of General Surgery, University of
Colorado, Denver, USA, Denver, US
★P008 PANCREATIC PENETRATION OF MEROPENEM AND DOSAGE
CONSIDERATIONS BASED ON SITE-SPECIFIC PHARMACOKINETICPHARMACODYNAMIC ANALYSIS Naru Kondo, MD, Kazuro Ikawa, PhD, Yoshiaki
Murakami, MD, Kenichiro Uemura, MD, Takeshi Sudo, MD, Yasushi Hashimoto, MD,
Hiroki Ohge, MD, Norifumi Morikawa, PhD, Taijiro Sueda, MD, Department of Surgery,
Institute of Biomedical and Health Sciences, Hiroshima University, Hiroshima, JP
★P009 RESCUE ERCP AND EMERGENCY PANCREATIC DUCT STENT PLACEMENT
FOR THE MANAGEMENT OF POST-ERCP PANCREATITIS: RESULTS OF A LARGE
CASE SERIES AT THE DISTRICT HOSPITAL IN JAPAN Hiroyuki Hisai, MD, PhD,
Tasuku Hirako, MD, Yohei Arihara, MD, Yuuki Ikeda, MD, Yutaka Koshiba, MD,
Etsu Miyazaki, MD, PhD, Department of Gastroenterology, Japan Red Cross Date
General Hospital, Date, Japan, Date, JP
★P077 HIGH PHOSPHATE SERUM LEVELS CORRELATE WITH THE SEVERITY OF
EXPERIMENTAL SEVERE ACUTE PANCREATITIS - INSIGHT INTO THE PURINERGIC
SYSTEM Guilherme S Mazzini, MD, Daniel T Jost, Denise B Ramos, MS, Jean
P Oses, PhD, Mateus A Zeni, Rafael Machoseki, Luiza W Kist, PhD, Mauricio R
Boggo, PhD, Carla D Bonan, PhD, Maria I Edelweiss, MD, PhD, Marta M Duarte,
MS, Luis V Portela, PhD, Alessandro B Osvaldt, MD, PhD, Diogo O Souza, MD, PhD,
Universidade Federal do Rio Grande do Sul, Universidade Catolica de Pelotas,
Instituto Nacional de Ciencia e Tecnologia Translacional em Medicina (INCT-TM),
Pontificia Universidade Catolica do Rio Grande do Sul, Universidade Luterana do
Brasil., Porto Alegre, BR
P010 TARGETED THERAPY OF THE HEDGEHOG EFFECTOR GLI IN PANCREATIC
AND AMPULLARY CANCER K
im C Honselmann, MD, Moritz Pross, MD, Thomas
Brabletz, MD, PhD, Tobias Keck, MD, Phd, Ulrich F Wellner, PhD, MD, Dirk Bausch,
MD, PhD, Department of General, Visceral-, Thoracic- and Vascular Surgery,
University of Luebeck, Germany &Clinic for General and Visceral Surgery,
University Medical Center Freiburg, Germany, Luebeck, DE
P011 COMPOSITE ALTERATIONS IN GLYCOLYTIC METABOLISM AND AUTOPHAGY
ARE ASSOCIATED WITH POOR PROGNOSIS IN PANCREATIC DUCTAL CARCINOMA
A K Witkiewicz, MD, W B Wachsmann, MD, G H Baek, MD, J C Mansour, MD, Michael
A Choti, MD, E S Knudsen, MD, Departments of 1Surgery and 2Pathology, University
of Texas Southwestern Medical Center, Dallas, TX USA, Dallas, US
P012 THE EFFECT OF NEOADJUVANT CHEMORADIATION ON GENE EXPRESSION
PATTERNS OF PANCREATIC ADENOCARCINOMA Andrew M Baschnagel, MD,
Bryan J Thibodeau, PhD, Laura E Fortier, MS, Tim J Geddes, BS, Barbara L Pruetz,
BS, Billie E Ketelsen, BS, Brandon M Stone, MD, George D Wilson, PhD, Robert P
Jury, MD, William Beaumont Hospital, Royal Oak, US
Poster Listings
TABLE OF CONTENTS
21
POSTER LISTINGS
P013 HIGH-VOLUME SURGEONS: ARE THERE DIFFERENCES AMONG THE
BUSIEST ONES? P
rashant B Sukharamwala, MD, Sharona B Ross, MD, Amanda
E Smart, Franka Co, BS, Carry E Ryan, MS, Thomas W Wood, MD, Alexander S
Rosemurgy, MD, Florida Hospital Tampa, Tampa, US
P014 FROM THE OR TO THE MOUSE: WHAT INFLUENCES SUCCESSFUL PDX
ENGRAFTMENT? Andrea Porpiglia, MD, Igor Astsaturov, MD, PHD, Vladimir
Khazak, PhD, Harry S Cooper, MD, John P Hoffman, MD, Fox Chase Cancer Center,
Philadelphia, US
P015 EXPRESSION OF B7-H5 IN NORMAL PANCREAS AND PANCREATIC CANCER
Joshua T Byers, Yuwen Zhu, PhD, Alessandro Paniccia, MD, Nate W Kahn, PhD,
Lieping Chen, MD, PhD, Richard D Schulick, MD, Barish H Edil, MD, Department of
Surgery, University of Colorado, Denver, Colorado; Department of Immunology,
Yale University, New Haven, Connecticut, Denver, US
P016 THE NEW FULLY AUTOMATED SYSTEM FOR KI67 EVALUATION IN
PANCREATIC NEUROENDOCRINE TUMORS (PNET). WOULD IT BE POSSIBILE TO
OBTAIN A STANDARD TO GRADE EVALUATION? N
iccola Funel1,2, PhD, Piniccia
Faviana1, MD, Luca E Pollina1, MD, Vittorio Perrone2, MD, Fabio Caniglia2, MD, Ugo
Boggi2, MD, Fulvio Basolo1, MD, BSD, Daniela Campani1, MD, 1 Departement of
Surgery, Division of Surgical Pathology, University of Pisa, Italy; 2 Department of
Oncology, Division of General and transpant Surgery., Pisa, IT
P017 EVALUATING COMPARATIVE EFFECTIVENESS WITH OBSERVATIONAL
DATA: ENDOSCOPIC ULTRASOUND AND SURVIVAL IN PANCREATIC CANCER
Abhishek D Parmar, MD, Kristin M Sheffield, PhD, Yimei Han, MS, Gabriela M
Vargas, MD, Praveen Guturu, MD, Yong-Fang Kuo, PhD, James S Goodwin, MD,
Taylor S Riall, MD, PhD, UCSF-East Bay, University of Texas-Medical Branch,
Galveston, US
P018 MINIMAL CLINICAL IMPACT OF DIAGNOSTIC ERRORS IN CYSTIC TUMORS
OF THE PANCREAS M
arco Del Chiaro, MD, PhD, Associate, Professor, Ralf
Segersvard, MD, PhD, Ralf Segersvard, MD, PhD, Raffaella Pozzi Mucelli, MD, Elena
Rangelova, MD, Nikolaos Kartalis, MD, PhD, Christoph Ansorge, MD, PhD, Urban
Arnelo, MD, PhD, John Blomberg, MD, PhD, Matthias Lohr, MD, PhD, Professor,
Caroline Verbeke, MD, PhD, Division of Surgery, Department of Clinical Science,
Intervention and Technology (CLINTEC). Karolinska Institutet - Stockholm, Sweden,
Stockholm, SE
P019 THE EFFECT OF PREOPERATIVE BILIARY DRAINAGE ON SURGICAL
OUTCOME FOLLOWING PANCREATICODUODENECTOMY FOR PANCREAS HEAD
CANCER Kenichiro Uemura, MD, Yoshiaki Murakami, MD, Kawai Kawai, MD, Kenichi Okada, MD, Ippei Matsumoto, MD, Sadaki Asari, MD, Sohei Satoi, MD, Hiroaki
Yanagimoto, MD, Masayuki Sho, MD, Takahiro Akahori, MD, Goro Honda, MD,
Masanao Kurata, MD, Fuyuhiko Motoi, MD, Michiaki Unno, MD, Multicenter Study
Group of Pancreatobiliary Surgery (MSG-PBS), Hiroshima, JP
TABLE OF CONTENTS
22
Poster Listings
POSTER LISTINGS
P020 DETAILED ANALYSIS OF EMT AND TUMOR BUDDING IDENTIFIES
PREDICTORS OF LONG TERM SURVIVAL IN PANCREATIC DUCTAL
ADENOCARCINOMA Peter Bronsert, MD, Silvia Timme, MD, Ilona Kohler, MD,
Martin Werner, Prof, Dirk Bausch, MD, Ulrich T Hopt, Prof, Tobias Keck, Prof, Ulrich
F Wellner, MD, Clinic for Surgery UKSH Campus Lubeck, Institute of Pathology
University Medical Center Freiburg, Lubeck, DE
P021 WHO TRAVELS FOR CANCER CARE? REGIONALIZATION OF
PANCREATECTOMY IN MASSACHUSETTS L
indsay A Bliss*, MD, Theodore P
McDade**, MD, Zeling Chau**, MD, MPH, Jillian K Smith**, MD, Catherine J Yang*,
MD, Sing Chau Ng*, MS, Bruce B Cohen***, PhD, Giles F Whalen**, MD, Mark P
Callery*, MD, Jennifer F Tseng*, MD, MPH, *Department of Surgery, Beth Israel
Deaconess Medical Center; **Department of Surgery, UMass Memorial Medical
Center; ***Center for Health Information, Statistics, Research, and Evaluation,
Massachusetts Department of Public Health, Boston, US
P022 SINGLE-INSTITUTION EXPERIENCE WITH RESECTION OF SIDE-BRANCH
IPMN: A REVIEW OF PRE-OPERATIVE CHARACTERISTICS AND FINAL
PATHOLOGIC DIAGNOSIS John Dortch, MD, Michael Antiporda, MD, John A
Stauffer, MD, Horacio J Asbun, MD, Mayo Clinic- Florida, Jacksonville, US
P023 DOES ROUTINE DRAINAGE OF THE OPERATIVE BED FOLLOWING ELECTIVE
DISTAL PANCREATECTOMY REDUCE COMPLICATIONS? - AN ANALYSIS OF
THE ACS-NSQIP PANCREATECTOMY DEMONSTRATION PROJECT Stephen W
Behrman, MD, Ben Zarzaur, MD, Abhishek Parmer, MD, Taylor Riall, MD, Bruce Hall,
MD, Henry Pitt, MD, University of Tennessee Health Science Center, Memphis, US
P024 STRONG MEMBRANOUS EXPRESSION OF PLECTIN IS AN INDEPENDENT
PREDICTOR OF IMPROVED SURVIVAL AFTER RESECTION OF PANCREATIC HEAD
DUCTAL ADENOCARCINOMA M
oritz Pross, MD, Peter Bronsert, MD, Martin
Werner, Prof, Silvia Timme, MD, Frank Makowiec, Ulrich Hopt, Prof, Dirk Bausch,
MD, Tobias Keck, Prof, Ulrich F Wellner, MD, Clinic for Surgery, UKSH Campus
Lubeck, Germany; Institute of Pathology, University Medical Center Freiburg,
Germany, Lubeck, DE
P025 IMPACT OF PANCREATIC FISTULA ON RECURRENCE AND LONGTERM PROGNOSIS OF PERIAMPULLARY ADENOCARCINOMAS AFTER
PANCREATICODUODENECTOMY D
owan Kim, BSc, Pablo E Serrano, MD, MPH,
MSc, Peter T Kim, MD, Paul D Greig, MD, Carol-Anne Moulton, MD, PhD, Steven
Gallinger, MD, MSc, Alice C Wei, MD, CM, MSc, Sean P Cleary, MD, MPH, MSc,
Department Of Surgery, Toronto General Hospital,Toronto,ON, Windsor, CA
P026 A NOVEL APPROACH TO PATIENT EDUCATION: THE ICAREBOOK FOR
PANCREATIC CANCER Christopher L Wolfgang, MD, PhD, Toby Cornish, MD,
PhD, Michael Erdek, Kyoung ran Eun, Na’im K Fanaian, MD, Elliot K Fishman, MD,
Joseph M Herman, Daniel Laheru, MD, Joanna K Law, MD, Anne Marie Lennon,
MD, Corinne Sandone, Ralph H Hruban, MD, Departments of Pathology, Oncology,
Surgery, Radiation Oncology, Radiology, Gastroenterology, Anesthesia and 8Art
As Applied To Medicine; Sol Goldman Pancreatic Cancer Research Center, Johns
Hopkins University, Baltimore, MD, Baltimore, US
Poster Listings
TABLE OF CONTENTS
23
POSTER LISTINGS
P027 MODIFIED RADICAL ANTEGRADE MODULAR PANCREATOSPLENECTOMY
FOR ADENOCARCINOMA OF THE LEFT PANCREAS-SIGNIFICANCE OF EN BLOC
RESECTION INCLUDING THE ANTERIOR RENAL FASCIA H
irohisa Kitagawa, MD,
Hidehiro Tajima, MD, Hisatoshi Nakagawara, MD, Isamu Makino, MD, Tomoharu
Miyashita, MD, Hirofumi Terakawa, MD, Shinichi Nakanuma, MD, Masatoshi Shouji,
MD, Hironori Hayashi, MD, Hiroyuki Takamura, MD, Tetsuo Ohta, MD, Kanazawa
University, Kanazawa, JP
P028 IDENTIFICATION OF RESECTION FOR BRANCH DUCT TYPE IPMN S
eiko
Hirono, MD, Masaji Tani, MD, Manabu Kawai, MD, Ken-ichi Okada, MD, Motoki
Miyazawa, Atsushi Shimizu, MD, Yuji Kitahata, Hiroki Yamaue, Wakayama Medical
University, Wakayama, JP
P029 ROBOTIC ASSISTED PANCREATICODUODENECTOMY MAY BE ASSOCIATED
WITH AN INCREASED LIKELIHOOD OF RECEIVING ADJUVANT CHEMOTHERAPY
M Khreiss, MD, Murtaza Shakir, MD, Brian Boone, MD, Mazen Zenati, MD, PHD,
David Bartlett, MD, Amer Zureikat, MD, Herbert Zeh III, MD, Melissa Hogg, MD,
University of Pittsburgh Medical Center, Pittsburgh, US
P030 LEARNING CURVE FOR ROBOTIC DISTAL PANCREATECTOMY M Shakir, MD,
M Khreiss, MD, P M Polanco, MD, B A Boone, MD, M Zenati, MPH, M Hogg, MD, H
Zeh, MD, A H Zureikat, MD, University of Pittsburgh Medical Center, Pittsburgh, US
P031 COMPARISON OF TUMOR MARKERS FOR PREDICTING NON-FUNCTIONING
PANCREATIC NEUROENDOCRINE TUMOR OUTCOME Jovenel Cherenfant, MD,
Susan J Stocker, Mistry K Gage, MS, Brittany Lapin, MS, Edward Wang, PhD,
Jonathan C Silverstein, MD, Kathy Mangold, PhD, Tiffany A Thurow, MD, Melanie
Odeleye, MD, Karen L Kaul, MD, Curtis R Hall, MD, Ihab Lamzabi, MD, Paolo
Gattuso, MD, David J Winchester, MD, Robert W Marsh, MD, Kevin K Roggin,
MD, David J Bentrem, MD, Marshall S Baker, MD, Mark S Talamonti, MD, Richard
A Prinz, MD, NorthShore University HealthSystems, Evanston, IL, Jesse Brown
Medical Center, Chicago, IL, University of Chicago, Chicago, IL, Rush University
Medical Center, Chicago, IL, Munster, US
P032 PREDICTING AGGRESSIVE BEHAVIOR IN NON-FUNCTIONING PANCREATIC
NEUROENDOCRINE TUMORS Jovenel Cherenfant, MD, Susan J Stocker, Mistry K
Gage, MS, Hongyan Du, MS, Tiffany A Thurrow, MD, Melanie Odeleye, MD, Scott
Schimpke, MD, Karen L Kaul, MD, Curtis R Hall, MD, Ihab Lamzabi, MD, Paolo
Gattuso, MD, David J Winchester, MD, Robert W Marsh, MD, Kevin K Roggin, MD,
David J Bentrem, MD, Marshall S Baker, MD, Richard A Prinz, MD, Mark S Talamonti,
MD, NorthShore University HealthSystems, Evanston, IL, Northwestern Finberg
School of Medicine, Chicago, IL, Jesse Brown Medical Center, Chicago, IL, University
of Chicago, Chicago, IL, Rush University Medical Center, Chicago, IL, Munster, US
P033 SOCIOECONOMIC STATUS AND SURGICAL OUTCOMES AFTER REGIONAL
PANCREATECTOMY H
eidi Schmidt, MD, Nakul Valsangkar, MD, Molly E Kilbane,
Alexandra P Turner, MD, Michael G House, MD, Nicholas J Zyromski, MD, Attila
Nakeeb, MD, C. Max Schmidt, MD, Eugene P Ceppa, MD, Indiana University School
of Medicine, Department of Surgery, Indianapolis, US
TABLE OF CONTENTS
24
Poster Listings
POSTER LISTINGS
P034 RISK FACTORS FOR PANCREATIC FISTULA AFTER ROBOTIC
PANCREATICODUODENECTOMY P
atricio M Polanco, MD, Melissa E Hogg, MD,
Murtaza Shakir, MD, Mazen S Zenati, MD, M.Haroon Choudry, MD, Brian A Boone,
MD, Bartlett L David, MD, Herbert J Zeh, MD, Amer H Zureikat, MD, University of
Pittsburgh Medical Center, Pittsburgh, US
P035 FIRST REPORT OF A PROSPECTIVE TRIAL OF PROTON THERAPY AND
CONCOMITTANT CAPECITABINE FOR PATIENTS WITH NON METASTATIC
UNRESECTABLE PANCREATIC ADENOCARCINOMA R
omaine C Nichols, MD,
Christopher G Morris, MS, Thomas J George, MD, Robert A Zaiden, MD, Elizabeth
Johnson, MD, Bestoun H Ahmed, MD, Meng Wei Ho, PhD, Soon N Huh, PhD, Nancy
P Mendenhall, MD, Bradford S Hoppe, MD, University of Florida Proton Therapy
Institute, Jacksonville, Florida, Jacksonville, US
P036 PORTAL VENOUS RESECTION IN CANCER OF THE PANCREATIC HEAD:
WHAT ARE THE RELEVANT PREDICTORS OF SURVIVAL? Hryhoriy Lapshyn,
PhD, Ulrich Wellner, PhD, Birte Kulemann, PhD, Jens Hoeppner, PhD, Frank
Makowiec, Prof, Peter Bronsert, PhD, Dirk Bausch, PhD, Tobias Keck, Prof, Ulrich
Hopt, Prof, Uwe Wittel, PhD, Clinic for General and Visceral Surgery, University of
Freiburg Medical Center, Germany. Department of Surgery, University Hospital
of Schleswig-Holstein Campus Lubeck, Germany. Institute of Clinical Pathology,
University of Freiburg. Germany., Freiburg Im Br., DE
P037 THE CHANGING SPECTRUM OF SURGICALLY TREATED CYSTIC NEOPLASMS
OF THE PANCREAS J ennifer K Plichta, MD, MS, Jacqueline A Brosius, BS, Sam
Pappas, MD, Gerard J Abood, MD, MS, Gerard V Aranha, MD, Loyola University
Medical Center, Maywood, US
P038 SHOULD ALL BRANCH-DUCT IPMN’S BE RESECTED? J ennifer K Plichta, MD,
MS, Zachary Fridirici, MD, Anjali S Godambe, DO, Sherri Yong, MD, Sam Pappas,
MD, Gerard J Abood, MD, MS, Gerard V Aranha, MD, Loyola University Medical
Center, Maywood, US
P039 COMPARISON OF ROBOTIC VERSUS OPEN PANCREATICODUODENECTOMY
Brian A Boone, MD, Stephanie Downs-Canner, MD, Jennifer Steve, BS, Mazen S
Zenati, MD, PhD, Melissa E Hogg, MD, A. James Moser, MD, David L Bartlett, MD,
Haroon A Choudry, MD, Herbert J Zeh, MD, Amer H Zureikat, MD, University of
Pittsburgh; Beth Israel Deaconess, Pittsburgh, US
P040 TRENDS IN THE USE OF PRE-OPERATIVE RADIATION FOR
ADENOCARCINOMA OF THE PANCREAS IN THE UNITED STATES E
rin E Burke, MD,
Resident, Schelomo Marmor, PhD, Pamela Portschy, MD, Resident, Beth A Virnig, PhD,
Todd M Tuttle, MD, MS, Eric H Jensen, MD, University of Minnesota, Minneapolis, US
P041 INCREASED NUMBER OF PERINEURAL INVASION IS INDEPENDENTLY
ASSOCIATED WITH POOR SURVIVAL OF PATIENTS WITH RESECTABLE
PANCREATIC CANCER Naru Kondo, MD, Yoshiaki Murakami, MD, Kenichiro
Uemura, MD, Takeshi Sudo, Yasushi Hashimoto, MD, Hayato Sasaki, MD, Taijiro
Sueda, MD, Institute of Biomedical and Health Sciences Applied Life Sciences
Surgery, Hiroshima University, Hiroshima, JP
Poster Listings
TABLE OF CONTENTS
25
POSTER LISTINGS
P042 DOES PANCREATIC INTRAEPITHELIAL NEOPLASIA PREDICT RECURRENCE
OF PANCREATIC ADENOCARCINOMA OR DEVELOPMENT OF A SECOND
PRIMARY IN THE REMNANT GLAND? T
rang K Nguyen, MD, Jennifer Steve, Amer
H Zureikat, MD, Aatur D Singhi, MD, Herbert J Zeh, MD, University of Pittsburgh
Medical Center, Pittsburgh, US
P043 IRREVERSIBLE ELECTROPORATION IS SAFE AND FEASABLE FOR THE
CONTROL AND TREATMENT OF LOCALLY-ADVANCED AND BORDERLINERESECTABLE PANCREATIC CANCER: SHORT TERM RESULTS M
egan Winner,
MD, Irene Epelboym, MD, Michael D Kluger, MD, John A Chabot, MD, Columbia
University Medical Center New York Presbyterian Hospital, New York, US
P044 IS ROUX-Y BINDING PANCREATICO-JEJUNAL ANASTOMOSIS (BPJA)
FEASIBLE FOR PATIENTS UNDERGOING DISTAL PANCREATECTOMY? A
nne
Antila, MD, Juhani Sand, MD, PhD, Sari Raty, MD, PhD, Isto Nordback, MD, PhD,
Johanna Laukkarinen, MD, PhD, Dept. of Gastroenterology and Alimentary Tract
Surgery, Tampere University Hospital, Tampere, Finland., Tampere, FI
P045 LENGTH OF STAY AFTER PANCREATICODUODENECTOMY: WHAT IS THE
GOAL? Thomas W Wood, MD, Sharona B Ross, MD, Amanda E Smart, Diana
Fisler, Carrie E Ryan, MS, Paul G Toomey, MD, Kenneth Luberice, BS, Alexander S
P046 PATENCY RATES OF PORTAL VEIN/SUPERIOR MESENTERIC
VEIN RECONSTRUCTION AFTER PANCREATECTOMY FOR PANCREATIC
ADENOCARCINOMA A N Krepline, K Duelge, K K Christians, B George, P S Ritch, B
A Erickson, J P Thomas, A Mahmoud, E J Quebbeman, K K Turaga, F M Johnston, T
C Gamblin, D B Evans, S Tsai, Medical College of Wisconsin, Milwaukee, US
P047 PROPHYLACTIC ANTICOAGULATION FOR SUPERIOR MESENTERIC VEIN
(SMV) OR PORTAL VEIN (PV) NARROWING/OCCLUSION IN BORDERLINE
RESECTABLE (BLR) PANCREATIC ADENOCARCINOMA (PC) PATIENTS A
N
Krepline, K Duelge, B George, P S Ritch, B A Erickson, J P Thomas, A Mahmoud, E
J Quebbeman, K K Turaga, F M Johnston, T C Gamblin, K K Christians, D B Evans, S
Tsai, Medical College of Wisconsin, Milwaukee, US
P048 CLINICAL OUTCOMES IN PANCREATIC ADENOCARCINOMA ASSOCIATED
WITH BRCA2 MUTATION O
jas H Vyas, MD, Keith Leung, MD, Wasif M Saif, MD,
MBBS, Tufts University School of Medicine, Tufts Cancer Center, Boston, US
P049 STEREOTACTIC BODY RADIATION THERAPY FOR PANCREATIC CANCER:
THE JOHNS HOPKINS EXPERIENCE Shalini Moningi, BA, Siva P Raman, MD, Avani
S Dholakia, BS, Amy Hacker-Prietz, MS, Timothy M Pawlik, MD, PhD, Lei Zheng,
MD, Matthew J Weiss, MD, Daniel A Laheru, MD, Christopher L Wolfgang, MD,
PhD, Joseph M Herman, MD, Msc, Johns Hopkins Hospital, Baltimore, US
P050 INVASIVE IPMN: TWO DISTINCT PATTERNS OF MICROSCOPIC INVASION
WITH DIFFERENT BIOLOGY J ason F Solus, MD, Ladan Fazlollahi, MD, MPH, Carlos
Fernandez-Del Castillo, MD, Giovanni Marchegiani, MD, Martha B Pitman, MD, Mari
Mino-Kenudson, MD, Massachusetts General Hospital, Boston, US
TABLE OF CONTENTS
26
Poster Listings
POSTER LISTINGS
P051 PRE-SBRT METABOLIC TUMOR VOLUME AND TOTAL LESION GLYCOLYSIS
PREDICT IMPROVED SURVIVAL IN PATIENTS WITH LOCALLY ADVANCED
PANCREATIC CANCER RECEIVING STEREOTACTIC BODY RADIATION THERAPY
Avani S Dholakia, BS, Muhammad Chaudhry, MD, Daniel T Chang, MD, Jeffrey P
Leal, BA, Amy Hacker-Prietz, PAC, Zheng Su, Matthew J Weiss, MD, Katherine
E Oteiza, MS, Mary E Griffith, BSN, Richard L Wahl, MD, Erik Tryggestad, PhD,
Timothy Pawlik, MD, MBA, Daniel A Laheru, MD, Christopher L Wolfgang, MD, PhD,
Albert C Koong, MD, PhD, Joseph M Herman, MD, MSc, Johns Hopkins Universtiy
School of Medicine and Stanford University School of Medicine, Baltimore, US
P052 WITHDRAW
P053 FINANCIAL BENEFITS OF A HEPATOPANCREATICOBILIARY PROGRAM
Sharona B Ross, MD, Richard L Klein, Carrie E Ryan, MS, Thomas W Wodd, MD,
Prashant B Sukharamwala, MD, Alexander S Rosemurgy, MD, Florida Hospital
Tampa, Tampa, US
P054 HIGH-VOLUME HOSPITALS WITH HIGH AND LOW VOLUME SURGEONS:
IS THERE A ‘FIELD EFFECT FOR PANCREATICODUODENECTOMY? T
homas W
Wood, MD, Sharona B Ross, MD, Amanda E Smart, Carrie E Ryan, MS, Prashant B
Sukharamwala, MD, Alexander S Rosemurgy, MD, Florida Hospital Tampa, Tampa, US
P055 WITHDRAW
P056 COST-EFFECTIVENESS AFTER PANCREATICODUODENECTOMY:
BOLSTERING THE VOLUME ARGUMENT Jeffrey M Sutton, MD, Gregory C Wilson,
MD, Koffi Wima, MS, Dennis J Hanseman, PhD, Ralph C Quillin III, MD, Ian M
Paquette, MD, Jeffrey J Sussman, MD, Michael J Edwards, MD, Syed A Ahmad,
MD, Shimul A Shah, MD, Daniel E Abbott, MD, Cincinnati Clinical Research Group
in Surgery, Department of Surgery, University of Cincinnati Medical Center,
Cincinnati, OH, Cincinnati, US
P057 PANCREATICODUODENECTOMY FOR PANCREATIC CANCER: IS THERE A
SURVIVAL DIFFERENCE FOR PLANNED VERSUS UNPLANNED PORTAL VEIN
RESECTION? Y
asushi Hashimoto, MD, Yoshiaki Murakami, MD, Kenichiro Uemura,
MD, Takeshi Sudo, MD, Naru Kondo, MD, Sasaki Hayato, MD, Ohge Hiroki, MD,
Taijiro Sueda, MD, Department of Surgery, Division of Clinical Medical Science,
Programs for Applied Biomedicine, Hiroshima University, Hiroshima, JP
P058 PERIOPERATIVE AND LONG TERM OUTCOME AFTER EXTENDED (PORTAL
VEIN, MULTIVISCERAL) RESECTION FOR CANCER OF THE PANCREATIC HEAD
Birte Kulemann, MD, Uwe Wittel, MD, Ulrich F Wellner, MD, Tobias Keck, MD,
Peter Bronsert, MD, Ulrich T Hopt, MD, Jens Hoeppner, MD, Frank Makowiec, MD,
Department of Genral &Visceral Surgery, Department of Pathology, University
Hosptial Freiburg, Freiburg, Germany, Freiburg, GE
P059 CT SIGNS SUGGESTING MALIGNANCY IN BRANCH DUCT TYPE IPMNS
Carla Cappelli, PhD, Rosa Cervelli, MD, Salvatore Mazzeo, MD, Mario Belluomini,
MD, Daniela Campani, MD, Ugo Boggi, MD, Carlo Bartolozzi, MD, Diagnostic and
Interventional Radiology-University of Pisa, Pisa, IT
Poster Listings
TABLE OF CONTENTS
27
POSTER LISTINGS
P060 IS ANTACID THERAPY AFTER PANCREATODUODENECTOMY NECESSARY?
CONTEMPORARY GLOBAL PRACTICE OF PANCREATIC SURGEONS James R
Butler, MD, Eugene P Ceppa, MD, Michael G House, MD, Attila Nakeeb, MD, C.
M Schmidt, MD, Phd, Nicholas J Zyromski, MD, Department of Surgery, Indiana
University School of Medicine, Indianapolis, US
P061 EFFECTS OF GEMCITABINE AND STEREOTACTIC BODY RADIOTHERAPY
ON QUALITY OF LIFE IN LOCALLY ADVANCED PANCREATIC CANCER A
vani S
Dholakia, BS, Daniel T Chang, MD, Karyn A Goodman, MD, Elizabeth Sugar, PhD,
Amy Hacker-Prietz, PAC, Laurie Ann Columbo, BSN, Mary E Griffith, BSN, Aaron
T Wild, BA, Timothy M Pawlik, MD, MBA, George A Fisher, MD, PhD, Susannah
Ellsworth, MD, Albert Koong, MD, PhD, Joseph M Herman, MD, MSc, Johns
Hopkins Universtiy School of Medicine, Stanford University School of Medicine,
and Memorial Sloan Kettering Cancer Center, Baltimore, US
P062 FEASIBILITY OF RESECTION AFTER INDUCTION THERAPY FOR LOCALLY
ADVANCED PANCREATIC CANCER A Amini, MD, A N Krepline, BS, A Mahmoud, BS,
K Duelge, BS, B George, MD, P S Ritch, MD, B A Erickson, MD, K K Christians, MD, D
B Evans, MD, S Tsai, MD, Medical College of Wisconsin, Milwaukee, US
P063 PROGNOSTIC IMPACT OF SINGLE LYMPH NODE STATIONS IN RESECTED
PANCREATIC HEAD CANCER G
iuseppe Malleo, MD, Laura Maggino, MD, Francesco
Gulino, Md, Eleonora Morelli, MD, Giovanni Butturini, PhD, Claudio Bassi, MD,
Roberto Salvia, PhD, Unit of Surgery B, The Pancreas Institute, University of
Verona Hospital Trust; Unit of Pathology, The Pancreas Institute University of
Verona Hospital Trust, Verona, IT
P064 PERIOPERATIVE RISK FACTORS FOR DELAYED GASTRIC EMPTYING
FOLLOWING PANCREATICODUODENECTOMY J amie Robinson, MD, Paula
Marincola, BA, Julia Shelton, MD, MPH, Kamran Idrees, MD, Nipun Merchant, MD,
Alexander Parikh, MD, MPH, Vanderbilt University Medical Center, Nashville, US
P065 INCIDENCE OF ADDITIONAL PRIMARY MALIGNANCIES IN PATIENTS WITH
PANCREATIC NEUROENDOCRINE TUMORS AND CARCINOID Jamie Robinson, MD,
Rondi Kauffmann, MD, MPH, Li Wang, MS, Sharon Phillips, MS, Kamran Idrees, MD,
Nipun Merchant, MD, Alexander Parikh, MD, MPH, Vanderbilt University Medical
Center, Nashville, US
P066 LAPAROSCOPIC PANCREATICOJEJUNAL ANASTOMOSIS DURING TOTAL
LAPAROSCOPIC PANCREATICODUODENECTOMY FOR PANCREATIC CANCER: IS
THERE A TEHNIQAL PREFERENCE? I gor E Khatkov - 1,2, Professor, MD, PhD, Victor
V Tsvirkun - 1, Professor, MD, PhD, Roman E Izrailov - 1,2, Professor, MD, PhD, Pavel
S Tyutyunnik, MD, 1 - Moscow Scientific Research Institute of Gastroenterology; 2 Moscow State University of Medicine and Dentistry, Moscow, RU
P067 THE SAFETY AND EFFICACY OF PANCREATIC DUCT STENT PLACEMENT
IN THE EMERGENCY ERCP OF ACUTE BILIARY PANCREATITIS H
iroyuki Hisai, MD,
PhD, Tasuku Hirako, MD, Yohei Arihara, MD, Yuuki Ikeda, MD, Yutaka Koshiba, MD,
Etsu Miyazaki, MD, PhD, Department of Gastroenterology, Japan Red Cross Date
General Hospital, Date, Japan, Date, JP
TABLE OF CONTENTS
28
Poster Listings
POSTER LISTINGS
P068 FEASIBILITY AND OUTCOMES OF ROBOTICS IN THE SURGICAL
MANAGEMENT OF PANCREATIC NECROSIS AND PSEUDOCYSTS R
amanathan M
Seshadri, MD, Ryan Z Swan, MD, David Sindram, MD, PhD, David A Iannitti, MD,
John B Martinie, MD, Carolinas Medical Center, Charlotte, US
★P069 QUANTIFYING THE BURDEN OF PERIOPERATIVE COMPLICATIONS
FOLLOWING TOTAL PANCREATECTOMY USING THE POSTOPERATIVE
MORBIDITY INDEX: A MULTI-INSTITUTIONAL PERSPECTIVE Jashodeep Datta,
MD, Russell S Lewis Jr., BA, Steven M Strasberg, MD, Bruce L Hall, MD, Charles M
Vollmer Jr, MD, The PMI Study Group, University of Pennsylvania Perelman School
of Medicine, Philadelphia, PA; Washington University School of Medicine, St. Louis,
MO, Philadelphia, US
★P070 BRAUN ENTEROENTEROSTOMY AFFECTS DELAYED GASTRIC
EMPTYING AFTER PYLORUS-PRESERVING PANCREATODUODENECTOMY:
A RETROSPECTIVE REVIEW Yusuke Watanabe, MD, Takao Ohtsuka, MD, PhD,
Hideyo Kimura, MD, Taketo Matsunaga, MD, Koji Tamura, MD, Noboru Ideno, MD,
Teppei Aso, MD, Yoshihiro Miyasaka, MD, PhD, Junji Ueda, MD, PhD, Shunichi
Takahata, MD, PhD, Masao Tanaka, MD, PhD, FACS, Department of Surgery and
Oncology, Graduate School of Medical Sciences, Kyushu University, Fukuoka,
Japan, Fukuoka, JP
★P071 SINGLE INSTITUTION EXPERIENCE WITH NEOADJUVANT TREATMENT
OF BORDERLINE RESECTABLE PANCREATIC ADENOCARCINOMA: ACHIEVING
R0 RESECTION WITH MODERN CHEMOTHERAPY N
athan Bolton, MD, William
Conway, MD, John Bolton, MD, Ochsner Clinic Foundation, New Orleans, US
★P072 A MULTIDISCIPLINARY CLINIC FOR PANCREATIC CANCER IMPROVES
UTILIZATION OF THERAPY Suzanne C Schiffman, MD, Yongli Shuai, PhD, Ying
Ding, PhD, Cindy Valko, Sharon Winters, David L Bartlett, MD, Amer H Zureikat,
MD, Herbert J Zeh, MD, Melissa E Hogg, MD, University of Pittsburgh Medical
Center, Pittsburgh, US
★P073 PANCREATICODUODENECTOMY WITH MAJOR VASCULAR RESECTION:
A COMPARISON OF LAPAROSCOPIC VERSUS OPEN APPROACHES K
ristopher P
Croome, MD, MS, Michael B Farnell, MD, Mark J Truty, MD, Kaye Reid-Lombardo,
MD, Florencia G Que, MD, David M Nagorney, MD, Michael L Kendrick, MD, Mayo
Clinic, Rochester, US
★P074 READMISSION AFTER PANCREATICODUODENECTOMY: THE INFLUENCE
OF THE VOLUME EFFECT BEYOND MORTALITY J effrey M Sutton, MD, Gregory C
Wilson, MD, Koffi Wima, MS, Ralph C Quillin III, MD, Dennis J Hanseman, PhD, Ian
M Paquette, MD, Jeffrey J Sussman, MD, Syed A Ahmad, MD, Shimul A Shah, MD,
Daniel E Abbott, MD, Cincinnati Clinical Research Group in Surgery, Department of
Surgery, University of Cincinnati Medical Center, Cincinnati, OH, Cincinnati, US
Poster Listings
TABLE OF CONTENTS
29
POSTER LISTINGS
★P075 COHORT STUDY OF THE INCIDENCE OF EXTRAPANCREATIC NEOPLASMS
DURING CLINICAL AND RADIOLOGIC SURVEILLANCE OF PATIENTS WITH
BRANCH-DUCT IPMN G
iuseppe Malleo, MD, Giovanni Marchegiani, MD, Alex Borin,
MD, Federico Accordini, Md, Claudio Bassi, MD, Roberto Salvia, Unit of Surgery B,
The Pancreas Institute, University of Verona Hospital Trust, Verona, IT
★P076 OPERATIVE MORTALITY AFTER MAJOR PANCREATIC CANCER SURGERY
IN NEW YORK STATE - HAS A REGIONALIZATION MADE A DIFFERENCE? A 10-YEAR
ANALYSIS P
ragatheeshwar Thirunavukarasu, MD, Chetasi Talati, MD, Kristopher
Attwood, Boris W Kuvshinoff, MD, Roswell Park Cancer Institute, Buffalo, US
★P077 Moved to Friday, May 2 viewing (see page 21 for details)
★P078 LONG-TERM OUTCOMES FAVOR PYLORUS PRESERVING
PANCREATICODUODENECTOMY OVER DUODENUM PRESERVING PANCREATIC
HEAD RESECTION FOR CHRONIC PANCREATITS: A META-ANALYSIS AND
SYSTEMATIC REVIEW Prashant B Sukharamwala, MD, Sharona B Ross, MD, S
Parikh, Carrie E Ryan, MS, Thomas W Wood, MD, Alexander S Rosemurgy, MD,
Florida Hospital Tampa, Tampa, US
P079 A COMPLEX CASE OF PANCREATIC DUCTAL ADENOCARCINOMA
FORMING TWO MASS LESIONS: MOLECULAR AND FUNCTIONAL ANALYSIS A
K Witkiewicz, MD, R Kittler, PhD, J C Mansour, MD, E S Knudsen, MD, M A Choti,
MD, Departments of Surgery and Pathology, University of Texas Southwestern
Medical Center, Dallas, TX USA, Dallas, US
P080 REDUCTION OF DEOXYCYTIDINE KINASE(DCK) PROTEIN EXPRESSION
LEVEL AND ENZYME ACTIVITY WERE CAUSE OF GEMCITABINE ACQUIRED
RESISTANCE IN PANCREATIC CANCER CELLS Kei Kawaguchi, PhD, Fuyuhiko Motoi,
PhD, Shinichi Egawa, PhD, Michiaki Unno, PhD, Division of Hepato-Bilialy Pancreatic
Surgery, Department of Surgery, Tohoku University Hospital, Sendai, Miyagi, JP
P081 REPEATED NON-INVASIVE RADIOFREQUENCY TREATMENT OF
PANCREATIC CANCER CELLS DEMONSTRATES SUSTAINED EFFECTIVENESS AND
IMPROVED SUPPRESSION OF CANCER CELL PROLIFERATION H
op S Tran Cao,
MD, Warna D Kaluarachchi, MS, Jonathan C Vo, BS, Douglas C Huynh, BS, Steven
A Curley, MD, Department of Surgical Oncology, U.T. MD Anderson Cancer Center,
Houston, TX; University of Texas Health Science Center at Houston Medical School,
Houston, TX, Houston, US
P082 OXALIPLATIN AND 5-FU UPREGULATE B7-H1 EXPRESSION IN HUMAN
PANCREATIC CANCER CELL LINES A
lessandro Paniccia, MD, Yuwen Zhu, PhD,
Joshua T Byers, MS, Nate W Kahn, PhD, Sanjana Mehrotra, MD, Richard D
Schulick, MD, MBA, Barish H Edil, MD, Department of General Surgery, University
of Colorado, Denver, Colorado, USA, Denver, US
TABLE OF CONTENTS
30
Poster Listings
POSTER LISTINGS
P083 GEMCITABINE- UKRAIN COMBINATION TREATMENT MODULATES MMP9
EXPRESSION IN PRIMARY PANCREATIC ADENOCARCINOMA CELL CULTURES
Lucia Botta1, MSD, Maria Denaro1, BSD, Alessandra Alvino1, BSD, Claudio Ricci1,
PhD, Luca E Pollina1, MD, Fabio Caniglia2, MD, Nelide De Lio2, MD, Ugo Boggi2, MD,
Daniela Campani1, MD, Niccola Funel1,2, PhD, 1 Department of Surgery, Division of
Surgical Pathology, University of Pisa, Italy; 2 Department of Oncology, Division of
General and transplant Surgery, University of Pisa, Italy, Pisa, IT
P084 IL-35 PROMOTES PANCREAS CANCER GROWTH THROUGH ENHANCEMENT
OF PROLIFERATION AND INHIBITION OF APOPTOSIS M
ichael B Nicholl, MD,
Chelsea L Ledgerwood, BS, Xuhui Chen, MD, Alberto Diaz-Arias, MD, Yujiang Fang,
MD, PhD, Qian Bai, BA, Chenglu Qin, MD, University of Missouri, Columbia, US
P085 SURGERY AS AN UNDERUTILIZED TREATMENT MODALITY IN PATIENTS
WITH LOCALIZED PANCREATIC CANCER - A NATIONAL ANALYSIS OF TRENDS
AND OUTCOMES M
adeleine Strohl, BA, Siavash Raigani, BA, John Ammori, MD,
Jeffrey Hardarce, MD, Julian Kim, MD, Case Western Reserve University School of
Medicine, Division of Surgical Oncology University Hospital Case Medical Center,
Cleveland, OH, Shaker Heights, US
P086 THE RIGHT HEPATIC ARTERY FROM THE GASTRODUODENAL ARTERY AT
PANCREATODUODENECTOMY D
isi Hao, Dongzhu Mao, Heilongjiang Provincial
Hospital, Harbin, CN
P087 AN ORGANIC IMPEDIMENT MIGHT BE ONE OF RISK FACTOR
OF DELAYED GASTRIC EMPTYING AFTER PYLORUS PRESERVING
PANCREATICODUODENECTOMY H
isashi Kosaka, MDPhD, Nobukazu Kuroda,
Kazuhiro Suzumura, Yugo Uda, Seikan Hai, Yuichi Kondo, Syogo Tanaka, Ikuo
Nakamura, Yasukane Asano, Toshihiro Okada, Tadamichi Hirano, Yuji Iimuro, Jiro
Fujimoto, Hyogo College of Medicine, Dept of Surgery, Nishinomiya, JP
P088 A CASE REPORT OF DISTAL PANCREATECTOMY WITH EN BLOCK CELIAC AXIS
RESECTION (DP-CAR) WITHOUT PREOPERATIVE INTERVENTIONAL ARTERIAL
EMBOLISM FOR PANCREATIC BODY CANCER INVADED TO CELIAC AXIS WITH
REPLACED RIGHT HEPATIC ARTERY T
oshiyuki Moriya, MD, PhD, Koichiro Ozawa, MD,
PhD, Shigeo Hasegawa, MD, PhD, Masaomi Mizutani, MD, PhD, Takayuki Higashi, MD,
Yukinori Kamio, MD, PhD, Moriyoshi Yokoyama, MD, Ai Takahashi, MD, Satoshi Takai,
MD, Osamu Usuba, MD, PhD, Okitama general hospital, Kawanishi-machi, JP
P089 LAPAROSCOPIC PYLORUS-PRESERVING PANCREATODUODENECTOMY
WITH DOUBLE JEJUNAL LOOP RECONSTRUCTION. INITIAL EXPERIENCE WITH
12 CASES Marcel Machado, MD, Fabio Makdissi, MD, Rodrigo Surjan, MD, Marcel C
Machado, MD, university of sao paulo, Sao Paulo, BR
P090 SINGLE PORT LAPAROSCOPIC DISTAL PANCREATECTOMY. INITIAL
EXPERIENCE WITH 14 CASES M
arcel A Machado, MD, Fabio Makdissi, MD, Rodrigo
Surjan, MD, Marcel C Machado, university of sao paulo, Sao Paulo, BR
P091 SAFE TECHNIQUE FOR DISTAL PANCREAS RESECTION WITH POLYSORB
CLIP IN THE VIEW OF 150 CASES G
yula Farkas Jr., PhD, Gyula Farkas, DSc, Gyorgy
Lazar, DSc, University of Szeged Department of Surgery, Szeged, HU
Poster Listings
TABLE OF CONTENTS
31
POSTER LISTINGS
P092 THE IMPACT OF PRESERVATION OF THE LEFT GASTRIC ARTERY IN
DISTAL PANCREATECTOMY WITH CELIAC AXIS EN-BLOC RESECTION (DP-CAR):
PROPOSAL OF A NOVEL SURGICAL TECHNIQUE TO REDUCE DELAYED GASTRIC
EMPTYING H
iroki Yamaue, MD, Manabu Kawai, MD, Ken-ichi Okada, MD, Masaji
Tani, MD, Seiko Hirono, MD, Motoki Miyazawa, MD, Atsushi Shimizu, MD, Yuji
Kitahata, MD, Second Department of Surgery, Wakayama Medical University,
Japan, Wakayama, JP
P093 PROGNOSTIC SIGNIFICANCE OF ZEB1 IN STROMAL AND CANCER CELLS IN
PANCREATIC HEAD CANCER P
eter Bronsert, MD, Dirk Bausch, MD, Silvia Timme,
MD, Martin Werner, Prof, Ulrich T Hopt, Prof, Tobias Keck, Prof, Ulrich F Wellner,
MD, Clinic for Surgery UKSH Campus Lubeck, Institute of Pathology University
Medical Center Freiburg, Lubeck, DE
P094 HOSPITAL READMISSION AFTER PANCREATICODUODENECTOMY IN A
HIGH VOLUME CENTER J. Bart Rose, MD, Flavio Rocha, MD, Adnan Alseidi, MD,
Thomas Biehl, MD, Farzad Alemi, MD, Scott Helton, MD, Virginia Mason Medical
Center, Seattle, US
P095 SHORT TERM OUTCOMES OF THE WHIPPLE AT THE SPLENIC ARTERY
(WATSA) PROCEDURE M
ajor K Lee, IV, MD, PhD, Roheena Z Panni, MD, William
G Hawkins, MD, Ryan C Fields, MD, David C Linehan, MD, Steven M Strasberg,
Washington University in St. Louis, St. Louis, US
P096 HEPATO-PANCREATO-BILIARY SURGERY IN CANADA: WORKFORCE AND
WAIT TIMES Janet Edwards, MD, MPH, Alexsander Bressan, MD, Sean C Grondin,
MD, MPH, Indraneel Datta, MD, MScHEPM, Elijah Dixon, MD, MScEpi, Chad G Ball,
MD, MScEpi, University of Calgary, Calgary, CA
P097 PANCREATIC TEXTURE-TAILORED RECONSTRUCTION TECHNIQUE IN
PANCREATIC HEAD RESECTIONS: SUPERIORITY OF PANCREATOGASTROSTOMY
(PG) VS. PANCREATICO-JEJUNOSTOMY (PJ) IN HIGH RISK ANASTOMOSES G
Alsfasser, MD, J Bochow, MS, A L Kutsch, MS, E Klar, MD, B Rau, MD, University of
Rostock, Rostock, DE
P098 PREDICTORS AND DIAGNOSTIC STRATEGIES OF EARLY STAGE
PANCREATIC DUCTAL ADENOCARCINOMA: A RETROSPECTIVE REVIEW H
ideyo
Kimura, Takao Ohtsuka, Taketo Matsunaga, Yusuke Watanabe, Koji Tamura,
Noboru Ideno, Teppei Aso, Yoshihiro Miyasaka, Junji Ueda, Shunichi Takahata,
Kazuhiro Mizumoto, Masao Tanaka, Department of Surgery and Oncology,
Graduate School of Medical Sciences Kyushu University, Fukuoka-city, JP
P099 CO-DELIVERY OF GEMCITABINE AND MI$-205 IN POLYMERIC MICELLES
FOR THE TREATMENT OF PANCREATIC CARCINOMA Deepak Chitkara, PhD,
Anupama Mittal, PhD, Stephen W Behrman, MD, Ram I Mahato, PhD, University
of Nebraska Medical Center; University of Tennessee Health Science Center,
Memphis, US
P100 DOES LAPAROSCOPIC DISTAL PANCREATECTOMY REDUCE THE RATE OF
READMISSIONS? J anak A Parikh, MD, MSHS, Scott Bendix, MD, Farrukh Jabbar, MD,
Michael J Jacobs, MD, FACS, St John Providence Hospital, Southfield, MI, Novi, US
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Poster Listings
POSTER LISTINGS
P101 EN BLOC TRANSECTION OF PANCREATIC PARENCHYMA AND SPLENIC
VESSELS IN DISTAL PANCREATECTOMY: A SAFE AND NOVEL TECHNIQUE Janak
A Parikh, MD, MSHS, Farrukh Jabbar, MD, Scott Bendix, MD, Michael J Jacobs, MD,
FACS, St John Providence Hospital, Southfield, MI, Novi, US
P102 ISOLATED ROUX-EN-Y DRAINAGE OF THE PANCREATIC STUMP
REDUCED THE AMYLASE LEVEL IN THE DRAINAGE FLUID AFTER DISTAL
PANCREATECTOMY WITH EN-BLOC CELIAC AXIS RESECTION K
en-ichi Okada,
Masaji Tani, Manabu Kawai, Seiko Hirono, Motoki Miyazawa, Atsushi Shimizu, Yuji
Kitahata, Hiroki Yamaue, Second Department of Surgery, Wakayama Medical
University, Wakayama, JP
P103 PANCREATIC ADENOCARCINOMA IN YOUNG PATIENTS: A SINGLE
INSTITUTION EXPERIENCE OVER 32 YEARS F
arzad Alemi, MD, Jessica Koller, MD,
Sameer Damle, MD, Thomas Biehl, MD, Adnan Alseidi, MD, Scott Helton, MD, Flavio
G Rocha, MD, Virginia Mason Medical Center, Seattle, US
P104 BENEFIT OF PANCREATICODUODENECTOMY WITH RESECTION OF PORTAL
OR SUPERIOR MESENTERIC VEIN FOLLOWING CHEMORADIOTHERAPY IN
PATIENTS WITH PANCREATIC DUCTAL ADENOCARCINOMA S
hugo Mizuno,
Masashi Kishiwada, Akihiro Tanemura, Yasuhiro Murata, Naohisa Kuriyama,
Yoshinori Azumi, Masanobu Usui, Hiroyuki Sakurai, Masami Tabata, Shuji Isaji,
Department of Hepatobiliary Pancreas and Transplant Surgery, Mie University,
Tsu, Mie, JP
P105 PREDICTORS OF OUTCOME IN RESECTED AMPULLARY CARCINOMA, A
SINGLE INSTITUTION EXPERIENCE Joyce Wong, MD, Zachary Thompson, PhD,
Barbara Centeno, MD, Evita Henderson-Jackson, MD, Christy Chai, MD, Pamela J
Hodul, MD, Moffitt Cancer Center, Harrisburg, US
P106 PANCREATICO-JEJUNOSTOMY ON ISOLATED LOOP AFTER
PANCREATICODUODENECTOMY: THE INCIDENCE AND SEVERITY OF
POSTOPERATIVE PANCREATIC FISTULA Gennaro Clemente, MD, AgostinoMaria
De Rose, MD, Alessandro Coppola, MD, Gennaro Grande, MD, Lucia Ionta, MD,
Marino Murazio, MD, Felice Giuliante, MD, Gennaro Nuzzo, MD, Department of
Surgery-Hepatobiliary Unit; A. Gemelli Med School - Rome, Italy, Rome, IT
P107 POSTOPERATIVE NUTRITIONAL EVALUATION USING GERIATRIC
NUTRITIONAL RISK INDEX (GNRI) FOR MATURE PATIENTS WITH
PANCREATODUODENECTOMY Y
uichi Kitagawa, MD, Yasuji Kawabata, MD, Ken
Fujishiro, MD, Shinji Fukata, MD, Department of Surgery and Intensive Care,
Division of Surgery National Center for Geriatrics and Gerontology, Obu, JP
P108 PROGNOSTIC IMPACT OF HUMAN EQUILIBRATIVE NUCLEOSIDE
TRANSPORTER 1 AND RIBONUCLEOTIDE REDUCTASE SUBUNIT 1 EXPRESSION
IN CHOLANGIOCARCINOMA PATIENTS TREATED WITH ADJUVANT
GEMCITABINE-BASED CHEMOTHERAPY Hayato Sasaki, Yoshiaki Murakami,
Kenichiro Uemura, Takeshi Sudo, Yasushi Hashimoto, Naru Kondo, Taijiro Sueda,
Department of Surgery, Institute of Biomedical and Health Sciences, Hiroshima
University, Hiroshima, JP
Poster Listings
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POSTER LISTINGS
P109 A NEW SURGICAL TECHNIQUE FOR PANCREATIC HEAD-BODY CANCER
WITH SPLENIC ARTERY INVASION: PANCREATICODUODENECTOMY WITH THE
SPLENIC ARTERY RESECTION (PD-SAR) Ryosuke Desaki, MD, Masashi Kisiwada,
MDPhD, Syugo Mizuno, MDPhD, Akihiro Tanemura, MDPhD, Yasuhiro Murata,
MDPhD, Yoshinori Azumi, MDPhD, Naohisa Kuriyama, MDPhD, Masanobu Usui,
MDPhD, Hiroyuki Sakurai, MDPhD, Masami Tabata, MDPhD, Syuji Isaji, MDPhD,
Department of Hepatobiliary Pancreas and Transplant Surgery, Mie University
Graduate School of Medicine, Tsu, JP
P110 SPYGLASS SINGLE OPERATOR PERORAL CHOLANGIOSCOPY (SOC) SEEMS
PROMISING IN THE EVALUATION OF PRIMARY SCLEROSING CHOLANGITIS
(PSC) RELATED BILIARY STRICTURES: A CASE SERIES AND INITIAL EXPERIENCE
FROM A TERTIARY REFERRAL CENTER Antti Siiki, MD, Irina Rinta-Kiikka, MD, PhD,
Tarmo Koivisto, MD, PhD, Kaija Vasama, MD, PhD, Juhani Sand, MD, PhD, Johanna
Laukkarinen, MD, PhD, Dept. of Gastroenterology and Alimentary Tract Surgery1,
Department of Clinical Radiology2, and Dept. of Pathology, Fimlab Laboratories3,
Tampere University Hospital, Tampere, Finland, Tampere, FI
P111 ROLE OF SURGICAL PALLIATION IN PATIENTS WITH PANCREATIC DUCTAL
ADENOCARCINOMA (PDAC) Ammara Abbasi, MD, Ruby J Lo, MD, A. James Moser, MD,
FACS, Jennifer F Tseng, MD, FACS, Charles M Vollmer Jr., MD, FACS, Mark P Callery, MD,
FACS, Tara S Kent, MD, FACS, Department of Surgery, Beth Israel Deaconess Medical
Center; Department of Surgery, University of Pennylvania, Boston, US
P112 STAPLED GASTROJEJUNOSTOMY AND JEJUNOJEJUNOSTOMY
ANASTOMOSIS REDUCES DELAYED GASTRIC EMPTYING AFTER
PANCREATODUODENECTOMY WITH CHILD RECONSTRUCTION Yoshihiro Okuda,
MD, Masashi Kishiwada, MD, PhD, Rie Sato, MD, PhD, Yasuhiro Murata, MD, PhD,
Akihiro Tanemura, MD, PhD, Naohisa Kuriyama, MD, PhD, Yoshinori Azumi, MD,
PhD, Shugo Mizuno, MD, PhD, Masanobu Usui, MD, PhD, Hiroyuki Sakurai, MD,
PhD, Masami Tabata, MD, PhD, Shuji Isaji, MD, PhD, Hepatobiliary Pancreatic and
Transplant Surgery, Mie University School of Medicine, Tsu, Japan, Tsu, JP
P113 USEFULNESS OF GRADING OF PANCREATIC NEUROENDOCRINE TUMOR
BY USING EUS-FNA SPECIMEN IN SELECTION OF OPERATIVE PROCEDURE BY
COMBINATION WITH UICC-T FACTOR K
azuhisa Fujinaga, Masanobu Usui, MD, PhD,
Akihiro Tanemura, MD, PhD, Naohisa Kuriyama, MD, PhD, Yoshinori Adumi, MD,
PhD, Masashi Kishiwada, MD, PhD, Shugo Mizuno, MD, PhD, Hiroyuki Sakurai, MD,
PhD, Masami Tabata, MD, PhD, Hiroyuki Inoue, MD, PhD, Hiroshi Imai, MD, PhD,
Shuji Isaji, MD, PhD, Hepatobiliary Pancreatic and Transplant Surgery, Tsu, Mie, JP
P114 PORTAL VEIN RESECTION IS ASSOCIATED WITH IMPROVED SURVIVAL
AFTER PANCREATICODUODENECTOMY FOR PANCREATIC CANCER P
rashant
B Sukharamwala, MD, Krishen Patel, BS, Richard L Klein, Thomas W Wood, MD,
Anthony F Teta, BS, Sharona B Ross, MD, Alexander S Rosemurgy, MD, Florida
Hospital Tampa, Tampa, US
P115 MULTIFOCAL PRE-INVASIVE PANCREATIC CANCER IN AN 18-YEAR-OLDWOMAN Lindsey L Manos, PAC, Ashley Salamone, CRNP, Elliot K Fishman, MD,
Anne Marie Lennon, MD, PhD, Ralph H Hruban, MD, Christopher L Wolfgang, MD,
PhD, The Johns Hopkins Medical Institution, Baltimore, US
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Poster Listings
POSTER LISTINGS
P116 SMOKING HISTORY DOES NOT APPEAR TO PREDICT PATHOLOGY IN
SURGICALLY RESECTED INTRADUCTAL PAPILLARY MUCINOUS NEOPLASMS
Neda Rezaee, MD, Saami Khalifian, MS, John L Cameron, MD, Timothy M Pawlik,
MD, MPH, PhD, Ralph H Hruban, MD, Elliot K Fishman, MD, Martin A Makary, MD,
MPH, Anne Marie Lennon, MD, PhD, Christopher L Wolfgang, MD, PhD, FACS,
Matthew J Weiss, MD, PhD, FACS, Department of Surgery, The Sol Goldman
Pancreatic Cancer Research Center, Johns Hopkins Medical Institutions, Baltimore,
Maryland, Baltimore, US
P117 WITHDRAW
P118 REGIONAL HOSPITAL CHARGES FOR PANCREATICODUODENECTOMY IN
FLORIDA: LOCATION MATTERS Sharona B Ross, MD, Amanda E Smart, Carrie
E Ryan, MS, Thomas W Wood, MD, Prashant B Sukharamwala, MD, Alexander S
P119 OUTCOMES FOLLOWING THE SELECTIVE APPLICATION OF LAPAROSCOPIC
PANCREATICODUODENECTOMY S
teven J Hughes, MD, Daniel Delitto, MD, Jose
G Trevino, MD, Kevin E Behrns, MD, Department of Surgery, University of Florida,
Gainesville, US
P120 WITHDRAW
P121 THE ROLE OF PORTOMESENTERIC VEIN RESECTION AT TIME OF
PANCREATODUODENECTOMY FOR PANCREATIC DUCTAL ADENOCARCINOMA
Kengo Asai, MD, Victor Zaydfudim, MD, Sarah Perkins, Guido Sclabas, MD,
Rory Smoot, MD, Mark Truty, MD, Kaye Reid Lombardo, MD, David Nagorney,
MD, Michael Kendrick, MD, Karla Ballman, PhD, Michael Farnell, MD, Division of
Gastroenterologic and General Surgery, Division of Biomedical Statistics and
Informatics, Mayo Clinic, Rochester, MN, USA, Rochester, US
P122 IRREVERSIBLE ELECTROPORATION CAN AUGMENT RESECTION IN
LOCALLY ADVANCED PANCREATIC ADENOCARCINOMA John E Mullinax, MD, Vic
Velanovich, MD, Robert C. G. Martin, MD, PhD, University of South Florida College
of Medicine, University of Louisville College of Medicine, Tampa, US
P123 DIVISION OF THE PANCREAS DURING DISTAL PANCREATECTOMY: A
RELIABLE AND SIMPLE TECHNIQUE WHICH RESULTS IN A VERY LOW FISTULA
RATE John A Stauffer, MD, FACS, Horacio J Asbun, MD, FACS, Mayo Clinic Florida,
Jacksonville, US
P124 PROGNOSTIC IMPACT OF PARA-AORTIC LYMPHNODES DISSECTION
DURING PANCREATICODUODENECTOMY FOR CANCER Gennaro Nappo, MD,
Domenico Borzomati, MD, PhD, FACS, Sergio Valeri, MD, Gianluca MascianA, MD,
Paolo Luffarelli, MD, Giuseppe Perrone, MD, Roberto Coppola, MD, FACS, Campus
Bio-Medico University of Rome, Rome, IT
P125 DOES LENGTH OF PREOPERATIVE ADMISSION IMPACT IN-HOSPITAL
MORBIDITY AND MORTALITY AFTER PANCREATECTOMY? A POPULATIONBASED STUDY C
lancy J Clark, MD, Shuja Ahmed, MD, Emeka Obiora, MD, Perry
Shen, MD, Wake Forest Baptist Health, Winston Salem, US
Poster Listings
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POSTER LISTINGS
P126 WITHDRAW
P127 SURVIVAL BENEFIT OF ADJUVANT THERAPY FOR RESECTABLE
PANCREATIC CANCER PATIENTS TREATED WITH NEOADJVUANT THERAPY K
J
Duelge, BS, A N Krepline, BS, A Mahmoud, BS, B George, MD, P S Ritch, MD, B A
Erickson, MD, K K Christians, MD, D B Evans, MD, S Tsai, MD, Medical College of
Wisconsin, Milwaukee, US
P128 NEOADJUVANT THERAPY FOR PANCREATIC CANCER IN PATIENTS > AGE
75 J Miura, MD, A N Krepline, BS, K Duelge, BS, B George, MD, P S Ritch, MD, B A
Erickson, MD, D B Evans, MD, K K Christians, MD, S Tsai, MD, Medical College of
Wisconsin, Milwaukee, US
P129 CLINICAL CHARACTERISTICS OF NEWLY DIAGNOSED PANCREATIC
ADENOCARCINOMA IN FAMILIAL PANCREATIC CANCER KINDREDS FROM A
INSTITUTIONAL PANCREATIC CANCER REGISTRY Patricio M Polanco, MD, Murawid
M Assifi, MD, Jordan M Knox, BA, Ruth E Dudley, MD, Amer H Zureikat, MD, David L
Bartlett, MD, Herbert J Zeh, MD, Aatur Singhi, MD, Randall E Brand, MD, Melissa E
Hogg, MD, Division of Surgical Oncology, Division of Gastroenterology, Department
of Human Genetics, University of Pittsburgh Medical Center, Pittsburgh, US
P130 LONG-TERM FOLLOW-UP OF RESECTED SMALL (< 2 CM) ASYMPTOMATIC
SPORADIC NON-FUNCTIONING PANCREATIC NEUROENDOCRINE TUMORS:
CORRELATION BETWEEN TYPE OF RESECTION, HISTOPATHOLOGIC FEATURES,
AND OUTCOME G
iuseppe Malleo, MD, Anna Malpaga, MD, Paola Capelli, MD,
Claudio Bassi, MD, Giovanni Butturini, PhD, Unit of Surgery B, The Pancreas
Institute, University of Verona Hospital Trust; Unit of Pathology, The Pancreas
Institute University of Verona Hospital Trust, Verona, IT
P131 LAPAROSCOPIC DISTAL PANCREATECTOMY WHAT IS THE DATA? Cherif N
Boutros, MD, MSc, FACS, Lance Uradomo, MD, Mukul Khandelwal, MD, University
of Maryland School of Medicine, University of Maryland Baltimore Washington
Medical Center, Baltimore, US
P132 WITHDRAW
P133 COST ANALYSIS OF OPEN AND LAPAROSCOPIC
PANCREATICODUODENECTOMY: A SINGLE INSTITUTION COMPARISON J ohn
A Stauffer, MD, FACS, Marc Mesleh, MD, Horacio J Asbun, MD, FACS, Mayo Clinic
Florida, Jacksonville, US
P134 MINIMALLY INVASIVE TREATMENTS OF PANCREATIC AND PERIAMPULAR
CANCER: SIXTY SUCCESSFUL CASES Igor E Khatkov - 1,2, Professor, MD, PhD, Victor
V Tsvirkun - 1, Professor, MD, PhD, Roman E Izrailov - 1,2, Professor, MD, PhD, Pavel
S Tyutyunnik, MD, 1 - Moscow Scientific Research Institute of Gastroenterology; 2 Moscow State University of Medicine and Dentistry, Moscow, RU
P136 OUTCOMES FOLLOWING DISTAL PANCREATECTOMY FOR CHRONIC
PANCREATITIS: A SINGLE INSTITUTION EXPERIENCE OF 33 PATIENTS Nathan
Avery, MD, Flavio Rocha, MD, Virginia Mason Medical Center, Seattle, US
TABLE OF CONTENTS
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Poster Listings
ORAL ABSTRACTS
S001 DIAGNOSTIC LAPAROSCOPY TO DETECT OCCULT METASTATIC DISEASE
PRIOR TO NEOADJUVANT CHEMORADIATION IN BORDERLINE RESECTABLE
PANCREATIC DUCTAL ADENOCARCINOMA - A COST ANALYSIS J une S Peng,
Jeffrey Mino, Noaman Ali, Kevin M El-Hayek, Colin O’Rourke, Sricharan Chalikonda,
R. Matthew Walsh, Cleveland Clinic Foundation, Cleveland, US
BACKGROUND: In patients with borderline resectable pancreatic ductal
adenocarcinoma (PDAC), neoadjuvant chemoradiation offers a potential for
curative resection. Current methods of radiographic staging can miss occult
metastatic disease, which is reflected in the wide range of resectability rates after
neoadjuvant therapy reported in the literature. This study aims to evaluate the
outcomes of borderline resectable PDAC and assess the relative cost of utilizing
staging diagnostic laparoscopy (SDL) as an adjunct to radiographic and endoscopic
staging.
METHODS: This study is a retrospective review of patients presenting to a single
tertiary care institution with borderline resectable PDAC since 2010. Patients
underwent SDL at the discretion of their surgeon prior to starting neoadjuvant
chemoradiation; SDL included biopsy of suspicious lesions, peritoneal washings,
and placement of a central venous port for access. Eligible patients were identified
from our institution’s electronic medical record and data on patient demographics,
staging workup, and oncologic and surgical interventions were collected and
analyzed. Patient level cost data, when available, was used to calculate total cost
of care related to each patient’s pancreatic cancer treatment and a cost ratio was
calculated to compare relative costs of SDL versus no SDL.
RESULTS: A total of 116 patients were identified for inclusion in the study. Five
patients (4.3%) declined surgery, 2 patients (1.7%) were not offered surgery due
to medical comorbidities, and 7 patients (6.0%) underwent attempted resection
up front. The remaining 102 patients (88%) were candidates for neoadjuvant
therapy and 76 (75%) underwent SDL. Nineteen of the 76 SDLs (25%) were positive
with metastatic implants or positive cytology. Patients undergoing SDL were
younger (63.6 vs 69.8 years, p=0.001); imaging characteristics of the primary
tumor were comparable in the two groups, including mean size (3.0 vs 3.0cm,
p=0.69) and encasement or involvement of an artery (13.4 vs 10.8%, p=0.77),
vein (64.2 vs 64.9%, p>0.99), or both artery and vein (22.4 vs 24.3%, p>0.99).
There were 81 patients who received neoadjuvant chemoradiation. In 55 patients
with a previously negative SDL, 5 (9.1%) were unable to complete neoadjuvant
therapy, 21 (38.2%) were found to have locally progressive or metastatic disease
on restaging, 29 (52.7%) underwent attempted resection, and 20 (36.4%) were
successfully resected. In 26 patients who underwent neoadjuvant chemoradiation
without SDL, 7 (26.9%) were unable to complete neoadjuvant therapy, 11
(42.3%) progressed, 8 (30.8%) underwent attempted resection, and 6 (23.1%)
were successfully resected. Relative cost of care, expressed as the ratio of the
geometric mean costs in the SDL versus no SDL groups is 1.3 (0.9-1.9, 95% CI) for
all patients in the study and 1.64 (1.1-2.6) for patients who ultimately underwent
resection.
Oral Abstracts
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ORAL ABSTRACTS
CONCLUSION: The optimal management of patients with borderline resectable
PDAC is debated. Experience at this institution demonstrates that 25% of patients
with radiographically borderline resectable disease have occult metastasis
detected by SDL at time of diagnosis, and these patients are spared aggressive
therapy which is of little benefit. A cost comparison shows no statistically
significant difference in overall costs for patients to undergo a SDL prior to
neoadjuvant therapy.
S002 RISK OF VENOUS THROMBOEMBOLISM DURING NEOADJUVANT
THERAPY FOR RESECTABLE AND BORDERLINE RESECTABLE (BLR) PANCREATIC
ADENOCARCINOMA (PC) A N Krepline, B George, P S Ritch, B A Erickson, J P
Thomas, A Mahmoud, E J Quebbeman, K Turaga, F M Johnston, T C Gamblin, K K
Christians, D B Evans, S Tsai, Medical College of Wisconsin, Milwaukee, US
BACKGROUND: PC increases venous thromboembolism (VTE) risk. The impact of
neoadjuvant therapy on VTE risk is unknown.
METHODS: From 2007-2013, neoadjuvant patients (pt) with resectable and
BLR PC were identified. Radiographic reports from diagnosis to restaging,
demographic, and clinicopathologic data were abstracted.
RESULTS: Seventy-nine resectable and 84 BLR PC pt undergoing neoadjuvant
therapy were identified. From diagnosis to start of treatment, 10 pt (5 resectable
and 5 BLR) were diagnosed with VTE - prevalence of 6.13%. VTE was associated
with lower hemoglobin (11.97 vs. 13.17, p = 0.03) and AB blood type (20.0% vs.
2.73%, p = 0.05). Incident VTE developed in 17 pt (11.11%) - 4 (25.5%) resectable and
13 (76.40%) BLR. Three pt (17.65%) had pulmonary embolisms (PE) and 14 (82.35%)
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Oral Abstracts
ORAL ABSTRACTS
had deep venous thromboses (DVT). Ten pt developed VTE (58.82%) within the
first 2 months of therapy. Thirteen (76.47%) were symptomatic (12 DVT and 1 PE).
Of incident VTE, 6 (35.29%) were catheter related, 9 (52.94%) occurred remote
from indwelling catheter, and 2 (11.76%) occurred in the absence of a catheter.
Use of granulocyte colony stimulating factor (GCSF) was associated with VTE
risk (41.18 vs. 16.91, p = 0.02). In a multivariate logistic regression, receipt of GCSF
(odds ratio 3.46, p = 0.07) and BLR clinical stage (odds ratio 3.08, p =0.07) were
associated incident VTE.
CONCLUSIONS: PC patients undergoing neoadjuvant therapy are at significant
risk of VTE. Advanced clinical stage and the use of GCSF may be associated with
greater VTE risk. Prophylactic anticoagulation may be indicated in high-risk
patients.
S003 IMPACT OF SURGICAL RESECTION AFTER CHEMORADIOTHERAPY
FOR LOCALLY ADVANCED UNRESECTABLE PANCREATIC DUCTAL
ADENOCARCINOMA Masashi Kishiwada, PhD, MD, Rie Sato, MD, Yasuhiro Murata,
PhD, MD, Akihiro Tanemura, PhD, MD, Naohisa Kuriyama, PhD, MD, Yoshinori
Azumi, PhD, MD, Shugo Mizuno, PhD, MD, Masanobu Usui, PhD, MD, Hiroyuki
Sakurai, PhD, MD, Masami Tabata, PhD, MD, Shuji Isaji, PhD, MD, Hepatobiliary
Pancreatic and Transplant Surgery, Mie University School of Medicine, Tsu, JP
BACKGROUND: Pancreatic ductal adenocarcinoma (PDAC) with involvement of
the superior mesenteric artery and/or celiac axis was commonly considered
unresectable. For selected patients with locally advanced PDAC, chemoradiotherapy
may offer the potential for margin-negative (R0) resection, resulting in improvement
of prognosis. At our institution, we have been performing chemoradiotherapy
followed by surgery (CRT-S) for PDAC. The aim of this study was to evaluate the
efficacy of CRT-S for PDAC, particularly in the locally unresectable (UR) cancer
defined by NCCN pancreatic cancer guidelines (2013). These include >180 degree
encasement of the superior mesenteric artery (SMA), unreconstructive portal vein
occlusion, aortic invasion, or celiac encasement.
METHODS: From February 2005 to October 2013, 191 consecutive patients with
cytologically/histologically proven PDAC (UICC-T3 87 cases,-T4 104 cases) had been
enrolled for our CRT-S protocol. CRT regimen: radiation therapy (total dose of 45
to 50.4 Gy, 25 to 28 fractions) with chemotherapy which included gemcitabine
(800mg/m2, day1,8,22,29, 2005.2-2011.10, n=124) or gemcitabine (600mg/
m2,day8,22,36,50)+ oral S-1, active combination of tegafur, gimeracil and oteracil
(60/m2, day1-21 and day 29-49, 2011.11-2013.10, n=67). These patients were
retrospectively classified into three respectability groups based on four-phase
dynamic CT. The patients underwent curative-intent resection after reassessment
by response of CRT completion. At the time of reassessment, we determined
that curative-intent resection was possible when the following findings on MDCT
were observed: no stenosis or change of shape in the celiac axis and SMA and the
absence of metastatic lesions in other distant organs. The primary endpoint was
overall survival, secondary one was R0 resection.
Oral Abstracts
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ORAL ABSTRACTS
RESULTS: The 191 patients were reclassified as resectable in 17 patients,
borderline resectable in 92 and UR in 82. Among UR patients, completion rate of
CRT was 95.1% (78/82). The 19 patients (23.1%) were precluded from surgery due
to distant metastasis at the time of restaging. The 35 patients (42.7%) underwent
surgical resection: the time from initial treatment to resection (median) was 3.2
months (range:2 to 12). The rate of R0 resection was 57.1% (20/35). The 2-year
survival rate and median survival time (MST) were 24.8% and 13.3 months in the
entire 82 patients, being significantly better in 35 patients with resection than in
47 patients without resection (38.2% vs. 20.1%, 23.8 vs.10.3 months, P=0.0088).
Interestingly, in the resected cases, there was no significant difference in survival
between R0 (n=20) and R1(n=13) (43.7% vs. 31.8%, 23.8 vs. 12.1 months, P=0.262).
CONCLUSION: CRT-S can select the patients with locally advanced unresectable
PDAC who are likely to benefit from aggressive resection.
S004 A COMPREHENSIVE ASSESSMENT OF NEOADJUVANT THERAPY FOR
PANCREATIC ADENOCARCINOMA: RESULTS FROM THE NATIONAL CANCER
DATABASE (NCDB) R
ussell S Lewis, BS, Jeffrey A Drebin, MD, PhD, Douglas L
Fraker, MD, Charles M Vollmer, MD, The Perelman School of Medicine, University of
Pennsylvania, Philadelphia, US
INTRODUCTION: Limited, early experience from specialty centers suggests
neoadjuvant therapy for pancreatic adenocarcinoma (PDAC) holds promise
for enhancing patient selection, improving survival, or both. A comprehensive,
contemporary assessment of its utilization on a national scale is lacking.
METHODS: Surgical patients with diagnoses of invasive PDAC between 1998-2010
were identified from the NCDB. Neoadjuvant patients (NA) were defined as those
who received chemotherapy and/or radiation before surgery. NA and surgery-first
patients (SF) were compared and survival analysis was conducted on patients
treated between1998-2005.
RESULTS: Among 232,539 PDAC patients overall, 43,724 were SF. 2,680 NA cases
(5% of surgeries) were contributed by 532 institutions, 10 of which provided 31%
of the cases. The use of NA doubled (6-12% of surgical PDAC) between 2006-2010.
One-third of NA patients had chemotherapy only. When compared to SF patients,
NA patients were treated in academic centers more often (66.4% vs. 51.9%;
P<0.001). Charlson comorbidity scores did not differ. Only 17% of NA patients were
clinical T4, suggesting few were locally advanced. Median days from diagnosis
to surgery were 122 in NA patients. Mean postoperative stay was shorter in NA
patients (11.0d vs. 12.0d; P<0.001). 30-day surgical mortality for NA was 2.8% vs.
4.9% for SF (P<0.001). Additional systemic therapy was applied to 29.3% of NA
patients postoperatively. NA patients had median survival from diagnosis of 19.9
vs. 15.3m in SF (P<0.001); however, long-term survival was equivalent (5-year=14%
in both). Survival benefit was observed for NA in all Stages except Stage I. There
was significant regional and institutional variation in NA survival rates.
CONCLUSION: National utilization of NA therapy has increased significantly in
recent years, and now represents a common treatment path for patients with
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ORAL ABSTRACTS
PDAC. Although this does not reflect an intention-to-treat analysis, NA functions
well as a patient selection technique, as it improves postoperative outcomes.
Furthermore, NA therapy appears to improve survival in advanced stage disease
but not in earlier tumors.
S005 DOES THE USE OF NEOADJUVANT THERAPY FOR PANCREATIC
ADENOCARCINOMA INCREASE POSTOPERATIVE MORBIDITY AND MORTALITY
RATES? Amanda B Cooper, MD, Abhishek Parmar, MD, Taylor S Riall, MD, PhD,
Bruce L Hall, MD, PhD, MBA, Matthew H Katz, MD, Thomas A Aloia, MD, Jason
B Fleming, MD, Henry A Pitt, MD, MD Anderson Cancer Center, University of
Texas Medical Branch at Galveston, Washington University at St. Louis, Temple
University School of Medicine, Houston, US
INTRODUCTION: The effects of neoadjuvant therapy on postoperative
complications following pancreatectomy for pancreatic cancer have not been
well studied. Using prospectively collected data from the NSQIP Pancreatectomy
Demonstration Project, we compared postoperative outcomes for patients with
pancreatic adenocarcinoma treated with a surgery-first vs. neoadjuvant therapyfirst approach.
METHODS: We included all patients with pancreatic adenocarcinoma captured
within the NSQIP Pancreatectomy Demonstration Project from November 2011 to
December 2012. Patients were classified according to neoadjuvant therapy status
(chemotherapy and/or radiation). Patients receiving neoadjuvant therapy were
then further classified as having received chemotherapy alone or radiation with or
without chemotherapy. The groups were compared using the Fisher’s exact test
with significance set at p<0.05.
RESULTS: Of the 1,567 patients with pancreatic cancer identified, 199 patients
received neoadjuvant therapy—99 patients (6.3%) received neoadjuvant
chemotherapy alone and 100 (6.4%) received neoadjuvant (chemo)radiation.
Demographic data were not notably different between the surgery-first and
the neoadjuvant therapy groups. Patients treated with neoadjuvant therapy
were more likely to need a vascular resection than patients treated with surgery
first (41.5% vs. 17.3%, p<0.0001). Patients treated with any neoadjuvant therapy
were also more like to undergo biliary stenting (58.9% vs. 44.5%, p=0.0006) and
were less likely to have a laparoscopic resection (6.0% vs. 8.6%, p=0.05) than
patients treated with surgery first. Patients in the neoadjuvant group had a mean
operative time of 6.9 hours compared to 5.9 hours for patients in the surgery-first
group (p<0.0001); however, their mean length of stay (10.4 days) was not longer
than that of the surgery-first group (11.1 days, p=0.32). The 30-day mortality rate
did not differ for patients in the neoadjuvant therapy compared to the surgeryfirst groups (2.0% vs. 1.5%, p=0.56). Overall postoperative morbidity also did not
differ between the two groups (56.3% vs. 52.9%, p=0.34). Postoperative mortality
and the incidence of most 30-day complications did not differ significantly based
on use of neoadjuvant therapy; however, patients treated with neoadjuvant
therapy were significantly less likely to have a deep organ space infection (3.0%
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vs. 11.5%, p=0.0004) and patients treated with neoadjuvant radiation were less
like to develop a pancreatic fistula (7.3% vs. 15.5%, p=0.03).
CONCLUSIONS: Only 12.7% of patients with pancreatic adenocarcinoma captured
in the Pancreatectomy Demonstration Project were treated with neoadjuvant
therapy. Our data suggest that patients receiving neoadjuvant therapy in this
dataset had more extensive disease (more frequently requiring vascular resection
with a longer mean operative time). Despite this, neoadjuvant therapy was
associated with lower rates of deep organ-space infections and neoadjuvant
radiation was associated with lower rates of pancreatic fistula. Concern over
increasing rates of postoperative complications should not deter the use of
neoadjuvant therapy for pancreatic cancer.
S006 NEOADJUVANT CHEMORADIATION VERSUS NEOADJUVANT
CHEMOTHERAPY PRIOR TO PANCREATICODUODENECTOMY FOR PANCREATIC
CANCER Pragatheeshwar Thirunavukarasu, MD, Kristopher Attwood, Boris W
Kuvshinoff, MD, Steven J Nurkin, MD, Department of Surgical Oncology, Roswell
Park Cancer Institute, Buffalo, US
BACKGROUND: Neoadjuvant therapy has been increasingly utilized for both
borderline and even earlier stage resectable pancreatic adenocarcinoma prior
to pancreaticoduodenectomy. Little is known regarding the relative benefit of
combination chemoradiation compared to chemotherapy alone in the neoadjuvant
setting. We sought to compare survival of patients who underwent neoadjuvant
chemoradiation (NeoCR) with those who underwent chemotherapy alone (NeoC)
prior to surgical resection.
METHODS: We extracted data on all patients who underwent
pancreaticoduodenectomy for pancreatic adenocarcinoma between 1998 and
2006 from the National Cancer Data Base (NCDB). Demographic, co-morbid
status and clinicopathologic variables were collected and reviewed. Patients
that received NeoC were compared to those that received NeoCR. Patients were
excluded if they had T4 or M1 disease on final pathology. Survival analysis was
performed using the Log-rank test.
RESULTS: We identified 285 patients that had neoadjuvant therapies prior to
a pancreaticoduodenectomy. 201 patients had NeoCR and 85 had NeoC only.
There were no statistically significant differences (P>.05) in the mean age, sex
distribution, co-morbid conditions or T-stage between both groups. NeoCR was
associated with a significantly higher rate of node-negative (N0) disease on
pathological staging compared to NeoC (67.5% vs. 48.1%, P=.004) and a statistically
non-significant trend towards lower margin positivity (13.1% vs. 22.8%, P=.07).
There was no difference in the 30-day readmission rate after surgery (9.6% NeoCR
vs. 6.2% NeoC, P=.50). The median survival with NeoC (24.4 months, 95% CI 28.2
– 41.5 months) and NeoCR (21.4 months, 95% CI, 18.0-24.82 months) were not
different (P=.40) (Figure 1). Subset analysis of pathologically N0 patients showed
marginal, although non-significant, survival benefit to NeoC over NeoCR (median
survival, 95% CI; 38.1 months, 27.4-44.7 vs. 23.9 months, 19.1-27.0, P=.12)
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CONCLUSION: Chemoradiation in the neoadjuvant setting of
pancreaticoduodenectomy for pancreatic cancer was associated with a higher rate
of pathologically node-negative disease and a marginally lower positive margin
rate than chemotherapy alone. Chemoradation did not improve overall survival.
On the contrary, there was a non-significant trend towards decreased early
survival associated with the use of radiation, especially in N0 disease. Prospective
studies are needed in the future given the lack of pre-operative staging
information and potential selection bias associated with the current study.
S007 CHANGES IN BODY COMPOSITION DURING PREOPERATIVE THERAPY
FOR RESECTABLE PANCREATIC CANCER: DO THEY MATTER? A
manda B Cooper,
MD, David Fogelman, MD, Holly M Holmes, MD, Rebecca S Slack, MS, Aparna
Balachandran, MD, Naveen Garg, MD, Maria Q Petzel, Douglas B Evans, MD, Gauri
R Varadhachary, MD, Robert A Wolff, MD, Christopher Crane, MD, Jeffrey E Lee,
MD, Jason B Fleming, MD, Matthew H Katz, MD, MD Anderson Cancer Center,
Medical College of Wisconsin, Houston, US
BACKGROUND: Sarcopenia (loss of muscle mass) predicts perioperative
complications and delayed recovery after cancer surgery, and poor survival
following de novo pancreatectomy in patients with pancreatic adenocarcinoma.
However, the impact of sarcopenia on outcomes of pancreatic cancer patients
treated with neoadjuvant therapy is unknown. We sought to characterize changes
in body composition of pancreatic cancer patients treated with preoperative
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chemoradiation to determine the prevalence of baseline and treatment-associated
sarcopenia and any association with survival.
METHODS: We examined the pretreatment and preoperative CT scans of all 90
patients with potentially resectable pancreatic cancer enrolled on a previouslyreported phase II trial of neoadjuvant chemotherapy and chemoradiation. We
computed normalized cross-sectional areas (CSA) of skeletal muscle (SKM),
visceral adipose tissue (VAT), and subcutaneous adipose tissue (SAT) at the L3
vertebral level. Sarcopenia was defined using gender-specific norms and evaluated
in the context of prospectively-acquired clinical data.
RESULTS: At trial enrollment, 46 (52%) patients were sarcopenic, 53 (59%) were
overweight or obese, and 21 (24%) were both. After neoadjuvant therapy (median
4.2 months), CSA (cm2/m2) decreased for each compartment [SKM 47.6 vs 46.3
(p=0.004), VAT 45.1 vs 41.2 (p=0.01), and SAT 53.0 vs 15.9 (p<0.001)] and 9 (23%)
patients without baseline sarcopenia developed sarcopenia. Among all enrolled
patients, neither pre- nor post-treatment sarcopenia were associated with
successful pancreatectomy, progression-free, or overall survival (all p >0.05).
However, among patients who underwent resection, patients who had large
decreases in SKM prior to pancreatectomy had a shorter median disease-free
survival than patients who had smaller decreases or increases in SKM during
therapy (p=0.05).
CONCLUSIONS: In this first report of the changes in body composition that may
occur in association with preoperative therapy, we demonstrated that sarcopenia
is prevalent in patients with resectable pancreatic cancer upon diagnosis, and
that preoperative therapy is associated with a further decline in SKM. Although
our data suggest that baseline or treatment-associated sarcopenia alone may
not portend a poor prognosis when neoadjuvant chemoradiation is employed, an
absolute decrease in SKM may be associated with shorter disease-free survival
among those patients who undergo resection after neoadjuvant therapy. Further
studies are necessary to determine which alterations in body composition impact
oncologic outcomes in patients treated with preoperative therapy, and how such
alterations can be modulated to optimize treatment outcomes.
S008 PROSPECTIVE RANDOMIZED CONTROLLED STUDY COMPARING OUTCOME
BETWEEN STANDARD RESECTION AND AN EXTENDED RESECTION THAT
INCLUDED DISSECTION OF THE NERVE PLEXUS AND VARIOUS LYMPH NODES IN
PATIENTS WITH PANCREATIC HEAD CANCER J in-Young Jang, Mee Joo Kang, Jin
Seok Heo, Seong Ho Choi, Dong Wook Choi, Sang Jae Park, Dong Sup Yoon, Hee
Chul Yu, Koo Jung Kang, Sang Geol Kim, Sun-Whe Kim, Department of Surgery,
Seoul National University & Korean Pancreatic Surgery Club, Seoul, KR
INTRODUCTION: Despite several previous RCTs on the extent of surgery in
pancreatic cancer, many surgeons have tried to perform more extended resection
due to several pitfalls of those studies. The aim of this study is to prospectively
evaluate survival benefit of dissection of the nerve plexus and lymphadenectomy
in the patients with the pancreatic head cancer.
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METHODS: A total of 244 patients was enrolled; of these, 200 were randomized
to undergo standard (SR) or extended resection (ER), with the latter including the
dissection of additional lymph nodes and the right half of the nerve plexus around
the superior mesenteric artery and celiac axis. We analyzed 167 patients from 7
centers who fulfilled all of the required criteria.
RESULT: Operation time was longer and estimated blood loss was higher in the ER
than in the SR group, but the R0 resection rate was comparable. Mean number of
lymph nodes retrieved per patient was higher in the ER than in the SR group (33.7
vs. 17.3, p<0.001). The morbidity rate was slightly higher in the ER than in the SR
group. There were 2 in-hospital deaths only in the ER group. Median survival after
R0 resection was similar in the ER and SR groups 18.0 vs. 19.0 months, p=0.239)
regardless of lymph node metastasis. Adjuvant chemoradiation had a positive
impact on overall survival.
CONCLUSION: This study suggests that extended lymphadenectomy with nerve
plexus dissection does not have a significant survival benefit compared with SR
in pancreatic head cancer. The authors note that this standard resection can be
done safely and efficiently, and does not in any way sacrifice oncologic efficacy
or long-term survivorship when compared to patients undergoing an extended
pancreaticoduodenal resection.
S009 MICROSCOPIC RESIDUAL TUMOR AFTER PANCREATICODUODENECTOMY
FOR CANCER. PRELIMINARY RESULTS OF A MULTICENTRIC PROSPECTIVE
RANDOMIZED TRIAL R
oberto Coppola, MD, FACS, Domenico Borzomati, MD, Phd,
FACS, Sergio Valeri, MD, Gennaro Nappo, MD, Michela Amato, MD, Giuseppe Perrone,
MD, Andrea Onetti Muda, MD, Campus Bio-Medico University of Rome, Rome, IT
INTRODUCTION/BACKGROUND: Resection margin and lymph-node status after
Pancreatico-Duodenectomy (PD) for cancer are the most powerful prognostic
factors. Recent studies showed that a standardized pathological evaluation of
the specimen increases the rate of microscopic residual tumour (R1) and nodal
metastases after PD for cancer. We report the preliminary results of a multicentric
prospective randomized study that compared standardized Vs non-standardized
methods to evaluate the surgical specimen.
MATERIAL AND METHODS: Surgical specimens after PD performed for ampullary,
biliary and pancreatic carcinoma were eligible for inclusion. Four different
pancreatic surgery Units took part into the study:
Campus Bio-Medico University of Rome; Humanitas Institute of Milan (Surgeons:
M. Montorsi, A. Zerbi. Pathologist: P. Spaggiari); University of Pisa (Surgeons: U.
Boggi, F. Vistoli. Pathologist: D. Campani); University of Katowice (Surgeon: S.
Mrowiec. Pathologist: L. Liszka)
Eligible cases were randomly allocated to receive two different methods of
pathological evaluation:
1) GROUP A: the specimen was evaluated with the standardized method (Verbeke
CS et Al. in Br. J. Surg. 2006; 93; 1232–1237).
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2) GROUP B: the specimen was evaluated with the method conventionally used by
each centre.
The primary endpoint of the study was to verify if the standardized method
determines a significant variation of R1 rate. The secondary endpoints were
the evaluation of “T” and “N” status, number of examined blocks and number of
examined lymph-nodes in the two groups.
RESULTS: From March 2013 until now, we randomly allocated 29 and 27
specimens to be managed with the standardized and the conventional method
respectively. At final histology:
• 13 cases (23.2%) resulted ampullary cancer (group A: 9 patients, group B: 4
patients, p = n.s.)
• 8 cases (14.3%) resulted distal common bile duct cancer (group A: 5 patients,
group B: 3 patients, p = n.s.)
• 35 cases (62.5%) resulted pancreatic head ductal adenocarcinoma (group A: 15
patients, group B: 20 patients, p = n.s.)
Mean size of the tumor was 2.59 cm (group A: 2.43 cm, group B: 2.77 cm, p = n.s.).
R1 resection rates were 58.6% (group A) and 40.7% (group B) (p < 0.05). Average
number of examined blocks was 44,4 (group A) and 23,4 (group B) (p < 0.05).
Mean number of examined lymphnodes was 34,8 (group A) and 21,9 (group B) (p <
0.05). Metastatic lymphnodes were found in 72.4% (group A) and in 63.0% (group
B) (p < 0.05).
DISCUSSION: This is the first prospective randomized study focusing the role of
pathological evaluation of the specimen after PD for cancer. Preliminary results
of our study confirm that the use of the standardized method increases the
incidence of R1 resections, the number of examined lymph-nodes and the rate
of nodal metastases. If definitive results of the present study will confirm these
preliminary data, we should assume that at least two third of PD for cancer can
not be considered “radical resections”.
S010 MINIMALLY INVASIVE PANCREATODUODENECTOMY: IS THE LEARNING
CURVE SURMOUNTABLE? A
ttila Nakeeb, MD, Abishek Parmar, MD, Taylor S Riall,
MD, PhD, E Molly Kilbane, RN, Bruce L Hall, MD, PhD, MBA, Henry A Pitt, MD,
Indiana University School of Medicine, University Texas Medical Branch Galveston,
Indiana University Health, Washington University School of Medicine, Temple
University School of Medicine, Philadelphia, US
BACKGROUND: Minimally invasive pancreatoduodenectomy (MIPD) has been
introduced in recent years at a few specialized centers. Both laparoscopic and
robotic Whipple procedures have been mastered by a small number of surgeons
around the world. Even in these expert hands, the learning curve has been steep,
but patient safety issues have not been reported. However, the generalizability of
this procedure has yet to be established. Therefore, the aim of this analysis was
to determine whether the outcomes of MIPD are comparable to open surgery in a
contemporary, multicenter cohort.
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METHODS: From November 2011 through December 2012, 1,781 patients
underwent pancreatoduodenectomy (PD) at 43 institutions participating in the
American College of Surgeons – National Surgical Quality Improvement Program
(ACS-NSQIP) Pancreatectomy Demonstration Project. MIPD included laparoscopic,
hand-assisted, robotic and robotic-assisted cases. MIPD was initiated in 131
patients (7.4%) at 21 centers. The mean and median cases per institution were
six and three, respectively, and 66 (50%) were converted to open surgery. MIPD
was completed at 13 institutions with the mean and median number of cases per
institution being five and two, respectively. Major morbidity was defined as ACSNSQIP serious morbidity plus clinically significant pancreatic fistulas. Outcomes
for MIPD (completed plus converted) were compared to open PD by standard
statistical analyses.
RESULTS: Minimally invasive (completed plus converted) and open patients were
similar with respect to age, gender, race, ASA class, BMI, cardiopulmonary disease,
diabetes, smoking, vascular resection and drain management. Minimally invasive
converted patients had higher BMI’s (p<0.02) and were more likely to undergo
vascular resection (p<0.01). Outcomes for Open and MIPD (completed plus
converted) were:
Procedure
Operative
Time
Septic Shock Reoperation
Major
Morbidity
30-day
Mortality
Open PD
6.1 hr
3.7%
3.5%
44.4%
1.8%
MIPD
7.5 hr*
11.5%*
11.0%*
55.0%†
4.7%†
*p<0.01, † p <0.04 vs Open PD
CONCLUSIONS: This analysis suggests that compared to open surgery minimally
invasive pancreatoduodenectomy (MIPD) takes longer and is associated with
significantly increased major morbidity and mortality. In 2012, MIPD was
attempted at many specialized centers, but half of the cases were converted
to open surgery. For MIPD to become generalizable, improved developmental
paradigms will be required.
S011 TOTAL LAPAROSCOPIC PANCREATICODUODENECTOMY FOR PANCREATIC
DUCTAL ADENOCARCINOMA: ONCOLOGIC ADVANTAGES OVER OPEN
APPROACHES? K
ristopher P Croome, MD, MS, Michael Farnell, MD, Mark J Truty,
MD, Kaye Reid-Lombardo, MD, Florencia G Que, MD, David M Nagorney, MD,
Michael L Kendrick, MD, Mayo Clinic, Rochester, US
OBJECTIVE(S): Advantages of total laparoscopic pancreaticoduodenectomy(TLPD)
include less blood loss and shorter hospital stay compared to open
pancreaticoduodenectomy(OPD). Published oncologic outcomes of TLPD are
limited by sample size and grouping of various cancer types. Our aim was to
evaluate the oncologic outcomes of TLPD and OPD in patients with pancreatic
ductal adenocarcinoma(PDAC).
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METHODS: Single institution, retrospective review of all patients undergoing
TLPD(n=108) and OPD(n=214) for PDAC from July 2007 to July 2013.
RESULTS: Neoadjuvant therapy, tumor size, node positivity and margin positive
resection were not different between the two groups. Median hospital stay was
greater in the OPD group (9 vs 6 days, p<0.001). A greater proportion of patients
in the OPD group had a delay of greater than 8weeks from surgery to adjuvant
chemotherapy, 41% and 27% respectively (p=0.01). The proportion of patients with
a delay of more than 90days or did not receive adjuvant treatment was also greater
in the OPD(12%) compared to the TLPD(5%) group(p=0.04). Median follow-up was
1.5years. Overall survival was not different between the two groups (p=0.22),
however, progression free survival was greater in the TLPD group(p=0.03).
CONCLUSIONS: TLPD not only provides the typical benefits of MIS approaches,
but in patients with PDAC it may also prevent delayed initiation or cancellation of
adjuvant therapy. In comparable patients, this study also demonstrated improved
progression free survival for patients undergoing TLPD.
S012 PRELIMINARY RESULTS OF A SWEDISH, MR BASED, SCREENING PROGRAM
FOR INDIVIDUALS AT RISK FOR PANCREAS CANCER Marco Del Chiaro, MD, PhD,
Caroline Verbeke, MD, PhD, Nils Albiin, MD, PhD, Associate, Professor, Nikolaos
Kartalis, MD, PhD, Stephan L Haas, MD, PhD, Ralf Segersvard, MD, PhD, Ake
Andren-Sandberg, MD, PhD, Professor, Matthias Lohr, MD, PhD, Professor, Division
of Surgery, Department of Clinical Science, Intervention and Technology (CLINTEC).
Karolinska Institutet - Stockholm, Sweden, Stockholm, SE
INTRODUCTION: Ten % of all pancreatic cancers can be hereditary. A screening
program for the individuals at risk (IAR) is recommended, but no defined
surveillance modalities are available.
AIM: To analyze the frequency of findings in IAR
METHODS: From 2010 to 2013, all the patients with a “genetic risk” to develop
pancreas cancer and referred to the Karolinska University Hospital, were included
in a MR based surveillance program. All patients were investigated for the most
common genetic mutation associated with pancreas cancer.
RESULTS: Forty patients were enrolled. There were 24 female and 16 man. The
mean age was 49.9. The mean length of follow-up was 12.9 (± xx) months. The
number of relatives affected by pancreas cancer was 5 in 2 patients (5%), 4 in
5 (12.5%), 3 in 17 (42.5%), 2 in 14 (35%) and 1 in 2 (5%). In 4 patients (10%) a p16
mutation was found, in 3 a BRCA 2 mutation (7.5%), in 1 a BRCA 1 mutation (2.5%).
In 16 patients (40%) a suspect lesion was found in the pancreas with MR. Fourteen
(35%) had an IPMN and 2 (5%) a pancreas cancer. Five patients (12.5%) required
surgery and the remaining 37 continue with the surveillance program.
CONCLUSIONS: During a median follow-up of just about a year, we detected
pancreatic lesions in about 40% of our patients, of which five underwent surgery.
Despite the relatively short time, the surveillance program in IAR seems to be
effective.
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S013 EARLY DETECTION OF PANCREATIC INTRAEPITHELIAL NEOPLASIA USING
NON-INVASIVE IMAGING TO LOCALIZE AND GRADE PROTEASE ACTIVITY
Dana A Dominguez, BS, Michael Paige, PhD, Fiore Cattaruzza, PhD, Anthony J
O’Donoghue, PhD, Nilotpal Roy, PhD, Elliot S Seeley, MD, PhD, Matthias Hebrok,
PhD, Kimberly S Kirkwood, MD, Charles S Craik, PhD, University of California, San
Francisco, San Francisco, US
Patients with hereditary or chronic pancreatitis or IPMN are at increased risk
of pancreatic cancer and undergo surveillance imaging with the hope of early
detection, yet differentiation between benign, atypical or dysplastic lesions, and
invasive cancers is inaccurate. Recently, the Sauer lab showed that cathepsin B
and L activities correlate with PanIN severity and PDAC. Non-invasive functional
imaging of proteolytic activity offers a promising strategy to grade the severity
of dysplasia in the pancreas. We determined if proteolysis could be labeled in live
animals and whether the activity relates to severity of dysplasia. We developed
a novel in-vivo probe that deposits near-infrared fluorophores or radioisotopes
at sites of proteolysis for non-invasive detection in live animals. Real-time
measurement is enabled through a non-interfering localization mechanism that
deposits probe on cellular membranes adjacent to the site of proteolytic activity
and is amplified by the presence of phosphatidylserine.
Our technology, called Restricted Interaction Peptides (RIPs) serves to take
advantage of this unregulated proteolysis. RIP probes are modified forms of
spontaneous membrane binding peptides with addition of a cleavable targeting
module and an imaging agent (Fig 1). For this study, we used a Cy5.5 tag, that was
visualized using near infrared spectrometry at a dose of 5 nmol with no obvious
harmful effects. For this proof of principle study, we compared probe deposition
in the following mice: LSL-Kras(G12D/+);Pdx-1-Cre PDAC, wild type C57BL/6,
cerulein-injected acute pancreatitis, and TNBS induced chronic pancreatitis and a
novel model of IPMN that develops sequential PanINs and invasive cancer (LSLKRAS(G12D/+) brg1 -/-).
As expected, there was a 5-fold increase in PANC-RIP probe deposition in acute
pancreatitis as compared with both chronic pancreatitis and no probe controls.
This activation was confirmed to be highly localized to the pancreas through
ex-vivo examination of organs in isolation including liver, heart and lung. PDAC
mice had significanty increased signal in both in-vivo imaging, as well as ex-vivo
imaging of the respective pancreata as compared with both healthy controls and
TNBS-chronic pancreatitis mice (Fig. 2). Ex-vivo immunofluorescence imaging
of cryosections from animals with PDAC showed site-specific accumulation on
epithelial cells, not on leukocytes or in stroma. A dose-response was seen with
less probe accumulation in PanINs 1 and 2 and more in PanIN-3, with brightest
signal in areas of invasion. All areas of PanIN-3 or invasive cancer showed
increased probe signal. Similarly, in the IPMN mouse, probe was identified in
PanINs and the highest activity was seen in cysts that had degenerated to PDAC
(Fig. 3).
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Our preliminary data suggests that proteolytic activity increases during
carcinogenesis and may be a useful tool for grading cellular atypia in the pancreas. Our
novel RIP probe may provide a useful tool for non-invasive functional imaging using
nanomolar doses, that offers the potential to detect PanIN-3s in patients with chronic
pancreatitis and to discriminate benign from malignant cystic lesions in IPMN.
Fig. 1:
Fig. 2:
Fig. 3:
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S014 ROLE OF CYB5A IN PANCREATIC CANCER: CORRELATION WITH CLINICAL
OUTCOME AND FUNCTIONAL CHARACTERIZATION IN THE MODULATION OF
AUTOPHAGY AND ONCOGENIC PHENOTYPES Elisa Giovannetti1, MD, PhD, Niccola
Funel2,5, PhD, Amir Avan1, PhD, Qiuyan Wang3, PhD, Tonny Lagerweij4, PhD, Luca
E Pollina, MD, Fabio Caniglia5, MD, Vittorio Perrone5, MD, Godefridus J Peters1,
PhD, Thomas Wurdinger4, Md, PhD, Giuseppe Giaccone3, MD, PhD, Ugo Boggi5,
MD, Departments of 1Medical Oncology, and 4Neurosurgery & Pediatric Oncology/
Hematology, VU University Medical Center; 2Division of General and Transplant
Surgery and 5Division of Surgical Pathology, University of Pisa, Pisa, 3Medical
Oncology Branch, Nati, Pisa, IT
INTRODUCTION: Pancreatic ductal adenocarcinoma (PDAC) carries one of the
worst prognoses of any major malignancy and exhibits profound chemoresistance.
The inefficacy of currently available therapeutic strategies has been attributed to
the dense desmoplastic reaction, which reduces drug penetration, and to the high
rate of genetic alterations affecting multiple pathways. We previously investigated
genomic imbalances using array comparative genomic hybridization in a cohort of
44 radically resected patients, the largest PDAC series ever investigated by arraycomparative genomic hybridization. In this series, the median overall survivals
(OS) for patients with and without loss of the cytoband 18q22.3 were 7.6 and
21.4 months, respectively. In agreement with previous findings, CPGL reduced
proliferation and inhibited migration in SU.86.86 cells carrying FLAG-tagged CPGL.
However, knockdown of CPGL in the PANC-1 cells did not affect proliferation,
cell cycle distribution, and wound healing. The aim of this study was to evaluate
whether the mRNAs and/or proteins coded by the genes in the 18q22.3 cytoband
were associated with outcome in two cohorts of radically resected patients and
one cohort of metastatic PDAC patients.
MATERIALS AND METHODS: We studied mRNA/protein expression in radically
resected (n = 130) and metastatic patients (n = 50). The role of CYB5A was tested
in 11 PDAC cell lines and five primary cultures through retrovirus-mediated
upregulation and small interfering RNA using wound-healing, invasion, annexin-V,
electron microscopy, and autophagic assays, as well as autophagy genes and
kinases arrays. CYB5A+ orthotopic models (n = 6 mice/group) were monitored by
Firefly and Gaussia-luciferase bioluminescence, magnetic resonance imaging, and
high-frequency ultrasound. Data were analyzed by t test, Fisher exact-test, log-rank
test and Cox proportional hazards models. All statistical tests were two-sided.
RESULTS: Both resected and metastatic patients with low mRNA or protein
expression of CYB5A (evaluated by computerized algorithm through digital
scanning: D-Dight, Menarini, Florence, Italy) had statistically significantly shorter
survival (eg, median = 16.7 months, 95% confidence interval [CI] = 13.5 to 19.9;
vs median = 24.8 months, 95% CI = 12.8 to 36.9; P =.02, two-sided log-rank test;
n=82 radically resected PDACs), and multivariable analyses confirmed prognostic
relevance. Moreover, we characterized a novel function to CYB5A, autophagy
induction, concomitant with reduced proliferation and migration/invasion of PDAC
cells. Network analysis of proautophagic pathways suggested CYB5A interaction
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with TRAF6, which was confirmed by TRAF6 downregulation after CYB5A
reconstitution (−69% in SU.86.86-CYB5A+; P =.005, two-sided t test). CYB5A
silencing had opposite effects, restoring TRAF6 expression and wound healing.
In vivo studies showed that CYB5A induced autophagy while inhibiting tumor
growth/metastasis and increasing survival (median = 57 days, 95% CI = 52 to 61; vs
median = 44 days, 95% CI = 21 to 57; P = .03, two-sided log-rank test).
CONCLUSIONS: These results define CYB5A as a novel prognostic factor for
PDAC that exerts its tumor-suppressor function through autophagy induction.
Morerover, strategies aimed at restoring CYB5A activity, or targeted therapy
inhibiting its deregulated downstream pathways, including TRAF6, may constitute
a novel approach favouring cancer cell death while preventing potentially
deleterious cross-talk between key oncogenic players in selected subgroups of
PDAC patients.
S015 CA 19-9 RESPONSE TO NEOADJUVANT THERAPY PREDICTS OUTCOME IN
PANCREATIC ADENOCARCINOMA B
rian A Boone, MD, Jennifer Steve, BS, Melissa
E Hogg, MD, Mazen S Zenati, MD, PhD, Amer H Zureikat, MD, Herbert J Zeh, MD,
University of Pittsburgh, Pittsburgh, US
INTRODUCTION: Baseline Ca 19-9 is a useful prognostic marker in pancreatic
ductal adenocarcinoma (PDA), however only a limited number of studies have
examined the significance of a change in Ca 19-9 following neoadjuvant therapy.
METHODS: All patients receiving neoadjuvant therapy for PDA from 7/2010 to
2/2013 were retrospectively reviewed. Patients who had a pre-treatment Ca
19-9 that was normal (<33 U/mL) were excluded. Resection rate, R0 resection
rate, need for venous resection and overall survival were correlated to Ca 19-9
response. Fischer exact test, Kaplan-Meier survival analysis and multivariate
analysis using cox regression were used to evaluate data.
RESULTS: 79 patients were eligible for study (22 patients with resectable
disease, 40 borderline resectable (BR) and 17 with locally advanced disease (LA)).
A variety of chemotherapies +/- radiation were utilized during the study period
(56% chemotherapy alone, 44% chemoradiation). The overall R0 resection rate
was 67% (82% resectable, 70% BR, 41% LA). 56 patients (71%) had a decrease in
Ca 19-9 with neoadjuvant treatment of >50%. For all patients, there was a trend
towards a Ca 19-9 response of > 50% predicting R0 resection (OR 2.5, p=0.077).
In BR patients, Ca 19-9 response of > 50% predicted R0 resection (OR 4.2,
p=0.05). In BR patients that had an increase in Ca 19-9, 0 of 5 (0%) underwent
R0 resection, while 80% of the remaining cohort had an R0 resection (p=0.001).
The rate of complete pathologic response was 29% in patients who had a Ca
19-9 response of >90% versus 0% in the remaining patients (p<0.001). A Ca 19-9
response of >50% resulted in improved overall survival (28.0 vs. 11.1 months,
p<0.0001, Figure 1). An increase in Ca 19-9 during treatment had an adverse
effect on survival (10.2 vs. 28.0 months, p<0.0001). Ca 19-9 response of > 50%
was an independent predictor of survival on multivariate analysis (p<0.0001, HR
0.26 [95% CI 0.13-0.55]).
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CONCLUSION: Ca 19-9 response to neoadjuvant therapy has prognostic value,
predicting R0 resection rate and survival. This data supports the use of CA19-9 as
an important biomarker of response to neoadjuvant therapy. Incorporation of this
easily obtainable and rapid biomarker into future clinical trials may facilitate more
rapid evaluation of novel regimens.
S016 DETECTION OF CLINICALLY RELEVANT GENETIC ALTERATIONS IN FINE
NEEDLE ASPIRATES OF PANCREATIC CANCER IS POSSIBLE USING NEXTGENERATION SEQUENCING Vicente Valero III, MD, Tyler J Saunders, BA, Matthew
J Weiss, MD, John L Cameron, MD, Ralph H Hruban, MD, Joseph M Herman, MD,
Christine A Iacobuzio-Donahue, MD, PhD, Christopher L Wolfgang, MD, PhD, The
Johns Hopkins University School of Medicine, Department of Surgery, Baltimore, US
INTRODUCTION: A personalized approach to the treatment of pancreatic cancer
that is based on genetic status depends on the tissue available for downstream
molecular analysis. Fine needle aspiration (FNA) is the most commonly used
method for obtaining tissue prior to surgical resection, or for patients in whom
surgical resection is not indicated. Potentially limiting factors of FNA include the
paucity of malignant cells within a fibroblast-rich stroma and tumor heterogeneity.
Therefore, we sought to determine: the ability to confidently detect mutant alleles
in low cellularity samples, the concordance between the FNA and the primary
tumor and the feasibility of identifying driver mutations in clinical FNAs.
METHODS: We determined the ability to detect cancer-specific mutations in a
wild-type stromal background in an in vitro model of Panc1 cells diluted into the
fibroblast cell line, CAF-35. To demonstrate proof of principle, we mixed Panc1 with
increasing cell ratios of CAF-35 (1:1, 1:10, 1:25, 1:50, 1:100, 1:200) to simulate the
tissue heterogeneity seen in FNAs. To explore the impact of genetic heterogeneity
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on FNAs, we next established the mutational concordance between an FNA
and its matched resected human adenocarcinoma tissue using next-generation
sequencing by Ion Torrent PGM. Finally, 17 patient FNAs were sequenced using
a targeted panel comprised of all exon coverage of 409 cancer related genes to
identify driver, actionable and passenger mutations via FNA.
RESULTS: The limit of confident detection occurred at a 1:25 ratio of malignant
to stromal cells for both the KRAS and TP53 mutant alleles corresponding to a
hypothetical carcinoma with 4% neoplastic cellularity. Confident mutant detection
was maintained at the 1:25 ratio when total cell count was varied with the lower
limit of detection occurring at 25,000 total cells. The concordance rates between
the FNA and tumor samples ranged from 83% to 100%, although there was 100%
mutational concordance for driver genes in all samples. Sequencing of clinical
FNAs revealed driver mutations of KRAS (93%), TP53 (53%), SMAD4 (40%) and
CDKN2A (7%) genes. The total number of somatic mutations identified in this
cohort was 80 (71 missense, 6 nonsense, 2 INDELs and 1 splice site) with a mean of
4.7 variants per patient. Other shared variants observed in these patients included
SF3B1 (27%), ARID1A (20%), ATM (13%), TRIM33 (13%) and GRM8 (13%).
CONCLUSION: This is the first study to prove that confident genotyping of low
cellularity FNA samples is possible and accurately detects the driver mutations
in primary tumors. Furthermore, next generation sequencing can provide
single base resolution for identification of clonal somatic variants found within
the primary tumor. Moving forward, obtaining the genetic signature of an
individuals pancreatic tumor will enable physicians to recommend personalized
treatment plans to patients according to chemosensitivity, metastatic efficiency,
perioperative outcome data and overall survival.
S017 NEW PLATFORMS FOR PDAC PRECLINICAL STUDIES: 3D TISSUEENGINEERED MODELS BASED ON PRIMARY CANCER CELLS AND SYNTHETIC
SCAFFOLDS * Claudio Ricci, PhD, * Serena Danti, PhD, + Lorenzo Moroni, PhD, +
Carlos Mota, PhD, ^ Stefania Moscato, PhD, * Delfo D’Alessandro, PhD, o Stefano
Ugel, PhD, o Silvia Sartoris, PhD, o Vincenzo Bronte, MD, PhD, * Daniela Campani,
MD, & Ugo Boggi, MD, * Niccola Funel, PhD; *Dept. of Surgical, Medical, Molecular
Pathology and Emergency Medicine, University of Pisa, Pisa, Italy; +Tissue
Regeneration Dept., University of Twente, Enschede, The Netherlands; ^ Dept. of
Clinical Medicine, University of Pisa, Pisa, Italy; oDept. O, Pisa, IT
INTRODUCTION: Pancreatic Ductal Adenocarcinoma (PDAC) is a malignant
neoplasm of epithelial origin which represents one of the major causes of death
in the western world. At present, the Tumor Tissue Microenvironment (TME) is
supposed to play a pivotal role on the aggressiveness of pancreatic epithelial
tumor cells. Aim of this study was to investigate the interactions between PDAC
cells (derived from patients who underwent surgical treatment) and different
biocompatible scaffolds to generate new 3D in vitro models for TME studies.
METHODS: To create 3D cellular models, three scaffolds were fabricated with
different polymers and techniques: polyvinyl alcohol/gelatin (PVA/G; weight
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composition ratio of 70/30) obtained via emulsion and freeze-drying; poly(ethylene
oxide terephthalate)/poly(butylene terephthalate) (PEOT/PBT) produced via either
compression molding and particle leaching (namely, CM) or electrospinning (namely,
ES). Human epithelial primary cultures were derived from PDAC explants. Both
tissues and derived cells were genetically characterized for K-ras and TP53. PDAC
cells were seeded on the sterile scaffolds at a density of 1×104 cells/mm3 and
cultured for 9 days in complete RMPI medium. Sample characterization included:
cell viability (using the AlamarBlue assay), cell morphology [via scanning electron
microscopy (SEM) and histology with H&E staining), expression of MMP9 and MMP2
proteins via Western Blot (WB) and immunohistochemistry (IHC).
RESULTS: At the endpoint cells were found to be viable in the scaffolds showing
AlamarBlue reduction of 47.5% (PVA/G), 40.6% (PEOT/PBT_CM) and 45.1% (PEOT/
PBT_ES). SEM analysis detected a good 3D colonization and a very strong cellular
adhesion in all three models. The histologic analysis highlighted the formation of
PDAC clusters showing a ductal-like morphology in both PVA/G and PEOT/PBT_
CM models. Finally, in the 3D models, a higher expression of MMP9 and MMP2
proteins was observed with respect to 2D cell cultures.
DISCUSSION: From our findings, the development of 3D cancer tissue-engineered
models using biocompatible scaffolds for cell growth seems to be feasible, versatile,
low time consuming and representative of PDAC features. This platform could be
used as a preliminary attempt before in vivo testing. In the close future, 3D models
could be used to screen experimental pharmacological treatments for the modulation
of different tumor proteins. Furthermore, in these 3D models an integration among
different cellular types involved in PDAC microenvironment could be generated and be
more representative of the human TME than the in vitro models used so far.
S018 BIOLUMINESCENT ORTHOTOPIC PANCREATIC-DUCTALADENOCARCINOMA (PDAC) MOUSE MODELS DERIVED FROM PRIMARY PDAC
CELLS AS A PLATFORM FOR THERAPEUTIC DISCOVERY Niccola Funel1,2, PhD,
Elisa Giovannetti3, MD, PhD, Tonny Lagerweij4, PhD, Amir Avan3, PhD, Daniela
Campani2, MD, Nelide De Lio1, MD, Vittorio Perrone1, MD, Dieter Fuchs5, PhD,
Henk M Verheul3, PhD, Gerrit-Jan S Schuurhuis4, PhD, Godefridus J Peters3,
PhD, Thomas Wurdinger4, MD, PhD, Ugo Boggi1, MD, 1Division of General and
Transplant Surgery and 2Division of Surgical Pathology, University of Pisa, Pisa,
Departments of 3Medical Oncology, and 4Neurosurgery & Pediatric Oncology/
Hematology, VU University Medical Center; 5VisualSonics, Amsterdam, NL, Pisa, IT
BACKGROUND & AIM: Pancreatic ductal adenocarcinoma (PDAC) remains a
major unsolved health problem. Most drugs that pass preclinical tests fail in
these patients, emphasizing the need of improved preclinical models to test
novel anticancer strategies. Early passages of primary PDAC cells may better
mimic the genetic characteristics of the disease and might be better predictors
of drug activity, including the standard treatment with gemcitabine. Recently,
some authors developed primary models by implanting pieces of human PDACs
subcutaneously into mice. However, subcutaneously implanted tumors may not
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optimally recapitulate many of the essential features of tumor growth in patients,
such as the ability to metastasize. The aim of the present study was to develop
orthotopic xenograft models using low passage primary PDAC cells injected in the
pancreas of mice, preserving the genetic background and heterogeneity of human
PDAC, while maintaining the macro- and micro-environmental interactions.
MATERIALS AND METHODS: We developed four orthotopic mouse models
using primary human PDAC cells genetically engineered to express firefly- and
Gaussia luciferase, simplifying the ability to monitor tumor growth and metastasis
longitudinally in individual animals. Transduction efficiency was evaluated using
fluorescence microscopy. Further imaging studies were performed with Magnetic
Resonance Imaging and high-frequency ultrasound. In these models, we conducted
detailed histopathologic and immunohistochemical analyses on paraffin-embedded
pancreatic tissues and metastatic lesions in liver, lungs, and lymph nodes using a
scanner for histopathology evaluation (D-SIght, Menarini, Florence, Italy). Genetic
characteristics were compared with the originator tumors and primary tumor cells
using array-based comparative genomic hybridization with the Agilent 4×180K
platform, using frozen specimens obtained by laser microdissection.
RESULTS: Orthotopic human xenografts in these models recapitulated the
phenotype of human PDACs, including hypovascular and hypoxic areas, as
assessed by immunohistochemical analyses of CD31 and Carbonic Anhydrase
IX, respectively. Pursuing genomic and immunohistochemical evidence revealed
an increased copy number and overexpression of c-Met in one of the models.
Therefore we examined the preclinical efficacy of c-Met inhibitors in vitro and in
vivo. We found that crizotinib decreased tumor dimension, prolonged survival, and
increased blood and tissue concentrations of gemcitabine.
Correspondingly, crizotinib reduced the activity of the gemcitabine catabolic enzyme
cytidine deaminase (CDA), both in tissue specimens and blood samples. Since intact
c-Met signaling is a critical factor in the protection against excessive generation of
endogenous ROS, we demonstrated that a similar mechanism of post-transcriptional
degradation induced by ROS was responsible for CDA reduction after exposure to
crizotinib, resulting in the increased stabilization of gemcitabine.
CONCLUSIONS: Our more readily imaged orthotopic PDAC models displayed
genetic, histopathologic, and metastatic features similar to their human tumors of
origin. Moreover, their use pointed to c-Met as a candidate therapeutic target in
PDAC and highlighted crizotinib and gemcitabine as a synergistic combination of
drugs warranting clinical evaluation for PDAC treatment.
S019 COUNTERACTING CANCER CELL SURVIVAL STRATEGY: SENSITIZATION OF
PANCREATIC CANCER CELLS TO TRAIL INDUCED CELL DEATH BY JAK2/STAT3
PATHWAY INHIBITION BY PREVENTING DEATH RECEPTOR DOWNREGULATION
Kaustav Majumder, MD, Steve Skube, MD, Rohit Chugh, MD, Sulagna Banerjee, PhD,
Ashok Saluja, PhD, Vikas Dudeja, MD, University of Minnesota, Minneapolis, US
INTRODUCTION: TRAIL (Tumor Necrosis Factor-Related Apoptosis Inducing
Ligand) is emerging as a promising anti-cancer therapy by virtue of its strong
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anti-tumor activity against a wide range of cancer cells and minimal toxicity to
normal cells. Unfortunately, pancreatic cancer is resistant to TRAIL. TRAIL binds
to Death Receptors (DR4 and DR5) and forms DISC (Death inducing signaling
complex) that further activates downstream caspases leading to cell death via
apoptosis. TRAIL receptor down-regulation by virtue of endocytosis has been
shown to be one of the mechanisms of TRAIL resistance in cancer cells. The aim
of the current study was to evaluate the combination of TRAIL and JAK-2 downregulation against pancreatic cancer as well as to examine the mechanism for
the proposed synergism.
METHODS: Highly aggressive metastatic pancreatic cancer cell lines (S2013,
S2VP10) and Hepatocellular cell lines (HUH-7) were treated with JAK-2 inhibitor
FLLL-31 (0-5µM), TRAIL (0-40ng/ml) and a combination of JAK-2 inhibitors and
TRAIL. The effect on viability (MTT) and parameters of apoptosis (Annexin V,
Caspase 3, 8 and 9 activation) was measured. Flow Cytometry was used to
evaluate cell surface expression of death receptors. Immuno-precipitation was
used to assess formation of DISC complex.
RESULTS: TRAIL in itself was ineffective in inducing cell death in pancreatic
cancer cells but combination of TRAIL and JAK2 inhibitor FLLL-31 induced
marked decrease in viability and increase in the markers of apoptosis (table).
TRAIL treatment led to down-regulation of both DR4 and DR5 receptors in
pancreatic cancer cell lines S2VP10 and S2013. Intriguingly, in presence of
JAK2/STAT3 inhibitor, TRAIL treatment did not downregulate death receptors
and was associated with increased DISC complex formation and increased
activation of Caspase-8 [DR5 receptor level, expressed as % of levels in
untreated cells (mean ± SEM) - S2013: TRAIL 20ng/ml 62±12.9%, TRAIL 20ng/
ml + FLLL-31 100.2±15; S2VP10: TRAIL 20ng/ml 46.4±18.7%, TRAIL 20ng/ml +
FLLL-31 101±8.8.]
CONCLUSION: Inhibition of JAK-2/STAT3 pathway sensitizes pancreatic cancer
cells to TRAIL induced apoptosis and cell death via inhibition of down-regulation
of DR4 and DR5. This leads to increased availability of death receptors and
increased formation of DISC and augmentation of downstream apoptotic pathway.
Combination of JAK-2/STAT3 silencing and TRAIL has immense potential to
emerge as novel therapeutic strategy against pancreatic cancer.
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S020 TOTAL PANCREATECTOMY WITH ISLET AUTOTRANSPLANTATION FOR
CHRONIC PANCREATITIS: THE PRICE PATIENTS PAY FOR IMPROVEMENTS
IN QUALITY OF LIFE K
atherine Morgan, MD, David B Adams, MD, Stefanie M
Owczarski, PAC, Hongjun Wang, PhD, Wendy Balliet, PhD, Jeffrey Borckardt, PhD,
Medical University of South Carolina, Charleston, US
BACKGROUND: For selected patients with debilitating pain from chronic
pancreatitis total pancreatectomy with islet autotransplantation (TPIAT) has been
undertaken with recently increased enthusiasm. Safety and efficacy, i.e. “patientcentered cost”, of this radical procedure has not been well assessed previously.
METHODS: A retrospective review of a prospectively collected database of
patients undergoing TPIAT was undertaken. Perioperative morbidity, quality of
life (QOL, SF-12), and insulin use were assessed preoperatively and at 12 and 24
months postoperatively.
RESULTS: One hundred twenty patients (93 women, mean age 41, mean BMI 26.2)
underwent TPIAT. Duration of pancreatitis prior to TPIAT averaged 7.6 years (0.540). Mean operative time was 237 minutes (75-395), EBL was 618 cc (50-7800),
and median islet equivalents transplanted were 256,470 (969-1,168,725), or 3640
IEQ/kg (14-16010). Average length of hospitalization was 12 days. Twelve patients
required reoperation in the 30-day post-operative period (10%). Postoperative
morbidity overall was 68% and 23% of patients had a complication requiring
intervention (Clavien-Dindo IIIa or greater). Perioperative mortality was 1.6%. Five
patients (4%) died in the follow-up period. Eighty-five patients were available for
at least 12 month follow-up. Physical QOL went from mean 27 preoperatively to 35
and 33 at 12 and 24 months (p=0.001, 0.003) and mental health QOL went from 38
to 42 and 41 (p=0.02, 0.2). Insulin independence was achieved in 26% and 29% at
12 and 24 months respectively.
CONCLUSION: Quality of life is significantly improved in patients who undergo
TPIAT for chronic pancreatitis, but with notable costs in perioperative morbidity
and diabetes. Improvements in physical and mental QOL are sustained up to two
years after surgery.
S021 COST-EFFECTIVENESS OF TOTAL PANCREATECTOMY WITH ISLET CELL
AUTOTRANSPLANTATION FOR THE TREATMENT OF SMALL DUCT CHRONIC
PANCREATITIS Gregory C Wilson, MD, Daniel E Abbott, MD, Daniel P Schauer,
MD, MSc, Mark H Eckman, MD, MS, Syed A Ahmad, MD, University of Cincinnati
Medical Center, Cincinnati, US
INTRODUCTION: Total pancreatectomy and islet cell autotransplantation (TPIAT)
has gained popularity for managing chronic pancreatitis (CP), but a cost-benefit
assessment has not been scientifically performed. We hypothesized that TPIAT
decreases long-term resource utilization and improves quality-of-life, justifying the
initial costs and risks of the procedure.
METHODS: From 1999-2013, 46 patients with small duct CP and detailed
treatment and outcomes data in the perioperative period (12 months before and
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after TPIAT) were analyzed. These data populated a Markov model comparing
ongoing medical management versus TPIAT for small duct CP. The surgery cohort
included perioperative mortality and complication rates, while CT imaging, insulin
use, morphine equivalent (MEQ) and endoscopic procedure (EGD, EUS, ERCP) and
readmissions were used in both surgical and medical cohorts. Survival (quality
adjusted life years, QALY) and cost (based on Medicare payment, 2013 US$) were
discounted at 3% per year.
RESULTS: Median patient age was 36 years (range = 15-61) with a predominance
of females (n=29, 63%). The etiologies of CP were primarily idiopathic (n=30,
65%) followed by genetic (n=12, 26%). In the 12 months prior to TPIAT (medical
management cohort), annual mean per patient hospital admissions were 1.6
(range = 0-11), endoscopic procedures 1.3 (range = 0-6), and imaging (CT/MRI) 1.3
(range = 0-4). In the surgical cohort there were no perioperative deaths, with
complication and 30-day readmission rates of 41% and 37%, respectively. 1 year
after TPIAT, annual mean per patient admissions, endoscopic procedures and
imaging had decreased to 0.9 (range = 0-4), 0.4 (range = 0-2) and 0.9 (range 0-5),
respectively. Furthermore, monthly narcotic use in the surgical cohort decreased
from 138 to 37 MEQ (p=0.012). Cost and survival for TPIAT versus continued
medical management were $153,575/14.9 QALYs and $196,042/12.8 QALYs,
respectively. Sensitivity analyses with variable perioperative mortality rates,
quality of life adjustment and TPIAT payment did not substantially change the
cost-effectiveness analysis.
CONCLUSIONS: In patients with refractory small duct CP, TPIAT is associated with
both decreased cost and increased quality-adjusted survival. Because TPIAT is a
cost-effective treatment for small duct pancreatitis, tertiary care centers should
look for opportunities to increase the use of TPIAT, and insurers should more
enthusiastically embrace its use.
S022 HIGH READMISSION RATES FOLLOWING SURGERY FOR CHRONIC
PANCREATITIS A V Fisher, J M Sutton, MD, G C Wilson, MD, D J Hanseman, D E
Abbott, MD, M T Smith, MD, N Schmulewitz, MD, K A Choe, MD, J Wang, MD, PhD,
J J Sussman, MD, S A Ahmad, MD, University of Cincinnati, Cincinnati, US
INTRODUCTION: Readmission after complex gastrointestinal surgery
is a frequent occurrence which burdens the healthcare system and leads to
increased cost. Recent studies have demonstrated 30-day and 90-day readmission
rates of 15% and 19%, respectively, following pancreaticoduodenectomy (PD)
for all indications. Given the psychosocial issues often associated with chronic
pancreatitis, we hypothesized that readmission rates following surgery for chronic
pancreatitis would be higher than previously reported for PD.
METHODS: We retrospectively reviewed patients undergoing surgery for headpredominant chronic pancreatitis at a single institution between 2001 and
2013. Patients in this cohort underwent PD, Berne, Beger, or Frey procedures.
Readmission to a primary or secondary hospital was evaluated at both 30 days
and 90 days following discharge. Multivariate logistical regression analysis was
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performed to identify patient demographics, comorbidities, peri-operative factors,
and complications associated with readmission.
RESULTS: The records of 111 patients were evaluated, of which 69 (62%)
underwent duodenal sparing head resection (DSHR; Berne, Beger, Frey), and
the remaining 42 (38%) underwent PD. Within the DSHR arm, readmission
rates at 30 days and 90 days were 30.4% and 43.5% respectively. Due to
multiple readmissions for several patients, there were a total of 57 readmissions
within 90 days. Within the PD arm, readmission rates were similar with
33.3% at 30 days, 40.5% at 90 days, and 34 total readmissions within 90
days. The most common reasons for readmission in both cohorts were pain
control, infectious complications, and recurrent pancreatitis. On multivariate
analysis of the entire cohort, wound infection during initial hospital stay was
a predictor of readmission at both 30 and 90 days (p=0.003). Within 90 days
following discharge, factors associated with readmission included dehydration/
malnutrition (p=0.047), and intractable pain (p=0.023). Factors not associated
with readmission included age, Charlson co-morbidity index, etiology of
pancreatitis, duration of disease, type of operation, operative time or blood
loss, presence of a post-operative pancreatic fistula, transfusion requirements,
respiratory complications (pneumonia, pleural effusion, respiratory failure/
insufficiency), and length of initial hospital stay.
CONCLUSIONS: To our knowledge, our data represents the first report
demonstrating very high readmission rates following surgery for chronic
pancreatitis, more than double the previously reported rates following PD for all
causes. This cohort of patients requires significant discharge planning focused on
pain control, nutritional optimization, and close post-operative monitoring. This
study may serve as a benchmark for further investigation into readmission rates
following the surgical treatment of chronic pancreatitis.
S023 PANCREATICODUODENECTOMY FOR CHRONIC PANCREATITIS: A LONGTERM FOLLOW-UP K
ristopher P Croome, MD, David M Nagorney, MD, Mark J
Truty, MD, Kaye Reid-Lombardo, MD, Florencia G Que, MD, Michael L Kendrick, MD,
Michael B Farnell, MD, Mayo Clinic - Rochester, Rochester, US
BACKGROUND: Over the last 30 years significant developments in the
management of chronic pancreatitis (CP) have occurred due to refinements in
surgical technique, improvements in diagnostic imaging and advancement in the
use of endoscopic therapies. This has led some authors to question the role of
pancreaticoduodenenctomy (PD) in chronic pancreatitis. The present study aimed
to examine the long-term outcomes of PD for CP as well as assess how practice
has changed over time.
METHODS: All patients who underwent PD for CP between the dates of January
1976 and July 2013 were identified. Patient records were reviewed. Patients were
contacted for response to a follow-up questionnaire and SF-12 Quality of Life
Health Survey administration. Patients were divided in 2 eras: Cohort 1 (19761999) and Cohort 2 (2000-2013).
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RESULTS: A total of 166 patients were identified (Cohort 1 (N=105) and Cohort
2 (N=61)). Median time from presentation until surgery was significantly longer
in cohort 2 (2.09 years (2months - 23 years)) compared to cohort 1 (1.13 years
(1month - 39 years)) (p=0.017). A higher proportion of patients in Cohort 2 (98%)
had intractable pain prior to surgery than in cohort 1 (82%) (p=0.002). Prior to PD
a higher proportion of patients in cohort 2 had undergone endoscopic stenting
compared to cohort 1, 67% and 10% respectively (p<0.001). A higher proportion of
patients had also undergone celiac plexus block 15% and 5% (p=0.026). Operative
mortality was not significantly different between cohort 2 (0%) and cohort 1 (3%)
(p=0.18). Median follow-up for all survey respondents was 17.8 years. On the SF12, mean physical component score (PCS) was 48.9±8.7 and mental component
score (MCS) was 56.8±5.22. Patients were not significantly different on the PCS
(p=0.65) and significantly better on the MCS (p=0.004) than the general US
population. Mean pain score out of 10 was significantly lower after surgery 1.3±2.6
than before surgery 8.0±3.8 (p<0.001). At time of last follow-up, diabetes had
developed in 38% of patients who were not diabetic prior to surgery.
CONCLUSION: Although practice has changed so that patients have a longer time
from presentation until surgery as less invasive techniques are attempted, PD
appears to provide effective long-term pain relief and quality of life in patients
who continue to have intractable pain after other interventions have failed.
S024 RISK OF RECURRENT PANCREATITIS AND PROGRESSION TO CHRONIC
PANCREATITIS AFTER ACUTE PANCREATITIS Usama Ahmed Ali, MD, MSc, Yama
Issa, MD, Julia C Hagenaars, MD, Olaf J Bakker, MD, Harry van Goor, MD, PhD,
Vincent B Nieuwenhuijs, MD, PhD, Thomas L Bollen, MD, Bert van Ramshorst,
MD, PhD, Ben J Witteman, MD, PhD, Menno A Brink, MD, PhD, Alexander F
Schaapherder, MD, PhD, Cornelis H Dejong, MD, PhD, Marcel B Spanier, MD, PhD,
Joos Heisterkamp, MD, PhD, Erwin van der Harst, Casper H van Eijck, MD, PhD,
Marc G Besselink, MD, PhD, Hein G Gooszen, MD, PhD, Hjalmar C van Santvoort,
MD, PhD, Marja A Boermeester, MD, PhD, Department of Surgery, Academic
Medical Center, Amsterdam, Utrecht, NL
BACKGROUND & AIMS: Most patients with acute pancreatitis (AP) achieve
complete recovery, but certain patients may develop recurrences and even
progress to chronic pancreatitis (CP). This study aims to evaluate these events and
their risk factors.
METHODS: A cross-sectional survey and retrospective review of an initially
prospectively collected cohort of patients with a first episode of acute pancreatitis
was performed. Primary endpoints were development of recurrent pancreatitis
(RP) and progression to CP. Risk factors for RP and CP were evaluated using
regression analysis, and cumulative risk was assessed using Kaplan-Meijer
analysis.
RESULTS: We included 670 patients that survived a first acute pancreatitis
episode. Median follow-up was 5 years. RP and CP were observed in 124 (19%)
and 42 (6.3%) patients, respectively. Rates of RP were in 13.0%, 24.8% and 25.8%
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of patients with biliary, alcoholic and idiopathic/other etiology, respectively.
Progression to CP occurred in 2.3%, 15.0% and 7.4% for these etiologies,
respectively. Etiology, smoking and pancreatic necrosis were independent risk
factors for both RP and CP. APACHE-II score was an additional independent risk
factor for RP. Cumulative risk for RP over 5 years was the highest among smokers
(about 42% over 5 years). A cumulative risk of progression to CP of about 15% was
observed in patients with alcohol etiology and in smoking patients. When both an
alcoholic etiology and smoking were present the cumulative risk increased to 30%.
CONCLUSIONS: The risk of developing RP and CP is highly dependent on risk
factors. Predominantly smoking is an independent risk factor for RP. For CP, the
combination of alcohol and smoking results in the highest cumulative risk. The
strong association of pancreatic necrosis with RP and CP provides support for the
‘necrosis-fibrosis-sequence’ theory for disease progression.
S025 SEVERE ACUTE PANCREATITIS: USING A MULTIDISCIPLINARY
PERCUTANEOUS DRAINAGE PROTOCOL THE MAIN PREDICTOR OF HOSPITAL
LENGTH OF STAY IS AMYLASE OR BACTERIA IN THE PERCUTANEOUS ASPIRATE
M Sugimoto, MD, G S Flint, C J Boyce, J C Kirkham, L Nesbit, S M Schutz, J T Witte,
M L Lloyd, J G Barton, T J Harris, D P Sonntag, S M Carr, B D Nelson, D A Bell, L W
Traverso, Departments of Radiology, Gastroenterology, and Surgery, St. Luke’s
Health Care System, Boise, US
INTRODUCTION: In addition to critical organ support many patients with severe
acute pancreatitis (SAP) will require drainage followed by nutritional support and
antibiotics. How important is drainage? A risk analysis of clinical parameters for
the outcomes of hospital length of stay (LOS) or mortality may provide an answer.
METHODS: During a 39 month period 98 patients were hospitalized with SAP
– defined as having clinical symptoms of pancreatitis, pancreatitis confirmed
by contrast enhanced CT, and the presence of one of the following CT findings:
peripancreatic fluid collections, pseudocyst, or lack of parenchymal contrast
enhancement (necrosis). Every CT scan for each patient was scored for severity
by 2 radiologists reaching consensus using the modified CT severity index
(CTSI, Mortele et al., AJR 2004;183:1261). The maximum CTSI was recorded.
Only symptomatic cases were treated with drainage based on a standardized
multidisciplinary approach beginning with a percutaneous drainage protocol
with frequent CT/drain exchanges and escalating to open necrosectomy for lack
of progress. Main outcomes were LOS and mortality. The clinical course was
analyzed for those risk factors associated with increased LOS.
RESULTS: The median CTSI was 6 for all patients (n=98) and 8 for percutaneous
drainage cases (n=41). The median LOS for all cases = 13 days and for percutaneous
drainage cases = 24 days. In this consecutive patient cohort, in-hospital mortality
was zero. Open necrosectomy was not required. Univariate analysis showed
a significant relationship with a longer LOS ≥ 14 days to the following clinical
parameters: older age (OR = 1.032, P = 0.019), systemic inflammatory response
syndrome (OR = 2.482, P =0.028), organ failure (OR = 6.622, P = 0.019), necrosis
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(OR = 2.700, P = 0.018), and presence of high amylase (more than 1000) or
bacteria in the initial drainage fluid (OR = 10.127, P <0.001). Multivariate analysis
showed age (OR = 1.032, P = 0.038) and presence of high amylase or bacteria in
the drainage fluid (OR = 7.416, P = 0.002) as independent risk factors for increased
LOS.
CONCLUSION: In symptomatic patients with SAP and a CTSI of 8, a standardized
multidisciplinary percutaneous drainage protocol was able to accomplish a zero inhospital mortality with a median LOS of 24 days. Among all measured parameters
associated with SAP the strongest OR for increased LOS was the presence of
amylase or bacteria in the aspirate at the time of initial percutaneous drainage.
This finding emphasizes the importance of continuous adequate drainage. In our
institution this was accomplished using a standardized protocol directing frequent
catheter exchanges resulting in no hospital mortality.
S026 SURGICAL RESECTION PROVIDES A SIGNIFICANT OVERALL SURVIVAL
BENEFIT FOR PATIENTS WITH SMALL PANCREATIC NEUROENDOCRINE TUMORS
Susan M Sharpe*, MD, Haejin In*, MD, MPH, MBA, David P Winchester`, MD, Mark
S Talamonti^, MD, Marshall S Baker^, MD, MBA, *Department of General Surgery,
University of Chicago, Chicago, IL; ^Department of General Surgery, NorthShore
University HealthSystems, Evanston, IL; `American College of Surgeons, Chicago,
IL, Chicago, US
INTRODUCTION/BACKGROUND: Pancreatic neuroendocrine tumors (PNETs)
have a widely variable potential for malignant behavior. Most series examining
the efficacy of surgical resection of these tumors are underpowered, single
institutional, retrospective studies. There continues to be controversy regarding
the optimal management of incidentally discovered small (<= 2 cm) non-functioning
PNETs. We evaluated the sub-population of small, non-functional PNETs in the
National Cancer Data Base (NCDB) to determine if an aggressive surgical approach
provides a significant survival advantage over observation.
METHODS: The National Cancer Data Base was queried to identify all patients
with PNETs <= 2 cm in size treated between 2003 and 2011. Patients with
metastatic disease at the time of presentation and those with unknown histologic
grade were excluded. Kaplan-Meier analysis, stratified by histologic grade and
treatment type, was used to evaluate the difference in 5-year overall survival (OS)
between patients who received surgery and those who did not. Multivariable Cox
regression was used to determine the relative importance of surgical intervention
in overall survival.
RESULTS: 749 patients met inclusion criteria. 93.2% underwent surgery and 6.8%
were managed with observation alone. 24.7% were size 0-1 cm and 75.3% were
1.1-2 cm. There were no significant differences between patients in the surgical
and observation cohort with regard to tumor size, tumor location, or comorbid
disease characteristics. A greater percentage of patients in the observation
cohort had moderately or poorly differentiated tumors than did patients in the
surgical cohort (37.3% vs. 11.3%, p<0.05). Five-year OS was 89.6% for patients
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who underwent surgery and 40.1% for those who did not (p<0.0001). Variables
included in the final multivariate Cox model were selected by backwards selection
and included: age, Charlson score, tumor location, histologic grade, and treatment
(surgery vs. observation). When controlling for Charlson score, age, and tumor
location, observation without surgical resection (OR 4.94, 95% CI [2.79, 8.76]) and
poorly differentiated histology (OR 8.15, 95% CI [4.47, 14.85]) were independently
associated with a significant increase in the risk of death (p<0.0001). Lymph node
positivity and tumor size were not associated with an increased risk of death.
DISCUSSION/CONCLUSION: In patients with localized, non-functional pancreatic
neuroendocrine tumors 2 cm in size or smaller, surgical resection provides a
significant overall survival advantage over observation. This benefit is independent
of patient age, co-morbid status, and histologic grade of the tumor.
S027 RISK OF MALIGNANCY IN RESECTED NONFUNCTIONING PANCREATIC
NEUROENDOCRINE TUMORS Michael J Ferrara, MS, Michael B Farnell, Kristopher
P Croome, Michael L Kendrick, Mayo Clinic Rochester, Rochester, US
BACKGROUND: Surgical resection is considered for nonfunctioning pancreatic
neuroendocrine tumors (nPNET) due to their malignant potential. Tumor size is a
known predictor of malignancy although the size warranting resection continues
to be debated. The aim of this study was to evaluate the risk of malignancy based
on clinicopathologic factors in patients undergoing resection of nPNET.
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METHODS: Retrospective review of all patients undergoing pancreatic resection of
sporadic nPNET at a single tertiary center from 2004 through 2012. Patients with
known metastasis or those with associated familial syndromes were excluded.
Preoperative imaging (MRI or CT) was reviewed to assess for features suspicious
for malignancy. Histopathology of resected specimens was reviewed for evidence
of malignancy (invasion or lymph node metastases). Median postoperative followup was 32 months.
RESULTS: Of 169 patients, median tumor size was 2.7 cm (range 0.6 cm – 16.5
cm). Malignancy was identified in 64 (38%) patients. Increasing tumor size
was associated with malignancy on logistic regression (p<0.001). Occurrence
of malignancy increased with tumor size: <1cm (0%), 1-1.9cm (22%), 2-3.9cm
(32%), ≥4cm (62%). Malignancy was also more common in patients with
suspicious features on imaging (58% vs. 23%, p<0.001). Occurrence of lymph
node metastases increased with tumor size: <1cm (0%), 1-1.9cm (12%), 2-3.9cm
(27%), 4cm (41%). Prediction of malignancy was investigated by tumor size.
Area under the curve for tumor size was 0.73 with an optimal cutoff of 2.6cm.
Tumor recurrence was identified in 21 (12%) patients, including 5 patients with no
evidence of malignancy at initial resection. Patients with lymph node metastases
were more likely to have tumor recurrence (28% vs. 9%, p=0.03).
CONCLUSIONS: Risk of malignancy in sporadic nPNET is significant even in small
tumors. Malignancy was identified in 22% of tumors between 1 and 1.9cm with
lymph node metastasis in 12%. These findings should prompt consideration of
resection for tumors greater than 1 cm and suggest that resection with regional
lymphadenectomy should be favored over enucleation.
S028 AN INVESTIGATION OF THE UTILITY OF KI-67 EXPRESSION IN PANCREATIC
NEUROENDOCRINE TUMOUR FINE NEEDLE ASPIRATION SAMPLES N
igel B
Jamieson, MD, PhD, Lewis Morrison, BSc, Ross Carter, MD, Euan J Dickson, MD, Colin
J Mckay, MD, Fraser Duthie, MD, Academic Unit of Surgery and West of Scotland
Pancreatic Unit, Glasgow Royal Infirmary, G31 2ER, Scotland, UK., Glasgow, GB
BACKGROUND: Pancreatic endocrine tumors (PETs) are uncommon and represent
1% to 2% of all pancreatic neoplasms. Endoscopic ultrasonography (EUS) in
combination with fine needle aspirate (FNA) is a highly accurate method for
the preoperative diagnosis and staging of pancreatic mass lesions. Despite the
utility of Ki-67 proliferative index of resected PETs for determining prognosis
postoperatively, the role of preoperative FNA sample derived Ki-67 expression
levels have yet not been investigated in depth.
AIMS: To assess the correlation between Ki-67 levels within PETs from
preoperative FNA and surgical resection specimens.
METHODS: Patients with PET tumors managed at the West of Scotland Pancreatic
Unit with full clinicopathological follow-up data were identified from a prospective
maintained database from 1999 to 2012. For this study, samples were only
included if adequate diagnostic preoperative cytology samples and subsequent
surgical resection were available. Immunocytochemical Ki-67 expression levels
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were assessed using validated manual counting techniques in both cytology and
resection specimens. A comparison of cytology and corresponding resection Ki-67
levels were performed.
RESULTS: 59 patients with PETs underwent resection during the study period.
Appropriate tissue was available from 22 patients. In these, significant correlation
was found between preoperative cytology and resection Ki-67 scores (Spearman’s
Rho = 0.6, P = 0.01). An elevated Ki-67 level was an independent predictor of
poor survival following resection (Hazard Ratio = 2.5, P=0.01). More importantly,
an elevated Ki-67 expression in preoperative EUS-FNA cytology specimens was
significantly associated with a reduced overall survival compared to those patients
with tumors expressing a low Ki-67 level (P=0.008, Log-rank).
CONCLUSION: Our study shows that cytological derived Ki-67 levels match closely
with those measured on resected specimens suggesting it can be a reliable predictor
of the behavior and prognosis of PETs. This data has important implications for the
staging and management of patients with PETs particularly those with borderline
fitness who would be best served by a non-operative approach.
S029 THE GASTRINOMA TRIANGLE REVISITED: DUODENAL WALL GASTRINOMA
AND PANCREATIC GASTRINOMA LOCATIONS PREDICT BIOLOGICAL BEHAVIOR
AND LONGEVITY S
am G Pappas, MD, Kara M Doffek, BS, Kathleen K Chrisitans,
MD, Edward J Quebbeman, MD, Douglas B Evans, MD, Stuart D Wilson, MD, Loyola
University Medical Center; Medical College of Wisconsin, Maywood, US
INTRODUCTION: This prospective 51 year observational study investigates the
biological behavior and longevity of sporadic gastrinomas (Zollinger-Ellison’s
syndrome) with specific reference to tumor location and longevity. Passaro’s
studies of the gastrinoma triangle suggest 2 types of gastrinomas based on origin
of location. Fendrich’s recent investigation with molecular markers further explain
a possible different genetic background between duodenal wall gastrinoma (DWG)
and pancreatic gastrinomas (PG).
METHODS: The study cohort consisted of 41 consecutive patients with sporadic
gastrinomas followed in the Clinical Research Center (CRC) and/or who underwent
operations over a 51 year period 1962- 2012. A diagnosis of sporadic form of
Zollinger-Ellison (ZE) syndrome was established in all patients.
RESULTS: Patients were divided into 2 groups based on tumor location. Thirtyfive patients with extrapancreatic gastrinoma found in the duodenal wall and/
or paraduodenal lymph nodes were assigned DWG group. Five patients with
primary pancreatic gastrinoma were assigned PG group. One patient with a
primary gastrinoma in the gastric antral wall was considered separately. Clinical
presentation (i.e. symptoms, ulcers, gastric acid, gastrin) were similar in DWG
and PG groups. Total gastrectomy (26 patients) was most common in the era
(1962-1979) prior to advent of effective acid suppression medications. Subsequent
operations have attempted to cure by excising DWG and/or paraduodenal lymph
nodes. Overall mean survival for 35 DWG patients has been 16.5 years vs. 2.3
years for 5 PG patients(p<.05). Remarkably none of the DWG patients died from
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tumor progression or developed liver metastasis even when operation was not
curative and hypergastrinemia persisted whereas all 5 PG patients died early with
progressing liver metastasis.
DISCUSSION: This 51 year observational study supports the concept that DWG
and PG are distinct clinical entities. The biological behavior of these 2 different
gastrinomas portends different outcomes. PG tumors metastasize early to the
liver and patients are short-lived. Whereas in DWG patients liver metastasis were
not observed and there were no deaths from tumor progression . Management of
DWG and PG entities should be different.
S030 PATTERNS OF PRACTICE AND SURVIVAL AMONG PATIENTS WITH NONMETASTATIC PANCREATIC NEUROENDOCRINE TUMORS UNDER 2 CM Jan Franko,
MD, PhD, Charles D Goldman, MD, Mercy Medical Center DSM, Des Moines, US
BACKGROUND: Discrepant evidence is available for treatment of small nonfunctional pancreatic endocrine tumors (NF-PET). We examined practice patterns
and overall survival among patients with NF-PET and tumor size 2 cm and smaller.
METHODS: The NCDB Participant Use Data File (PUF) for pancreas covering 19982011 was queried for clinical characteristics, demographic, treatment and outcome
data for all cases coded as NF-PET. Survival analysis was performed for patients
diagnosed 1998-2006 to allow at least five years of follow-up.
RESULTS: Data on initial resection versus observation were available on 6,689
cases of non-metastatic NF-PET. 270 (4%) of small non-metastatic NF-PETs were
initially observed. This proportion was 14% among those with stage I-II disease.
There was no trend in resection and observation rates over the study period.
Initial observation rather then resection among non-metastatic patients was to some
extent predicted by multinomial logistic regression (pseudo R2=0.276, p<0.001).
Observation was more common with younger age, pancreatic head location, and
tumors ≤2cm, but not influenced by modified Charlson-Deyo comorbidity index.
Among resected non-metastatic NF-PETs sized ≤2 cm 72.8% were node-negative,
whereas 27.2% were node-positive. Higher proportion of node-positive disease
was observed among corresponding patients with tumor size over 2 cm (49.5%
node-positive, p<0.001).
Survival among non-metastatic small PET was better among those resected
(p<0.001) even when analysis was restricted to those with clearly resectable
disease (stage I-II, p=0.014). Cox model demonstrated that age, resection rather
then observation (HR=0.25), nodal status (HR=1.47), and size >2 cm (HR=1.55) were
predictive of survival, but not comorbidity and tumor location (head vs. body/tail).
CONCLUSION: A small proportion of non-metastatic NF-PET is not initially
resected, but observed. Clinical characteristics explain only 27% variability in
decision to operates versus observe. Resection of even small NF-PETs measuring 2
cm and less is associated with improved survival. This analysis supports resection
of all NF-PETs, including those smaller than 2 cm.
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S031 RE-CLASSIFICATION OF COMBINED-TYPE IPMNS ALLOWS FOR A BETTER
DEFINITION OF TWO DISEASE ENTITIES G
iovanni Marchegiani, MD, Mari MinoKenudson, MD, Klaus Sahora, MD, Cristina Ferrone, MD, Sarah Thayer, MD,
Andrew L Warshaw, MD, Keith D Lillemoe, MD, Carlos Fernandez-del Castillo, MD,
Massachusetts General Hospital - Harvard Medical School, Cambridge, US
BACKGROUND / AIM: Malignant potential of IPMNs is associated with involvement
of the main pancreatic duct (MPD). Mixed-type or combined IPMNs have been
historically categorized together with main duct tumors. However, combined
IPMNs encompass a spectrum which differs in terms of extent of MPD
involvement. We sought to re-classify combined IPMNs to better define groups
that may diverge in pathological features and biological behavior.
METHODS: Slide re-classification by a single pancreatic pathologist of all IPMNs
operated between 1990 and 2013 at the MGH. IPMNs were divided into lesions
with predominant involvement of the MPD (pred-MD) and into those with
predominant involvement of the branch ducts (pred-Bd).
RESULTS: Out of 421 patients who underwent surgery for IPMN, 386 patients
had enough material for re-review. 176 (46%) were pred-MD and 210 (54%)
pred-Bd. Median age was 67 in both groups; male-to-female ratio was 1.1:1 in
pred-MD and 1:1.3 in pred-Bd (P=0.02). Pred-MD were significantly more likely to
be smokers, diabetic, jaundiced and to have a history of pancreatitis, weight loss
and an elevated CA 19.9 (all P<0.05). Pred-MD were of the intestinal and gastric
epithelial subtype in 48% and 34% of cases, respectively, while in pred-Bd these
frequencies were 14% and 80% (P<0.001). 72% of pred-MD had high-grade
dysplasia or more, whereas 79% of pred-Bd were either low- or intermediategrade (P<0.001). Invasive carcinoma was found in 39% of pred-MD compared
to only 5% of pred-Bd (P<0.001); the latter were mostly tubular (83%), whereas
pred-MD were spread between colloid (31%), tubular (59%) and oncocytic (10%)
(P=0.08). Distinct PDAC was present in 2.8% of pred-MD and in 6.1% of pred-Bd
(P=0.1)
Median follow-up was 90 months and 5-year overall survival 77%. 5-year diseasespecific survival was 83% and 96% for the pred-MD and pred-Bd, respectively
(P=0.002). For invasive cancers, 5-year DSS was 64% for the pred-MD and 41% for
the pred-Bd (P=0.2). At 10 years overall recurrence rates were 25% and 17% for
pred-MD and pred-Bd respectively (P=0.08), but for invasive tumors they were
48% in pred MD and 81% in pred Bd (P=0.04).
CONCLUSIONS: Re-classification of combined IPMN based on the actual extent
of MPD involvement identifies two different entities in terms of epidemiology,
biology and outcome. Pred-MD are more symptomatic and malignant than
pred-Bd, and are associated with a worse prognosis. However, invasive predBD recurs more often and tends to have a worse disease specific survival than
invasive pred-MD.
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S032 CLINICAL VALIDATION OF NEW INTERNATIONAL CONSENSUS GUIDELINES
FOR THE RESECTION OF BRANCH DUCT TYPE INTRADUCTAL PAPILLARY
MUCINOUS NEOPLASMS (BD-IPMN) Jin-Young Jang, Selyeong Lee, Mee Joo
Kang, Taesung Park, Kyoung Bun Lee, Wooil Kwon, Ye Rim Chang, Seung Yeoun
Lee, Sun-Whe Kim, 1Department of Surgery and Cancer Research Institute, Seoul
National University College of Medicine, Seoul, Korea 2Department of Statistics,
Seoul National University College of Natural Sciences, Seoul, Korea 3Department
of Pathology, Seoul National Univ, Seoul, KR
BACKGROUND: Despite new consensus guidelines, classifications of intraductal
papillary mucinous neoplasm(BD-IPMN) remain ambiguous, especially for mixed
type, and factors predicting malignancy remain unclear. The aim of this study was
to evaluate the clinical usefulness of each factor predicting malignancy in the new
consensus guidelines for resection of branch duct type (BD-IPMN) and to validate
new guideline comparing with previous one.
METHODS: The sensitivity, specificity, balanced accuracy and area under the
receiver operating characteristic (ROC) curve for the first and second consensus
guidelines were compared. The statistical importance of each variable was analyzed
in a prospectively collected database of 350 patients with biopsy proven BD-IPMN.
RESULTS: Random Forest models showed that the sensitivity, specificity, and area
under the ROC curve (AUC) were 0.639, 0.822, and 0.774, respectively, for the first
consensus guidelines; and 0.724, 0.779, and 0.801, respectively, for the second
consensus guidelines, with balanced accuracies of 0.730 and 0.751, respectively.
Multiple logistic regression analysis showed that main pancreatic duct dilatation
>5 mm (hazard ratio [HR] 4.538; 95% confidence interval [CI], 2.449-8.408;
P<0.001), mural nodules (HR 6.267; 95% CI, 3.271-12.009; P<0.001), and CA19-9 >37
U/ml (HR 4.032; 95% CI, 1.826-8.903; P=0.001) were independent predictors of
malignancy of BD-IPMNs.
CONCLUSION: The second consensus guidelines showed better sensitivity, AUC
and balanced accuracy than the first consensus guidelines in the diagnosis of
BD-IPMN malignancy. However, size alone was limited in predicting malignancy.
Additional tumor markers and imaging findings may be used as indicators for
resection of BD-IPMN. The variability in clinical significance of each variable
of the consensus guidelines indicates the need for a tailored approach in the
management of patients with BD-IPMN.
S033 INTRADUCTAL PAPILLARY MUCINOUS NEOPLASM OF THE PANCREAS,
ONE MANIFESTATION OF A MORE SYSTEMIC DISEASE? A
lexandra M Roch, MD,
Carlo M Rosati, MD, Eugene P Ceppa, MD, Mohammad A Al-Haddad, MD, John
M DeWitt, MD, C Max Schmidt, MD, PhD, MBA, FACS, 1 Department of Surgery,
Indiana School of Medicine, Indianapolis, IN, USA; 2 Department of Medicine,
Division of Gastroenterology, Indiana University Hospital, Indianapolis, IN, USA,
Indianapolis, US
BACKGROUND: Several studies have demonstrated a high prevalence of extra
pancreatic malignancies in patients with intraductal papillary mucinous neoplasm
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(IPMN) of the pancreas. Similarly, recent case reports have described an
association between IPMN and autoimmune pancreatitis.
Hypothesis: We hypothesized that IPMN were associated with an increase rate of
systemic disease (extra pancreatic malignancies and autoimmune disease).
METHODS: From 1996 to 2012, 841 patients with IPMN were seen at the pancreatic
cyst clinic of a single academic institution. A retrospective analysis of a prospectively
collected database was performed and supplemented with electronic medical
charts review of clinical, radiological and (cyto) pathological parameters. Difference
between observed and expected frequencies was assessed using Chi-square
test. Fisher’s exact test compared IPMN type distribution - main pancreatic duct
involved IPMN (MPD-involved IPMN) or branch-duct IPMN (BD-IPMN) - and rate of
malignancy/invasiveness. P<0.05 was considered significant.
RESULTS: Among the 841 patients, 500 (59.5%) were followed whereas 341
(40.5%) underwent surgical resection for IPMN. Mean age was 68 years.
220 extra pancreatic malignancies were found in 185 patients (22%). The most
common malignancies were colorectal adenocarcinoma (26/841, 3.1%), lung
carcinoma (14/841, 1.7%) and renal cell carcinoma (14/841, 1.7%) with observed/
expected frequencies ratio <0.0001 in those 3 cancers. However, the presence of
extra pancreatic malignancy did not influence the subtype of IPMN (p=0.79), the
rate of malignancy (p=0.81) or the rate of invasive carcinoma (p=0.89).
110 synchronous autoimmune diseases were found in 96 patients (11.4%). Systemic
lupus erythematosus was found in 6/841 (0.7%), rheumatoid arthritis in 12/841
(1.4%) and inflammatory bowel disease in 15/841 (1.8%) with observed/expected
frequencies ratio <0.0001, 0.014 and <0.0001, respectively. Patients associated
autoimmune disease had a significantly higher rate of BD-IPMN (77.1% vs. 66.7%,
p=0.048), resulting in lower rates of malignancy and invasive carcinoma (5.2%
vs. 15.3% and 3.1% vs. 10.9%, p=0.005 and 0.017, respectively). However, when
analyzed separately according to IPMN type, there was no influence of an
associated autoimmune disease on malignancy/ invasiveness. Finally, in patients
with autoimmune disease there was no impact of immunosuppressive treatment
(steroids or immunosuppressant) on the subtype distribution (p=0.61), malignancy
(p=0.66) or invasive carcinoma rates (p=0.9).
CONCLUSION: IPMN are associated with surprisingly high rates of extra pancreatic
malignancies and autoimmune diseases (22% and 11.4%), suggesting that IPMN
might be one manifestation of a more systemic disease.
S034 THE BIOLOGY OF SMALL IPMN CANCERS (< 20 MM INVASIVE
COMPONENT): A MULTI-INSTITUTIONAL ANALYSIS Jordan M Winter, MD, Zhi
V Fong, MD, Wei P Tan, MD, Wei Jiang, MD, PhD, Basturk Olca, MD, Mari MinoKenudson, MD, Harish Lavu, MD, Dana Haviland, David S Klimstra, MD, Murray
F Brennan, MD, Keith D Lillemoe, MD, Charles J Yeo, MD, Carlos Fernandez-Del
Castillo, MD, Peter J Allen, MD, Thomas Jefferson University, Massachusetts
General Hospital, Memorial Sloan-Kettering Cancer Center, Philadelphia, US
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Recurrence risk of small invasive IPMN (p=0.4)
No recurrence
0 to 4.9 mm
29 (85%)
5 to 9.9 mm
11 (79%)
10 to 14.9 mm
4 (57%)
15 to 19.9 mm
7 (88%)
Total
51 (81%)
Recurrence
5 (15%)
3 (21%)
3 (43%)
1 (12%)
12 (19%)
BACKGROUND: Early invasive malignancy may be encountered in the background
of intraductal papillary mucinous neoplasms (IPMN). The natural history of these
invasive lesions is unknown.
METHODS: Pancreatic surgical databases from 3 high-volume centers (Thomas
Jefferson University, Massachusetts General Hospital, and Memorial Sloan-Kettering)
were queried for IPMN with invasive components <20 mm. Cases were reviewed
by GI pathologists. A concensus between institutional pathologists was reached for
difficult cases. Pathologic features were analyzed to identify predictors of recurrence.
RESULTS: A total of 63 small invasive IPMN (< 20 mm invasive component) were
identified, comprising 35% of resected invasive IPMN (1993 to 2013). The median
follow-up was 26 months (0.2 to 179). There were 16 deaths (25%), with a median
estimated survival of 8 years. The overall recurrence rate was 19% (n=12) and the
average time to recurrence was 15 months (4 to 132). Recurrence patterns were
local in 33%, distant in 42%, and both in 25%. The majority of invasive foci were
multifocal (73%) and involved the main duct (95%), with neither feature associated
with recurrence. Papillary patterns included intestinal (51%), pancreatobiliary (17%),
gastric (16%), oncocytic (10%), and mixed (6%), with comparable recurrence rates
(18% to 50%, p=0.4). Cancer subtypes included tubular (52%), colloid (32%), oncocytic
(11%), mixed (3%), and signet ring (2%), again with comparable recurrence rates
(10 to 43%, p=0.4). Microscopic vessel invasion was identified in one patient (2%),
perineural invasion in 19%, and microscopic lymphatic invasion in 15%. Regional
lymph node metastasis was present in 16%, and correlated with lymphatic invasion
(p<0.001). Unadjusted predictors of recurrence included lymph node metastasis
(60% vs. 11%, p=0.001), lymphatic invasion (50% vs. 18%, p=0.04), and perineural
invasion (42% vs. 14%, p=0.03). Dysplasia at the neck margin was observed in 19%
of cases, but was not associated with recurrence (33% vs. 13%, p=0.1). The size
of invasive foci was not associated with recurrence risk (p=0.4, table). Adjuvant
treatment (16% of patients) was associated with a non-significant increase in
recurrence risk (40% vs. 17%, p=0.1). In a multivariate model (dysplastic margin,
perineural invasion, lymph node metastasis), lymph node metastasis was associated
with recurrence (OR 11, p=0.005). Patients harboring small invasive IPMN without
lymph node metastasis or perienural invasion still had a 9% recurrence risk.
CONCLUSION: The majority of small IPMN cancers are successfully treated with
resection. However, recurrence risk is significant, and greatest in patients with
lymph node metastases. Whether recurrences represent progression of residual
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disease or metachronous disease is unknown. Due to incomplete follow-up, these
data likely underestimate the true recurrence rate.
S035 A NATIONAL PERSPECTIVE OF INVASIVE INTRADUCTAL PAPILLARY
MUCINOUS NEOPLASM (IPMN) R
ussell S Lewis, BS, Jeffrey A Drebin, MD, PhD,
Douglas L Fraker, MD, Charles M Vollmer, MD, The Perelman School of Medicine,
University of Pennsylvania, Philadelphia, US
INTRODUCTION: Great understanding of IPMN has occurred in the last two
decades, however questions remain which cannot be adequately answered by
currently available institution-based literature. Specifically, 1) What are predictors
of survival in these malignancies? 2) What is the impact of adjuvant therapy
in this cohort? 3) How do outcomes compare to standard pancreatic ductal
adenocarcinoma (PDAC)? A large scale assessment of invasive IPMN using a
national dataset would provide greater clarity to these clinical dilemmas.
METHODS: Surgical patients from the National Cancer Database (NCDB) with
histologically confirmed invasive IPMN were studied from 1998-2005 and compared
to those with PDAC. Patients were excluded if they received preoperative systemic
or radiation therapy, or if they died within 30 days of the operation. Survival was
assessed using the log-rank test statistic and Cox regression.
RESULTS: 1739 patients underwent pancreatic resection for invasive IPMN (54% N0,
70% R0, median tumor size=3.5cm). 31% of patients were Stage 1, 33% Stage 2, 20%
Stage 3, 11% Stage 4, and 5% were unclassified. For the overall cohort, median, 1-yr,
and 5-yr survivals were 26.7m, 74%, and 32%. Adjuvant therapy was used in 45%
of patients (24% in Stage 1 vs. 58% in Stages II-IV). The majority of treated patients
received combined Chemo/XRT (70%). When assessed by Cox regression, improved
survival for invasive IPMN was associated with receipt of adjuvant therapy (HR=
0.76; p<0.001), treatment at academic facilities, low grade tumors, N0 status, R0
resection, lower AJCC stage, and younger age. Furthermore, Cox models by stage
revealed a survival advantage associated with adjuvant therapy in patients with
Stage II-IV disease (HR 0.66; p<0.001), but not in Stage I (HR 1.21; p=0.223). IPMN had
significantly better stage-adjusted survival than PDAC (table).
CONCLUSIONS: Invasive IPMN appears to be more indolent than standard PDAC,
even after stage adjustment. Overall, adjuvant therapy improves survival for
invasive IPMN, especially in higher-staged disease (by 34%). However, this benefit
is not evident in early stage disease, negating the necessity of post-operative
therapy in these situations.
AJCC Stage
1
2
3
4
Overall
IPMN, suvival (mo.)
80.4
24.1
16.8
10.1
26.7
PDAC, survival (mo.)
24.6
17.6
14.4
9.8
16.2
P-value
<0.001
<0.001
0.010
0.318
<0.001
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S036 CHARACTERIZATION OF PANCREATIC STROMAL CELLS ISOLATED FROM
PANCREATITIS AND PANCREATIC ADENOCARCINOMA SURGICAL SPECIMENS
Song Han, PhD, Daniel Delitto, MD, Jose G Trevino, MD, Kevin E Behrns, MD, Steven
J Hughes, MD, Department of Surgery, University of Florida, Gainesville, US
INTRODUCTION: Accumulating evidence implicates the desmoplastic stromal
compartment of the pancreatic cancer microenvironment as an integral factor in
tumor development. However, the precise mechanisms of stromal contribution
to cancer progression and the development of chemoresistance remain poorly
characterized. We present a reproducible model capable of isolating pancreatic
stromal cells from surgical specimens for further investigation into tumorstromal interactions.
METHODS: Primary human pancreatic tissue was received fresh from surgical
resections at the University of Florida’s high volume pancreatic surgery center.
Pancreatitis, heavily implicated as a precancerous state, was included in a
separate group from normal pancreas and pancreatic adenocarcinoma. Tissue
fragments were minced and cultured in Dulbecco’s Modified Eagle Medium
(DMEM) with 10% fetal bovine serum (FBS). Resulting stromal cells isolated in
this manner were cultured and population doubling times were recorded. After
5-7 passages, cultured cells were further characterized with flow cytometry
and immunohistochemical analysis. Specifically, markers of epithelial (ESA) or
stromal (GFAP, α-SMA) differentiation as well as senescence (α-H2AX, Ki-67)
were examined. Pancreatic stromal cells were then co-cultured with established
pancreatic cancer cell lines (BxPC3, L3.6pl and PANC-1) and supernatants were
assayed for differential cytokine secretion using Luminex analysis.
RESULTS: A total of 35 surgical specimens were investigated. Successful
outgrowth of stromal cells was achieved in 3/5 (60%) normal pancreas samples,
5/6 (83%) pancreatitis samples and 23/24 (96%) pancreatic adenocarcinoma
samples. Senescence occurred at 9.37+/- 0.38 (mean +/- SD) population doublings
without significant variation between groups. Flow cytometry revealed α-SMA
expression in over 95% and ESA expression in less than 5% of cultured stromal
cells in all groups. These results were compared to a commercially available
immortalized pancreatic fibroblast cell line, characterized by less than 1% α-SMA
expressing cells and 58% ESA expressing cells. Co-culture of cancer-associated
stroma with established pancreatic cancer cell lines revealed a 100-1,000-fold
increase in SDF-1 expression compared with cancer cells cultured alone. This
trend was observed across all established cancer cell lines co-cultured with three
different stromal grafts.
CONCLUSION: Our model provides a reliable method for in vitro isolation of
pancreatic stromal cells from human specimens in order to further characterize
the microenvironment in pancreatitis and pancreatic cancer. Outgrowth of
stromal cells in this manner demonstrates high levels of α-SMA expression and
minimal ESA expression, indicative of pancreatic myofibroblastic differentiation.
Additionally, co-culture of cancer-associated stroma obtained from our model
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with established cancer cell lines resulted in significantly elevated SDF-1 secretion,
which is in agreement with current literature regarding paracrine signaling
between cancer-associated stroma and pancreatic cancer cells.
S037 CURRENT INDICATIONS FOR SURGERY OF IPMN’S MAY OVERLOOK SOME
PATIENTS WITH CANCER: RECOMMENDATIONS FOR CHANGE Andrew H Nguyen*,
Paul Toste*, James J Farell#, Barbara M Clerkin*, V. Raman Muthusamy^, Rabindra
Watson^, James S Tomlinson*, O. Joe Hines*, Howard A Reber*, Timothy R Donahue*,
* Department of Surgery, David Geffen School of Medicine at UCLA, # Yale Center
for Pancreatic Disease, Yale University School of Medicine, ^ UCLA Division of
Digestive Diseases, David Geffen School of Medicine at UCLA, Los Angeles, US
INTRODUCTION/BACKGROUND: Over the past decade, the management of
intraductal papillary mucinous neoplasms (IPMN) has continued to evolve. Due
to the high risk of cancer, almost all patients with main or mixed duct IPMN are
recommended to undergo surgical resection. However, there continues to be
debate in the management of patients with branch duct IPMN (BD-IPMN), which is
associated with a lower risk of invasive malignancy. The revised Sendai Criteria of
2012 place less emphasis on the size of the lesion, and recommends that BD-IPMN
≥3 cm on noninvasive imaging (NIM) be interrogated by endoscopic ultrasound
(EUS) for further “worrisome features.” Those lesions without a mural nodule/
solid component or atypical cells on fine needle aspiration (FNA) should undergo
observation rather than surgical resection. This change has generated significant
concern amongst physicians treating pancreatic cystic lesions. Therefore, the aim
of this study was to perform a retrospective review of BD-IPMN resected at a
high volume pancreatic surgical center to determine: (i) the preoperative variables
associated with malignancy and (ii) the optimal size cutoff on NIM to identify
patients who should undergo EUS to identify those with advanced pathology.
METHODS: 66 patients with BD-IPMN between July 1996 to June 2012 at a high
volume pancreatic surgical program at an academic medical center were identified
in a prospectively maintained database of patients who underwent pancreatic
resection. BD-IPMN were initially characterized by pre-operative CT/MRI and later
confirmed by pathologic review. BD-IPMN was defined as a cystic dilation of the
pancreatic duct, but not involving the main duct. Demographic, pathologic, and
imaging data were extracted. Pathologic grade was dichotomized into (i) low (low
or intermediate grade lesions) versus (ii) high (high grade, carcinoma in situ or
invasive cancers). Fisher’s exact test, t-test, and receiver operator characteristic
(ROC) analysis were performed.
RESULTS: The median cyst size on NIM was 2.7 cm (range: 0.6-9.6 cm), which
correlated with final pathologic size (R2 = 0.819, p<0.001). Fifty-one (77%) low
and 15 (23%) high grade BD-IPMN were identified. ROC analysis demonstrated
that lesion size (on NIM) is a reasonable predictor of grade with an area under the
curve of 0.691. Two-thirds of high grade BD-IPMN were <3 cm (n = 10). Compared
with a cutoff of 3.0 cm, a NIM size cutoff of 2.0 cm: was associated with higher
sensitivity (73.3% vs. 33.3%) and negative predictive value (83.3% vs 80%) for high
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grade IPMN. In fact, all smaller size cutoffs had higher NPVs than 3.0 cm. Mural
nodules or atypical cells on FNA were identified in all cysts <2.0 and only 50% of
those <3.0 cm.
DISCUSSION/CONCLUSIONS: Small cysts less than 3.0 cm can harbor high grade
lesions or even invasive cancer. Our data suggests a need for further evaluation
by EUS of smaller cysts. These results are opposite the trend of the revised 2012
Sendai Criteria towards greater observation and surveillance of larger cyst sizes.
S038 MAIN PANCREATIC DUCT SIZE AND RISK OF MALIGNANCY IN
INTRADUCTAL PAPILLARY MUCINOUS NEOPLASM N
eda Rezaee, MD, Lindsey
L Manos, PAC, Siva P Raman, MD, Elliot K Fishman, MD, Ralph H Hruban, MD,
Timothy M Pawlik, MD, MPH, PhD, Matthew J Weiss, MD, Anne Marie Lennon, MD,
PhD, Christopher L Wolfgang, MD, PhD, FACS, Department of Surgery, The Sol
Goldman Pancreatic Cancer Research Center, Johns Hopkins Medical Institutions,
Baltimore, Maryland, Baltimore, US
BACKGROUND: Main pancreatic duct involvement by intraductal papillary
mucinous neoplasm (IPMN) of the pancreas is associated with a high risk of
invasive adenocarcinoma. The definition of what constitutes main duct or mixed
type IPMN based on duct size is variable. Very few published work is available
that documents risk of malignancy as a function of the size of the main pancreatic
duct. The aim of this study was to identify an optimal duct size to contribute to
main duct type IPMN.
METHODS: Data of patients with preoperative CT scan study who underwent
surgical resection for an IPMN from 1996 to 2013 was analyzed. CT scans of
the patients were reviewed by a radiologist where imaging was available. Main
pancreatic duct (MPD) size was determined by the maximal cross-sectional
diameter perpendicular to the long axis of the duct. IPMNs with low or
intermediate grade of dysplasia were stratified as “low-risk”, and lesions with
high-grade dysplasia or invasive carcinoma as “high-risk” disease.
RESULTS: A total of 420 consecutively resected IPMNs with adequate preoperative
imaging data were identified. On final pathology 67 (16%) IPMNs were classified as
low-grade dysplasia, 160 (38%) with intermediate grade dysplasia, 95 (23%) with
high-grade dysplasia, and 98 (23%) with invasive carcinoma. MPD was < 5mm
(small duct) in 224 (53%), 5-9 mm (intermediate duct) in 128 (30%), and >9 mm
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(large duct) in 68 (17%) patients. High risk IPMN was found in 26% small duct, in
63% intermediate, and 78% large duct IPMNs. Area under the receiver operating
characteristics curve (AUR) of the MPD for predicting high risk IPMN was 75% (95%
CI: 0.70- 0.80). The duct size of 5-mm was associated the optimal intersection of
sensitivity (69%) and specificity (73%). The positive predictive value of the 5-mm
duct threshold for high risk lesions was 68% and the negative predictive value was
74%. When the duct was dilated to ≥ 5mm, the incidence of high-risk IPMN wasnot
different in lesions with diffuse (73%) or focal (59%) duct dilatation (p=0.06).
CONCLUSION: Preoperatively identified main pancreatic duct dilatation is an
important factor in guiding the management of the IPMNs. Based on the increased
risk of high-grade dysplasia and invasive carcinoma, surgical resection should be
strongly considered when the MPD is diffusely or focally dilated to ≥ 5mm.
S039 DOES EUS IMPROVE OUTCOME IN SURVEILLANCE OF NON-RESECTED
PRESUMED BRANCH-DUCT INTRADUCTAL PAPILLARY MUCINOUS NEOPLASMS?
Anna C Evans, MD, Tarun Rustagi, MD, James J Farrell, MD, Yale-New Haven Hospital
Internal Medicine Department; Yale Center for Pancreatic Disease, Interventional
Endoscopy, Yale School of Medicine, New Haven, CT, New Haven, US
BACKGROUND: Current guidelines support surveillance with non-invasive imaging
for presumed branch duct intraductal papillary mucinous neoplasms (BD-IPMN),
not initially managed with surgery. There is little data regarding the optimal
frequency, modality and long-term outcomes of both non-invasive (CT/MRI) and
invasive (EUS) surveillance in these patients. We aim to perform a systematic
review of all published studies to better define current surveillance strategies and
outcomes in these patients.
METHODS: MEDLINE and Embase database searches were performed to identify
studies with BD-IPMN patients that were initially managed non-surgically and
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surveyed for ≥ 3 months. Data regarding study design, number of patients,
modality and frequency of surveillance, followup duration, change in cyst
characteristics, development of pancreatic malignancy, and impact of surveillance
on management was extracted.
RESULTS: Of 677 citations identified, 39 studies with 3745 BD-IPMN patients were
included for analysis. Overall mean per-patient follow-up was 40.1±20.7 months.
Morphologic progression of cystic lesions including new signs concerning for
malignancy (increase in size, development of nodularity) was noted in 22.24% of
patients (n=31 [79%] studies). 15.28% patients underwent surgical resection of
cysts (n=37 [95%] studies). Pancreatic cancer developed in 141 (4.42%) patients
(n=32 [82%] studies). Calculated risk of developing pancreatic cancer in BD-IPMN
patients was 1.3% per year. 70 (4.36%) patients died during follow-up (1.38% per
year; n=17 studies). Surveillance was done using CT (n=34 [87%] studies), MRI/
MRCP (n=31 [79%] studies) and EUS (n=24 [62%] studies), with all three modalities
of surveillance being used in 21 (54%) studies involving 55% of all BD-IPMN
patients. 28 of 39 studies (81% of all BD-IPMN patients) reported change in
management based on surveillance results. There was a statistically significant
lower rate of surgical resection (p<0.00001) and overall mortality (p=0.0004) in
patients undergoing surveillance which included EUS, compared with those who
did not undergo EUS as part of their surveillance (Table 1).
CONCLUSIONS: Although this study has the limitations of a systematic review,
it represents the most comprehensive study regarding long-term outcomes and
surveillance techniques in BD-IPMNs. In addition to confirming the 1% yearly rate
of cancer development in surveillance, this study strongly suggests that including
EUS in surveillance of BD-IPMN may decrease mortality and reduce the need for
surgery, and warrants further study.
Table 1. Outcomes for EUS surveillance in presumed BD-IPMN patients
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S040 RESECTED PANCREATIC ADENOCARCINOMAS WITH RECURRENCE
LIMITED IN LUNG HAVE A SIGNIFICANTLY BETTER PROGNOSIS THAN THOSE
WITH OTHER RECURRENCE PATTERNS L
ei Zheng, MD, PhD, Tamna Wangjam, MD,
Zhe Zhang, MS, Xiao Chong Zhou, MS, Laxmi Lyer, MD, Farzana Faisal, BS, Kevin
C Soares, MD, Elliott Fishman, MD, Ralph H Hruban, MD, Joseph Herman, MD,
Daniel Laheru, MD, Matthew Weiss, MD, Ana De Jesus-Acosta, MD, Christopher L
Wolfgang, MD, PhD, Johns Hopkins University School of Medicine, Baltimore, US
INTRODUCTION/BACKGROUND: Majority of resected pancreatic adenocarcinoma
(PC) recurs within 5 years of resection. However, the prognosis of different
patterns of recurrence, particularly in the lung, has not been well studied.
METHODS: Between 1998 and 2007, 209 consecutive patients had surgical
resection of PC and had postoperative follow-up primarily at the Johns Hopkins
Hospital. A retrospective analysis of the 174 cases of recurrent PC out of the
209 patients was performed. Survival distributions among different patterns of
recurrence were described using the Kaplan-Meier method and compared using
Cox proportional hazards models.
RESULTS: With a median follow-up of 16 months (range 0.8-142.9), 174 of the 209
patients had recurrent diseases. Of those, 28 (13.4%) had metastatic recurrent
diseases limited to lung only, 20 (9.6%) had recurrence in lung with one or more
sites excluding liver, 73 (34.9%) had liver metastasis alone or with any other site
except lung, 28 (13.4%) had local recurrence only, and 25 (12.0%) had peritoneal
recurrence alone or together with local recurrence.
Patients with recurrence limited to lung had a 8.5 Mo median survival time from
recurrence to death (RTD) and a 27.8 Mo median survival time from surgery to
death (STD), which was significantly better than recurrence at any other site such
as liver, peritoneum and local site in multivariate analyses after adjusting for age,
tumor margin, tumor size, lymph nodes, and time from surgery to diagnosis of
recurrence (for RTD, Liver vs. Lung: HR 1.90, p=0.022; Peritoneum vs. Lung: HR 6.32,
p<0.0001; Local vs. Lung: HR 2.09, p=0.025). Interestingly, among all groups with
different recurrence patterns, the time from surgery to the diagnosis of recurrence
(STR) in patients who recurred in lung only (12.7 Mo) is also the longest. However,
75% of patients were found to have undetermined lung nodules in their surveillance
CT scans prior to the diagnosis of recurrence in lung, suggesting they may have
developed lung metastases long before the diagnosis. The median time from the
surgery to the initial presentation of lung nodules is only 10.2 Mo, similar to the time
of STR in liver (8.9 Mo), peritoneum (10.6 Mo) or local site (10.4 Mo). Nevertheless,
whether there was a delay in the diagnosis of the lung nodules as the recurrence in
lung did not have an impact on the survival (for RTD, HR=1.39, p=0.499).
DISCUSSION/CONCLUSIONS: The frequency of surgically resected PC with lung
recurrence is much higher than was thought historically. PC with lung recurrence
has a significantly better prognosis than recurrence in other sites although the
diagnosis of lung recurrence was often delayed. Further studies are needed to
investigate how different diagnostic and treatment modalities affect the survival
of this unique subpopulation of PC patients.
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S041 THE INDOLENT NATURE OF PULMONARY METASTASES FROM
PANCREATIC CANCER Stephanie Downs-Canner, MD, Mazen Zenati, MD, MPH,
PhD, Brian A Boone, MD, Patrick R Varley, MD, Melissa E Hogg, MD, Amer H
Zureikat, MD, Herbert J Zeh, MD, Kenneth K Lee, MD, University of Pittsburgh
Medical Center, Pittsburgh, US
INTRODUCTION: Pulmonary metastases from pancreatic cancer are less common
than intra-abdominal metastases and little is known about their natural history.
Based on our observations, we hypothesize that among patients with lung
metastases, those with pulmonary metastases first will have improved survival
compared to those with intra-abdominal metastases as a first or synchronous site
of disease.
METHODS: We performed a retrospective review of patients from 2001-2010
with a diagnosis of pancreatic cancer and pulmonary metastases. Demographic
and clinicopathologic data were obtained from the electronic medical record
and data was analyzed using Cox regression and the log rank test for survival
analysis. The cohort was divided into four groups defined by first radiologic site
of metastases: lung as the only site, lung as the first but not only site, abdomen as
the first site and synchronous intra-abdominal and lung metastases.
RESULTS: 174 patients with pulmonary metastases from pancreatic cancer were
identified. The average age was 66.9 (S.D. 10.7). 55.7% of patients were female.
44% of patients in the cohort had resection of their primary tumors prior to
development of metastatic disease. There were no differences in age, race, gender,
BMI, ASA, age adjusted Charlston Comorbidity Index (CCI) and history of alcohol
or tobacco use based on the first site of metastases. Utilizing Kaplan-Meier
survival analysis, we demonstrated significant differences in survival between all
four groups, with patients developing lung metastases only or lung metastases
first having improved survival compared to those with abdominal metastases
first. Compared with patients who only developed lung metastases, patients
with lung metastases first followed by intra-abdominal metastases had a hazard
ratio of death of 1.42 (95% C.I. 0.89-2.25, p=0.140). Those with intra-abdominal
metastases before lung metastases had a hazard ratio of death of 2.36 (95% C.I.
1.56-3.56, p<0.0001) and those with synchronous metastases had a hazard ratio
of death of 3.78 compared to those with lung metastases only (95% C.I. 2.465.8, p<0.0001). These differences were independent of age, CCI, neoadjuvant
chemotherapy, resection of the primary tumor and the T and N stage of primary
tumors. There was also improved survival when patients with lung metastases
as either the only or the first site of metastases were compared to those with
intra-abdominal metastases first and synchronous metastases (p-value <0.0001).
Again, this difference was independent of patient factors. Upon analysis of only
those patients who underwent resection of their primary tumor, the difference in
survival between groups remained statistically significant. Median survival among
those who developed lung only or lung first recurrence was 37.5 months and
33.8 months respectively compared to 21 months for those with intra-abdominal
recurrence or synchronous recurrence.
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CONCLUSION: In this large retrospective cohort of pancreatic cancer patients
with lung metastases, those with lung metastases first had improved survival
compared to those with intra-abdominal metastases first. These results suggest
an indolent nature to pulmonary metastases. Further research is needed to
determine how these results may impact clinical treatment decisions in patients
with isolated pulmonary metastases.
S042 PANCREATIC STELLATE CELL SECRETED IL-6 MEDIATES STAT3
DEPENDENT CANCER CELL INVASION Jason A Castellanos, MD, M Ambrose, Y
Beesetty, N Nagathihalli, PhD, N B Merchant, MD, Vanderbilt University Medical
Center, Nashville, US
INTRODUCTION: Pancreatic cancer is the fourth most common cause of cancerrelated death in the United States. Pancreatic ductal adenocarcinoma (PDAC) is an
inflammatory disease and includes several stromal elements such as immune cells,
fibroblasts, and stellate cells. Pancreatic stellate cells (PSCs) are myofibroblast-like
cells responsible for the dense tumor stroma, which is a hallmark of PDAC. The
role of tumor-associated stroma in PDAC is not well understood. The purpose of
this study was to determine if factors produced by PSCs could effect signaling and
tumorigenicity in cancer cells. We hypothesized Interleukin (IL)-6 secreted from
PSCs activates STAT3 signaling and enhance tumor invasion in PDAC cells.
METHODS: Total and activated STAT3 expression was determined in human
and mouse PSCs, human PDAC cell lines, a human pancreatic ductal epithelial
(HPDE) cell line and cell lines generated from Pdx-cre/LSL-KrasG12D and Pdx-cre/
LSL-KrasG12D/LSL-p53R273H mice. A panel of cytokines and chemokines were
analyzed in PSC culture supernatants. IL-6 concentrations were determined in PSC
supernatants by ELISA. Lysates from cells treated with PSC-conditioned medium
(PSC-CM) were assayed for protein expression for STAT3, pSTAT3, STAT5, pSTAT5,
STAT1 and pSTAT1 by immunoblot. Colony formation and cell invasion assays were
performed with and without neutralizing IL-6 antibody, STAT3 inhibitor (AZD1480)
and in STAT3 shRNA Panc1 cells.
RESULTS: STAT3 activation is necessary for malignant phenotype and affects
survival in PDAC. PSCs produced cytokines that have a documented role in
promoting tumor progression. Supernatants from PSCs contained significantly higher
concentrations of IL-6 compared with other cytokines. Exposure to PSC-CM activated
STAT3 signaling in Panc1 and MiaPaca PDAC cells and significantly enhanced both
cell invasion and colony formation. Neutralization with IL-6 antibody in the PSC-CM
prevented phosphorylation of STAT3 and abrogated the ability of PSCs to induce
cell invasion and stimulate colony formation. Pharmacologic inhibition of STAT3
(AZD 1480) or siRNA knockdown of STAT3 in Panc1 cells similarly inhibited both cell
invasion and colony formation associated with exposure to PSC-CM.
CONCLUSIONS: PSCs release IL-6, which promotes STAT3-dependent signaling
and tumorigenecity in PDAC. These findings demonstrate a novel role of PSCs in
supporting an inflammatory tumor microenvironment and extend the evidence of
crosstalk between the tumor stroma and epithelium. Furthermore, these results
show that STAT3 may represent a therapeutic target in PDAC.
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S043 NEUTROPHIL EXTRACELLULAR TRAPS (NETS) ARE UPREGULATED
IN PANCREATIC CANCER AS A RESULT OF AUTOPHAGY AND CONTRIBUTE
TO HYPERCOAGULABILITY Brian A Boone, MD, Nicole Schapiro, MS, Lidiya
Orlichenko, PhD, Matthew D Neal, MD, Jarrod Ellis, Michael T Lotze, MD, Herbert J
Zeh, MD, University of Pittsburgh, Pittsburgh, US
INTRODUCTION: Neutrophil extracellular traps (NETs) occur when activated
neutrophils release their intracellular contents containing DNA, histones and
granule constituents to trap and kill bacteria. While traditionally associated
with sepsis, NETs have also been demonstrated in sterile inflammation and
have been linked to thrombosis. Recently, the process of autophagy has been
implicated in NET formation. We have previously reported that pancreatic
ductal adenocarcinoma (PDA) is associated with increased autophagy in the
tumor microenvironment and systemically. Here were explored NETs and
autophagy in models of murine and human PDA as well as their potential role in
hypercoagulability of cancer.
METHODS: Neutrophils were isolated from both an orthotopic and a genetically
engineered murine model of PDA (Pdx-1-Cre/LSL-KRasG12D, KC) utilizing density
gradient centrifugation. NETs were induced with platelet activating factor
(PAF,0-40μM) and visualized by Hoechst staining to identify both nuclear and
extracellular DNA. Levels of free DNA were measured as a surrogate marker of
NET formation in PDA in murine and patient serum. Animals were treated with the
autophagy inhibitor chloroquine (CQ, 100 mg/kg/day PO) as well as DNase (100U
IP x 4 doses). Thromboelastograms (TEG) were performed on blood from tumor
bearing and control animals.
RESULTS: Neutrophils from tumor bearing animals (KC and orthotopic) were
more prone to NET formation following PAF stimulation (Figure). Pre-treatment
of harvested neutrophils with CQ prior to PAF stimulation reversed the tumor
bearing effect. Treatment of tumor bearing animals with CQ also reversed the
propensity to form NETs. Serum DNA was elevated in the orthotopic animals
compared with sham controls (80 vs. 38 ng/mL, p<0.05) and in the KC animals
compared with wild type (WT) (56 vs. 42 ng/mL, p<0.05). Treatment with CQ
decreased serum DNA in both tumor bearing models. 80% of patients had a
decrease in serum DNA following treatment with gemcitabine + CQ. Treatment
with DNase also decreased serum DNA in the orthotopic animals. Orthotopic
tumor bearing animals were hypercoagulable on TEG compared to sham
controls. These effects were partially reversed with chloroquine or with DNase
treatment.
CONCLUSION: Mice from both orthotopic and genetically engineered models of
pancreatic cancer demonstrate increased propensity for NET formation associated
increased free serum DNA . In vitro and in vivo treatment with the autophagy
inhibitor chloroquine reversed this process. This suggests that pancreatic cancer
results in an increase in NET formation through an autophagy mediated process.
Additionally, NETs in pancreatic cancer may contribute to hypercoagulability.
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Figure 1
S044 ISOLATION AND CHARACTERIZATION OF DCLK1+ TUMOR CELLS OF
PANCREATIC ADENOCARCINOMA PATIENTS J eremy L Irvan, MD, Dongfeng Qu,
PhD, Alexander Raines, MD, Parthasarathy Chandrakesan, Nathaniel Weygant,
Randal May, Shubham Pant, MD, Courtney W Houchen, MD, Russell G Postier, MD,
University of Oklahoma, Oklahoma City, US
BACKGROUND: Pancreatic ductal adenocarcinoma (PDAC) has the worst prognosis
of any major malignancy with less than a 6% 5-year survival rate. It is one of
the leading causes of cancer-related death in the developed world and is the
fourth leading cause of cancer death in the United States. Patients with PDAC
are often diagnosed at late stages with extensive local tumor invasion and early
metastasis, presenting a major obstacle to all forms of therapy. Cells with cancer
stem cell (CSC) properties were identified in PDAC. CSCs are often resistant to
chemotherapy and radiation therapy, this may explain why current treatments do
not cure PDAC or prevent recurrences. It is suggested that stem cells may be the
root of PDAC. Targeting CSCs is a very promising therapeutic approach for PDAC.
Doublecortin-like kinase 1 (DCLK1), a microtubule-associated kinase, is a putative
pancreatic stem cell marker and is upregulated in pancreatic cancer, colorectal
cancer, and many other solid tumor cancers. It marks tumor stem cells in mouse
models of intestinal neoplasia. The aim of this study is to evaluate the stemness,
pluripotency, and clonogenicity of DCLK1+ tumor cells isolated from PDAC patients.
METHODS: Tumor tissues were obtained after resection from three stage IIA and
IIB PDAC patients. Tumor tissues were digested with collagenase IV and single
cell suspensions were filtered and cultured. Cultured PDAC tumor cells were
passed and expanded for eight passages. DCLK1+ tumor cells were isolated using
anti-DCLK1 antibody and FACS-based cell sorting. Gene expressing levels in both
DCLK1+ and DCLK1- cells were analyzed by real-time RT-PCR. The proliferative,
invasive, and clonogenic activities of DCLK1+ and DCLK1- cells were compared
using MTT assay, migration assay in 24-well transwell coated with Matrigel, and
clonogenicity assay in soft agar.
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RESULTS: We successfully cultured the primary tumor cells isolated from PDAC
tumor tissues, and passed the cells more than ten generations. We found that the
expressing levels of pluripotency factors, SOX2, NANOG, OCT4, and LIN28, were
2 fold higher in the isolated DCLK1+ cells compared to that in DCLK1- cells. The
expression levels of pancreatic cancer related oncogenes, KRAS, NOTCH, and REG4,
were significantly increased in the DCLK1+ cells compared to that in the DCLK1- cells.
The expression levels of epithelial mesenchymal transition (EMT) related genes,
ZEB1, ZEB2, SNAIL, SLUG, and TWIST, were also significantly increased in the
DCLK1+ cells compared to that in the DCLK1- cells. Both isolated DCLK1+ and DCLK1cells were subjected to MTT assay, the isolated DCLK1+ cells exhibited increased
proliferation activity compared to that in the DCLK1- cells. Furthermore, DCLK1+ cells
have increased migration activity and clonogenic activity compared to DCLK1- cells.
CONCLUSION: These results demonstrated that DCLK1+ cells have increased
pluripotency, stemness, migrative, and clonogenic activities, suggesting that DCLK1
marks pancreatic tumor stem cells. These results also suggest that targeting
DCLK1 may have therapeutic potential in PDAC.
S045 SEQUENCE ALTERATIONS IN THE WEE1 NON-CODING REGION IS A
FACILITATOR AND MARKER FOR PANCREATIC TUMORIGENESIS Shruti Lal,
PhD, Joseph A Cozzitorto, Fernando F Blanco, PhD, Janae Romeo, Charles J Yeo,
MD, Jonathan R Brody, PhD, Jordan M Winter, MD, Thomas Jefferson University,
Philadelphia, US
INTRODUCTION: We discovered an abnormal sequence motif in a 56 bp noncoding region of the mitotic kinase inhibitor WEE1 in pancreatic adenocarcinoma,
which contains the binding site of an RNA binding protein, HuR (important
for cancer cell survival). WEE1 promotes DNA repair by triggering a mitotic
checkpoint in the setting of DNA damage. We hypothesized that a germline
sequence alteration (INDEL, insertion/deletion of bases) in WEE1 impairs HuR
stabilization of the WEE1 transcript and abrogates this critical checkpoint in cells,
thereby enhancing proliferation. Paradoxically, this phenotype could render cells
susceptible to DNA damaging agents.
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EXPERIMENTAL METHODS: The 56 bp HuR binding site on the WEE1 transcript was
sequenced in 21 cancer cell lines, 30 familial pancreatic cancers, and 68 patients with
normal pancreata. Functional assays were performed in cell lines with wild type and
abnormal WEE1 sequence after treatment with mitomycin C (MMC).
RESULTS: An INDEL was identified in the poly-T track of the 56 bp region
(ATGTACCTGTGTGTCCATCTTATATTTCTTTTTTTTTTAATTGTGAATTAGAC), which
has 10 T’s in the wild type sequence. In the control group, 51 patients had two wild
type alleles, and 17 were heterozygous for a TT insertion (12 T’s), establishing an
abnormal allelic frequency of 12.5%. In 21 cancer cell lines, 10 were homozygous for
the wild type sequence, and 11 exhibited a TT insertion. In 5 of these cell lines, the
second allele exhibited a separate abnormality (11 T’s). In total, the abnormal allelic
frequency was three-fold increased at 38%. In 30 familial pancreatic cancers, 12
were homozygous for the wild type sequence and 18 had the TT insertion (abnormal
allelic frequency of 30%, p<0.0003 vs. controls). MMC (i.e., DNA damage) treatment
of pancreatic cancer cell lines results in HuR movement from the nucleus to the
cytoplasm with its bound mRNA (e.g., the WEE1 transcript). MMC induced WEE1
protein expression by Western blot in cell lines with wild type sequence, but not in
cell lines containing INDELs in both alleles. Reporter constructs with luciferase in
front of the HuR-WEE1 binding site (both wild type and abnormal sequence motifs)
were generated. Upon treatment with MMC, reporter activity was reduced with
plasmids containing the TT insertion (Figure). Interestingly, biallelic abnormal binding
site sequences (while observed in 5/21 cancer cell lines) were never identified in the
germline of any patients (n=98, expected in 5% of individuals), suggesting that the
abnormal HuR binding site sequence is functionally important and embryonic lethal.
CONCLUSIONS: The incidence of a TT insertion in the HuR binding site on WEE1 is
increased in familial pancreatic cancer and results in decreased WEE1 expression
upon DNA damage. These findings may have important implications for 1) genetic
screening, 2) predicting chemo-responsiveness, 3) and the development of novel
therapies.
S046 CHEMOTHERAPY RESISTANT PANCREATIC CANCER TUMOR-ASSOCIATED
FIBROBLASTS ARE PROTUMORIGENIC P
aul A Toste, MD, Andrew H Nguyen, MD,
Brian E Kadera, MD, Mindy Duong, Nanping Wu, PhD, Luyi Li, MS, Timothy R Donahue,
MD, Department of Surgery, University of California, Los Angeles, Los Angeles, US
INTRODUCTION: As a result of late diagnosis and frequent resistance to cytotoxic
chemotherapy, pancreatic ductal adenocarcinoma (PDAC) has a notoriously
poor prognosis. An important component of chemoresistance in PDAC is the
dense tumor-associated stroma (TAS) characteristic of the disease. PDAC tumorassociated fibroblasts (TAFs), the predominant cell type of the TAS, enhance
tumor growth, invasion, metastasis, and chemoresistance. However, the impact of
chemotherapy on TAF biology has not yet been reported.
METHODS: Immortalized human TAFs were grown in either standard media
or media containing IC50 doses of gemcitabine for 4 weeks to generate
chemotherapy-naïve and chemotherapy-resistant lines. Gene expression
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microarray analysis was performed to compare naïve and chemoresistant TAFs.
Expression of selected targets was confirmed by qRT-PCR and/or antibody-based
cytokine array. IL-8 expression was quantified by ELISA. Conditioned media (CM)
was produced from both naïve and resistant TAFs. MTT assay was used to assess
tumor cell (TC) viability in naïve versus resistant CM. TC migration and invasion as
well as endothelial cell migration were assessed using modified Boyden chambers
with naïve or resistant CM. For in vivo studies, TCs were subcutaneously coimplanted with naïve or resistant TAFs in immunodeficient mice.
RESULTS: Microarray analysis demonstrated that TAFs undergo a large number
of molecular changes in response to cytotoxic chemotherapy. Molecules involved
in important TAF functions such as stellate cell activation, cellular movement,
extracellular matrix production and remodeling, and cytokine signaling were altered.
Of note, the expression of multiple inflammatory molecules was increased. Cytokine
array and qRT-PCR confirmed elevated levels of multiple inflammatory cytokines
(IL-6, IL-8, CXCL-1, CXCL-6) in chemoresistant TAF conditioned media. Furthermore,
ELISA demonstrated that IL-8 concentration was 6-fold higher in chemoresistant
TAF CM compared to naïve TAF CM. TCs (Miapaca-2 and Panc1) demonstrated
increased viability when grown in the presence of resistant as compared to naïve
TAF CM (p<0.001). TCs also showed increased migration (Miapaca-2, p<0.001 and
Panc1, p=0.002) and invasion (Panc-1, p<0.001) in the presence of resistant CM.
Resistant TAF CM was also pro-angiogenic, as evidenced by increased endothelial
cell migration (p=0.01). In vivo, TCs (Miapaca-2) implanted along with chemoresistant
TAFs grew larger tumors compared to those implanted with naïve TAFs (p=0.004).
CONCLUSION: After treatment with cytotoxic chemotherapy, TAFs manifest
multiple molecular changes including a pro-inflammatory gene expression
signature. Chemoresistant TAFs support tumorigenesis and angiogenesis in vitro
and in vivo via paracrine signaling. While further studies are needed to evaluate
regulation and mediators of the TAF response to chemotherapy, it represents a
potential therapeutic target to improve efficacy of current treatments in PDAC.
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S047 PTK6 INCREASES APOPTOSIS WITH GEMCITABINE TREATMENT IN
PANCREATIC CANCER CELLS BY ENHANCING DNA DAMAGE Hiroaki Ono, MD,
PhD, Marc D Basson, MD, PhD, Hiromichi Ito, MD, Michigan State University, East
Lansing, US
BACKGROUND: Protein Tyrosine Kinase 6 (PTK6) is a non-receptor type tyrosine
kinase known to be aberrantly expressed in various cancers including pancreatic
cancer. The role of PTK6 in cancer chemo-resistance remains unknown. We tested
our hypothesis that PTK6 regulates gemcitabine (GEM) resistance in pancreatic
cancer, and explored its mechanism.
METHODS: We studied 2 human pancreatic cancer cell lines, Panc1 and MIAPaCa2.
For some studies, GEM resistant clones of Panc1 and MIAPaCa2 were isolated
by culture with GEM for 2 months. Cell survival was measured by WST-8 assay.
GEM-induced apoptosis and DNA damage were evaluated by Western blotting.
The effect of PTK6 overexpression on the efficacy of GEM therapy for pancreatic
cancer in vivo was assayed using a xenograft mouse model.
RESULTS: Endogenous PTK6 expression was increased at 24-48 hours with
GEM treatment in Panc1 and MIAPaCa2 cell lines. PTK6 gene-silencing increased
cell survival after GEM treatment and decreased cleaved Caspase3 and PARP,
indicating decreased apoptosis, while PTK6 overexpression decreased cell survival
and increased apoptosis. Basal PTK6 expression was significantly reduced in the
GEM resistant clones compared with the parental lines (0.29 fold decrease in
MIAPaCa2 and 0.60 fold decrease in Panc1, respectively, p<0.05). Restoration of
PTK6 expression using an over-expression vector made the resistant MIAPaCa2
clone cells sensitive to GEM (0.77 fold decreased survival compared to the
resistant clone, p<0.05). To explore the mechanism in which PTK6 regulates
the cytotoxic effect of GEM on pancreatic cancers, we tested the effect of
altered PTK6 expression on DNA damage induced by GEM. GEM-induced H2AX
phosphorylation (γ-H2AX), which is a specific marker for DNA double-strand
breaks, was significantly reduced by PTK6 gene-silencing, while GEM-induced
γ-H2AX was increased by PTK6 overexpression. Furthermore, PTK6 gene silencing
also inhibited the GEM-induced activation of ataxia-telangiectasia mutated
(ATM) protein kinase, a central initiator of key signal responses to DNA damages
in both cell lines. Conversely, ATM kinase activation was enhanced by PTK6
overexpression (Figure). In the mouse xenograft model, subcutaneous tumors with
PTK6-overexpressing MIAPaCa2 showed significant growth reduction compared
with tumors with control MIAPaCa2 after 5 weeks treatment with GEM (150 mg/
kg IP, twice a week) (606 mm3 vs 252 mm3 in size, 609 mg vs 128 mg in weight,
p<0.01, respectively) .
CONCLUSION: PTK6 is endogenously activated by GEM treatment in pancreatic
cancers, and forced-overexpression of PTK6 increases the efficacy of GEM on
pancreatic cancer with enhancing DNA damage. Further study to elucidate the
mechanism by which PTK6 regulates GEM-induced DNA damage may identify
therapeutic targets to improve the outcomes of patients with pancreatic cancer.
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S048 THE VALUE OF DRAINS AS A FISTULA MITIGATION STRATEGY FOR
PANCREATODUODENECTOMY: SOMETHING FOR EVERYONE? RESULTS OF
A RANDOMIZED PROSPECTIVE MULTI-INSTITUTIONAL STUDY Matthew T
McMillan, BA, William E Fisher, MD, Jeffrey Drebin, MD, PhD, Stephen Behrman,
MD, Mark Bloomston, MD, Kimberly M Brown, MD, Steven J Hughes, MD,
Katherine A Morgan, MD, Vic Velanovich, MD, Jordan Winter, MD, Nicholas J
Zyromski, MD, Charles M Vollmer, MD, University of Pennsylvania School of
Medicine, Baylor College of Medicine, Philadelphia, US
INTRODUCTION: A recent randomized controlled trial investigating intraperitoneal
drain use during pancreatoduodenectomy (PD) had a primary goal of assessing
overall morbidity. It was terminated early with findings that routine elimination
of drains in PD increases mortality and the severity and frequency of overall
complications. Here, we provide a subset analysis of drain value in reference to
clinically-relevant postoperative pancreatic fistula (CR-POPF), with emphasis on
risk-adjusted outcomes.
METHODS: Nine institutions performed 137 PDs, with patients randomized to
intraperitoneal drainage (D; n=68) or no drainage (ND; n=69). CR-POPFs were
categorized, at POD 60, as ISGPF Grade B or C. The Fistula Risk Score (FRS), a
10-point scale derived from four validated risk factors for CR-POPF (soft gland,
small duct, high-risk pathology, increased blood loss), facilitated risk adjustment
between groups. FRS risk zones include: Negligible (FRS 0), Low (FRS 1-2),
Moderate (FRS 3-6) & High (FRS 7-10).
RESULTS: There was no difference in overall fistula risk between the two groups
as judged by mean FRS (D=3.51 vs. ND=3.57; p=0.897), rates of each of the
aforementioned individual risk factors, or stent use. When used, drains were
typically removed POD 7. Overall, CR-POPF rates were higher in the no drain
group compared to the drain group (20.3% vs. 13.2%; OR: 1.67; p=0.269), as were
rates of the severe Grade C POPFs (8.7% vs. 2.9%; OR: 3.14; p=0.274). The use of
drains in the presence of known individual FRS factors was associated with lower
CR-POPF rates, particularly for soft glands (11.8% vs. 34.3%; OR: 0.26; p=0.027).
For each cohort, CR-POPF occurrence was assessed across the various FRS risk
zones. CR-POPF never occurred in the 10 patients with negligible risk. In patients
with Low risk, the rate of CR-POPF was actually higher when drains were utilized
(19.0% vs. 4.8%; OR: 4.71; p=0.343). Conversely, there were significantly fewer CRPOPFs (12.2% vs. 29.5%; p=0.050) when drains were used in Moderate and High
risk scenarios (Figure). The benefit of drains in these particular patients is detailed
in Table 1. Lastly, patients who suffered CR-POPFs experienced shorter duration
of stay (15.2 d vs. 34.7 d, p=0.010) and reduced 90-d mortality (11.1% vs. 42.9%; OR:
0.17; p=0.176) when a drain was used.
CONCLUSION: Controversy exists over the efficacy of drains as a fistula
mitigation strategy in cases of PD. The results of this analysis suggest that
drains diminish the rate and severity of CR-POPF in patients with Moderate and
High fistula risk, but they might be avoided in the roughly one-third of patients
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with Negligible or Low risk. The premature discontinuation of this study, due
to obvious deleterious outcomes in the absence of drains, limits its statistical
power; yet, the randomization process and risk adjustment with the FRS ensures
absence of bias.
S049 A RANDOMIZED PROSPECTIVE MULTICENTER TRIAL OF
PANCREATICODUODENECTOMY WITH AND WITHOUT ROUTINE
INTRAPERITONEAL DRAINAGE G
eorge Van Buren, II, MD, Mark Bloomston, MD,
Steven J Hughes, MD, Jordan Winter, MD, Stephen W Behrman, MD, Nicholas J
Zyromski, MD, Charles Vollmer, MD, Vic Velanovich, MD, Taylor Riall, MD, Peter
Muscarella, MD, Jose Trevino, MD, Attila Nakeeb, MD, Max Schmidt, MD, Kevin
Behrns, MD, Christopher Ellison, MD, Omar Barakat, MD, Kyle Perry, MD, Jeffrey
Drebin, MD, Michael House, MD, Sherif Abdel-Misih, MD, Eric J Silberfein, MD,
Steven Goldin, MD, Kimberly Brown, MD, Somala Mohammed, MD, Sally E Hodges,
BS, Amy McElhany, MPH, Mehdi Issazadeh, BS, Eunji Jo, MS, Qianxing Mo, PhD,
William E Fisher, MD, 1Baylor College of Medicine, The Elkins Pancreas Center,
Michael E. DeBakey Department of Surgery, and Dan L. Duncan Cancer Center,
Houston, TX, Houston, US
OBJECTIVE: To test by randomized prospective multicenter trial the hypothesis
that pancreaticoduodenectomy (PD) without the use of routine intraperitoneal
drainage does not increase the frequency or severity of complications.
BACKGROUND: Some surgeons have abandoned the routine use of drains placed
at the time of pancreas resection.
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METHODS: One hundred-thirty seven patients were randomized to PD with (n=68,
drain group) and without (n=69, no-drain group) the use of routine intraperitoneal
drainage and the safety of this approach and spectrum of complications between
the two groups were compared.
RESULTS: There were no differences between drain and no-drain cohorts in
demographics, comorbidities, pathology, pancreatic duct size, pancreas texture,
baseline quality of life, or operative technique.
Pancreaticoduodenectomy without routine intraperitoneal drainage was
associated with an increase in the number of complications per patient (1(0-2) vs.
2(1-4), p=.029); an increase in the number of patients who had at least one ≥ grade
2 complication (35 (52%) vs. 47 (68%), p=0.047); and a higher average complication
severity (2 (0-2) vs. 2(1-3), p=0.027). Pancreaticoduodenectomy without routine
intraperitoneal drainage was associated with a higher incidence of gastroparesis,
intra-abdominal fluid collection, intra-abdominal abscess (10% vs 25%, p= 0.027),
severe (≥ grade 2) diarrhea, need for a postoperative percutaneous drain, and a
prolonged length of stay.
The study was stopped early by the Data Safety Monitoring Board due to a fourfold increase in mortality from 3% to 12%mortality in the patients undergoing PD
without routine intraperitoneal drainage, many of whom had pancreatic fistulas.
CONCLUSION: This randomized prospective multicenter trial provides level one data
suggesting that elimination of intraperitoneal drainage in all cases of PD increases
the frequency and severity of complications and likely increases mortality.
S050 RISK-ADJUSTED OUTCOMES OF CLINICALLY-RELEVANT POSTOPERATIVE
FISTULA FOLLOWING PANCREATODUODENECTOMY: A MODEL FOR
PERFORMANCE EVALUATION C
harles M Vollmer, MD, Matthew T McMillan, BA,
Sameer Soi, MS, Benjamin C Miller, BA, Pancreas Fistula Study Group, University of
Pennsylvania School of Medicine, Philadelphia, US
INTRODUCTION: Accurate assessment of surgeon and institutional performance
requires: 1) establishment of a standard for comparison; 2) the ability to adjust for
variability in patient risk and characteristics of surgeon and institution. We sought
to evaluate surgical performance in pancreatoduodenectomy using clinicallyrelevant postoperative fistula (CR-POPF) occurrence as a quality indicator.
METHODS: This multinational, retrospective study of 4,187 pancreatoduodenectomies
involved 55 surgeons at 15 institutions. Risk was assessed using the previously
validated Fistula Risk Score (FRS) and fistulas were stratified by International Study
Group criteria. CR-POPF variability was evaluated and hierarchical regression analysis
assessed individual surgeon and institutional performance.
RESULTS: There was variability in both CR-POPF risk and occurrence (Table). Risk
alone did not explain all observed outcomes; surgeon-specific effects (fistula
mitigation choices) and institutional volume were important in accounting for
discrepancies. The model identified variables that were associated with lesser
(Stents – Odds Ratio[OR]=0.69; Drains OR=0.69) or greater (Octreotide OR=2.28;
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Pancreatogastrostomy OR=1.91) CR-POPF occurrence. When controlling for risk,
performance outliers were identified, at both the surgeon and institutional levels
(Figure).
CONCLUSIONS: This largest analysis of pancreatic fistulas following
pancreatoduodenectomy demonstrates considerable variability in risk and
occurrence of CR-POPF among surgeons and institutions. Beyond inherent patient
risk factors, surgical decision-making influences fistula outcomes.
S051 HIGH PERFORMING WHIPPLE PATIENTS: FACTORS ASSOCIATED WITH
SHORT LENGTH OF STAY AFTER OPEN PANCREATICODUODENECTOMY G
race
C Lee, BS, Zhi Ven Fong, MD, Cristina R Ferrone, MD, Sarah P Thayer, MD, PhD,
Andrew L Warshaw, MD, Keith D Lillemoe, MD, Carlos Fernandez-del Castillo, MD,
Department of Surgery, Massachusetts General Hospital, Boston, MA, United
States, Boston, US
INTRODUCTION: In this cost-conscious era of health care reform, much attention
has been focused on minimizing length of hospital stay (LOS) and readmission
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rates after surgical procedures. Despite the decreasing morbidity and mortality of
pancreaticoduodenectomy (PD), it continues to be associated with prolonged LOS.
As preliminary data of minimally invasive PD emerges, we sought to determine
the average LOS after open PD at a high-volume tertiary care hospital in an
attempt to set a standard to which minimally invasive PD can be compared. We
also determined the factors that could predict “high performance” after PD.
METHODS: The demographic, perioperative, and readmission data of 634
consecutive patients who underwent open PD between January 2007 and
December 2012 at the Massachusetts General Hospital were reviewed. “High
performers” were defined as patients with a LOS ≤5 days.
RESULTS: The median LOS was 7 days (interquartile range 6-10 days). A total
of 61 patients (9.6%) had a LOS ≤5 days and were deemed “high performing”.
Postoperative delayed gastric emptying, ICU admission, and discharge to a
rehabilitation facility each perfectly predicted LOS >5 days. In multivariate logistic
regression analysis, neoadjuvant therapy (26.2 vs 15.9%, OR 3.31, p=0.003), epidural
success (92.9 vs 85.1%, OR 3.73, p=0.030), epidural duration ≤3 days (40.4 vs 19.5%,
OR 2.90, p=0.002), surgery on Thursday or Friday (59.3 vs 46.1%, OR 3.10, p=0.001),
and discharge on Monday through Wednesday (80.3 vs 50.7%, OR 6.54, p<0.001)
were independently associated with LOS ≤5 days. Age ≤70 years, male gender,
Charlson comorbidity index <5, and high surgeon volume were predictive of “high
performance” on univariate analysis, but were not significant in the multivariate
model. When comparing “high performing” patients to those with LOS>5 days,
readmission rate (16.4% vs 22.2%, p=0.298) and time to readmission (5.5 vs 12 days,
p=0.661) were not different. Body mass index, diabetes, prior abdominal surgery,
prior ERCP, vessel resection, and tumor pathology also did not correlate with LOS.
CONCLUSION: In our contemporary experience of patients undergoing
pancreaticoduodenectomy, median LOS after open PD was 7 days, with a 9.6%
rate of “high performers”. LOS ≤5 days was associated with neoadjuvant therapy,
epidural success, and undergoing surgery at the end of the week. “High performing”
patients experienced no difference in readmission rates as a result of their early
discharges. Minimally invasive PD should be compared to this high standard for LOS,
among other quality metrics, to justify its increased cost and operative duration.
S052 THE ASSOCIATION BETWEEN PANCREATIC FISTULA GRADE C AND SURVIVAL
AFTER PANCREATIC RESECTION FOR PANCREATIC CANCER M
anabu Kawai, MD,
PhD, Masaji Tani, MD, PhD, Seiko Hirono, MD, PhD, Ken-ichi Okada, MD, PhD, Fuyuhiko
Motoi, MD, PhD, Michiaki Unno, MD, PhD, Masayuki Sho, MD, PhD, Yoshiyuki Nakajima,
MD, PhD, Kenichiro Uemura, MD, PhD, Sohei Satoi, MD, PhD, A-Hon Kwon, MD, PhD,
Ippei Matsumoto, MD, PhD, Tadahiro Goto, MD, PhD, Goro Honda, MD, PhD, Masanao
Kurata, MD, PhD, Yoshiaki Murakami, MD, PhD, Hiroki Yamaue, MD, PhD, Multicenter
Study Group of Pancreatobiliary Surgery (MSG-PBS), Wakayama, JP
BACKGROUND: Several studies demonstrated that postoperative complications
after pancreatic resection for pancreatic cancer adversely affect survival outcome.
Pancreatic fistula grade C is one of the most serious complications after pancreatic
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resection. However, it remains unclear whether pancreatic fistula grade C affects
long-term outcome after resection for pancreatic cancer.
AIMS: The aim of this study is to elucidate the adverse effect of pancreatic fistula
grade C on recurrence and survival after resection for pancreatic cancer by a
survey of high volume center of pancreatic resection in Japan.
METHODS: Medical records were reviewed in 1,015 patients with pancreatic
cancer who underwent pancreatic resection between 2001 and 2010 at 7 highvolume surgical institutions in Japan. Pancreatic fistula was defined based on the
International Study Group on Pancreatic Fistula (ISGPF) guideline.
RESULTS: Overall morbidity following pancreatic resection was 42.6%, and 30day mortality was 0.3%. Pancreatic fistula occurred in 22.9% (232 of enrolled 1,015
patients) ; grade A 9.4%, grade B 10.7%, grade C 2.8%. Concerning with disease-free
survival, patients with pancreatic fistula grade C had a significantly shorter time
to recurrence than those without it (5.8 vs. 12.6 months, p=0.019). Concerning with
overall survival, patients with pancreatic fistula grade C had a significantly poorer
survival than those without it (8.1 vs. 22.3 months; median survival, 14.3 vs. 32.6%
months; 3-year survival, p<0.0001). Pancreatic fistula grade C was an independent
prognostic factor after multivariate analysis (hazard ratio 2.49; 95% confidence
interval 1.56-3.96; P< 0.001). Moreover, independent prognostic significance was
also detected for glasgow prognostic score (GPS) 2 (P=0.021), blood transfusion (P<
0.001), International Union Against Cancer (UICC) pT3 or T4(P= 0.003), pathological
plexus invasion (P= 0.001), lymph node status (N1) (P= 0.024), no adjuvant therapy
(P< 0.001). Furthermore, multivariate analysis demonstrated that independent risk
factors for pancreatic fistula grade C was glasgow prognostic score (GPS) 2 (hazard
ratio 5.37; 95% confidence interval 1.31-22.0; P=0.019) and male (hazard ratio 6.02;
95% confidence interval 1.77-20.5; P=0.004)
CONCLUSIONS: pancreatic fistula grade C had a significant impact on the longterm survival of patients with pancreatic cancer. The improvement of operative
procedure or perioperative management to reduce the incidence of pancreatic
fistula grade C may lead to a favorable survival in these patients.
S053 DOES DRAIN FLUID AMYLASE ACCURATELY PREDICT PANCREATIC FISTULA?
Christina W Lee, MD, Henry Pitt, MD, Taylor Riall, MD, Sean Ronnekleiv-Kelly, MD,
Jacqueline Israel, MD, Glen Leverson, PhD, Abhishek Parmar, MD, Molly E Kilbane,
RN, Bruce L Hall, MD, PhD, MBA, Sharon M Weber, MD, University of Wisconsin
Hospital and Clinics, Madison, WI; Temple University Health System, Philadelphia,
PA; University of Texas Medical Branch, Galveston, TX; Indiana University Health,
Indianapolis, IN; Washington University, St. Louis, MO, Madison, US
BACKGROUND/INTRODUCTION: Improvements in the ability to predict pancreatic
fistula (PF) could enhance patient outcome by early drain removal and avoidance of
drain-related morbidity in those who will not develop PF. Although clinical predictors
are associated with an increased risk for PF, these are imprecise. Previous studies
have shown that drain fluid amylase on post operative day 1 (DFA1) >5000 is
predictive of PF. Therefore, we sought to assess the accuracy of DFA1 to predict PF.
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METHODS: Patients undergoing pancreatic resection from 11/1/11 to 12/31/12
were selected from the American College of Surgeons National Surgical Quality
Improvement Program (ACS NSQIP) Pancreatectomy Demonstration Project
(PDP) database. PF was defined as persistent drainage of amylase-rich fluid in
addition to drain continuation > 7 days, percutaneous drainage of pancreatic fluid
collection, or re-operation. Factors significantly associated with pancreatic fistula
on univariate analysis (p < 0.1) were included in logistic regression analysis to
evaluate factors independently associated with PF. An ROC curve was utilized to
determine the best predictive performance between DFA1 and PF.
RESULTS: DFA1 was recorded in 536 of 2724 patients who underwent PR,
including patients undergoing pancreaticoduodenectomy (n=380), distal
pancreatectomy (n=140), and enucleation (n=16). PF occurred in 92 subjects
(17.2%). On univariate analysis, DFA1, increased body mass index (BMI), small
pancreatic duct size and soft pancreatic texture were significantly associated
with PF (p < 0.05). On multivariate analysis, all four of these factors were
independently associated with PF (p<0.05). Among multiple DFA1 cutoff values,
60 U/L demonstrated the highest sensitivity (Se) and negative predictive value
(NPV, Table 1). 141 (26.3%) subjects satisfied this DFA1 cutoff. ROC confirmed the
significant relationship between DFA1 and PF, with a c-statistic of 0.761 (Figure 1).
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CONCLUSIONS: Although DFA1 >5000 U/L was associated with high specificity,
the sensitivity was low, thus decreasing its clinical usefulness. Lower DFA1 levels
resulted in improved NPV; for example, a cut-off of 100 would incur only 4% FN
rate while allowing 31% (170/536) of patients to undergo early drain removal
safely. Therefore, in patients with low DFA1, early drain removal is recommended.
S054 EARLY DRAIN REMOVAL: THE MIDDLE GROUND BETWEEN
THE DRAIN VERSUS NO DRAIN DEBATE IN PATIENTS UNDERGOING
PANCREATICODUODENECTOMY. A PROSPECTIVE VALIDATION STUDY Z
hi Ven
Fong, MD, Camilo Correa-Gallego, MD, Cristina R Ferrone, MD, Gregory R Veillette,
MD, Sarah P Thayer, MD, Andrew L Warshaw, MD, Keith D Lillemoe, MD, Carlos
Fernandez-del Castillo, MD, Massachusetts General Hospital, Boston, US
INTRODUCTION: Surgeons have been pushing the envelope on abandoning routine
intraperitoneal drainage after pancreaticoduodenectomy (PD). We performed an
unbiased assessment of drain amylase level as a predictor of pancreatic fistula
(PF) development.
METHODS: We prospectively measured daily drain amylase levels, and correlated
them with the development of PF in two independent cohorts of patients undergoing
PD: training- (n=126; year 2008) and validation-cohort (n=369; years 2009-2012).
RESULTS: First postoperative day (POD 1) drain amylase level had the highest
predictive ability (concordance-index: 0.911, figure 1) for development of PF in the
training cohort. An amylase level ≥612 showed the best accuracy (86%), sensitivity
(93%), and specificity (79%). In the validation cohort, 229 (62.1%) patients had a POD
1 drain amylase level of <600 U/L, and PF developed in only 2 (0.9%) cases, whereas
in patients with POD 1 drain amylase level of ≥600 U/L (n=140) the PF rate was
31.4% (OR 52, p<0.0001). On multivariate logistic regression analysis, POD 1 drain
amylase level of <600 U/L (p<0.0001) was a stronger predictor of the absence of PF
than pancreatic gland texture (OR 5.2, p=0.002) and duct diameter (OR 0.9, p=0.835).
CONCLUSIONS: Following PD, the risk of PF is <1% if POD 1 drain amylase level is
<600 U/L. We propose that in this group, which comprise >60% of patients, drains
should be removed on POD 1, and are currently validating this strategy.
S055 THE HYSLAR TRIAL: A PROSPECTIVE RANDOMIZED TRIAL ON THE
USE OF A RESTRICTIVE FLUID REGIMEN WITH 3% HYPERTONIC SALINE
(HS) VERSUS LACTATED RINGERS (LR) IN PATIENTS UNDERGOING
PANCREATICODUODENECTOMY (PD) H
arish Lavu, MD, Naomi Sell, MHS, Jordan
Winter, MD, Timothy Carter, MD, David Maguire, MD, David Gratch, MD, Marian
Feil, CRNA, Richard Berman, MD, Zvi Grunwald, MD, Benjamin Leiby, PhD, Edward
Pequignot, MS, Ernest Rosato, MD, Charles Yeo, MD, Thomas Jefferson University,
Philadelphia, PA, Philadelphia, US
INTRODUCTION: Restrictive fluid regimens have been shown to reduce
perioperative complications in patients undergoing surgery. The objective of this
study was to determine if the volume and type of fluid administered during and
after PD impacts postoperative outcomes.
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METHODS: Between May 2011 and November 2013, patients undergoing PD were
consented and enrolled in an IRB approved, prospective, randomized trial (NCT
01428050). At laparotomy, patients were stratified by gland texture (soft vs hard) and
randomized to LR (15ml/kg/hr LR intraop, and 2ml/kg/hr LR postop until the morning
of POD #1) or HS (9ml/kg/hr LR and 1ml/kg/hr HS intraop, and 1ml/kg/hr HS postop
until the morning of POD #1). The trial was powered to detect a 30% reduction in the
overall rate of complications (80% power, alpha= 0.05, chi-squared test).
RESULTS: There were 245 patients, with 122 and 123 in the LR and HS groups,
respectively. Demographic variables between groups were similar (Table). The LR
patients had a significantly greater net fluid balance (91 vs 65 ml/kg, p=0.02) for
the entire admission. The overall complication rate (54% vs 41%, p<0.05) and the
cumulative number of complications (120 vs 80, p=0.01), were significantly greater
in the LR group. Reoperation rate, length of stay, readmission rate, and 30 day
mortality were similar between groups.
CONCLUSIONS: A restrictive fluid regimen with 3% HS significantly reduces
complications in patients undergoing PD.
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S056 CURRENT MANAGEMENT OF DELAYED BLEEDING AFTER
PANCREATICODUODENECTOMY Young Joon Ahn, PhD, Jin He, Jia-hua Leng,
John L Cameron, Nita Ahuja, Martin A Makary, Kenzo Hirose, Timothy M Pawlik,
Matthew Weiss, Christopher L Wolfgang, Johns Hopkins Medical Institution,
Baltimore, US
INTRODUCTION :Delayed bleeding after pancreaticoduodenectomy (PD),
defined as bleeding after post-operative day 5, is a rare but life threatening
complication. Options for management include angiography with embolization,
endoscopic procedures, supportive therapy or re-operation. However, the
optimal management remains unclear. We summarized our experience on the
management of delayed bleed in order to better define the outcomes associated
with different types of management.
PATIENTS & METHODS :The electronic records of 4513 patients who underwent
pancreaticoduodenectomy between October 1987 and July 2013 were analyzed
regarding postoperative bleeding complications.
RESULTS :Delayed bleeding occurred in 86 patients (1.9 %) following
pancreaticoduodenectomy (classical PD: 48, pylorus preserved PD: 38) with
median time of occurrence of 12.5 days from operation (range: 5 to 96). The
pattern of bleeding was classified into intraluminal bleeding only (n=51; 59.3%)
extraluminal bleeding only (n=22; 26.6%), and both (n=13; 15.1%). Within this cohort,
50 patients (58.1%) had an associated postoperative pancreatic fistula (ISGPF
grade A: 5, B: 26, C: 19). The majority of delayed bleeding was the result of a
pseudoaneurysm (n=40, 46.5%), while other sources included suture lines (n=12),
marginal ulcer or gastritis (n=12), drain-related bleeding (n=5), others (n=5) and
unknown cause (n=12). A total of 82 angiographies were performed in 65 patients
(65/86:75.6) The embolization was performed in 44 patients. Immediate control
of bleeding was achieved in 32 cases (72.7%) with coil embolization or covered
stent insertion. Of those patients who failed initial embolization, 9 cases with
ongoing bleeding were explored surgically and 3 underwent repeated angiography
with re-embolization. Among these 3 patients, 2 survived and 1 died. As for
pseudoaneurysmal bleeding, 27 of 39 patients who attempted angiography first
achieved effective bleeding control with embolization and 4 cases were controlled
by surgery. Endoscopy found bleeding focus in 18 out of 44 patients (41%) who
underwent endoscopy and 13 hemodynamically stable patients were clipped and
cauterized subsequently. Other 5 patients underwent exploration for ongoing
bleeding after endoscopy. Surgery was attempted in total 21 patients to control
bleeding and 11 of the 21 patients survived eventually. 6 patients were explored
as 1st line treatment and 4 patients survived. The other 10 patients with delayed
bleeding were managed conservatively. Overall mortality was 18.6 % (16 / 86).
CONCLUSIONS :Delayed bleeding after pancreatic surgery should prompt the
suspicion of a pseudoaneurysm even in intraluminal bleeding only. Angiography
with embolization showed better outcome as 1st line approach for urgent bleeding
suspicious of pseudoaneurysm. For patients with pseudoaneurysm, operative
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exploration should be reserved for unstable patient or failed angiographic
intervention. Endoscopy seems to play minimal role in urgent bleeding.
S057 BILE-CULTURE BASED ANTIMICROBIAL PROPHYLAXIS REDUCES
SURGICAL SITE INFECTIONS (SSIS) IN PANCREATIC SURGERY Alessandro Zerbi,
MD, Maria Rachele Angiolini, MD, Francesca Gavazzi, MD, Cristina Ridolfi, MD,
Paola Morelli, MD, Erminia Casari, MD, Maria Carla Tinti, MD, Marco Montorsi, MD,
Section of Pancreatic Surgery, Department of Surgery; Infectious Diseases Unit,
Hospital Health Direction; Humanitas Research Hospital, Rozzano, Milan, Italy.
University of Milan School of Medicine, Milan, Italy, Rozzano (mi), IT
BACKGROUND: Cefazolin is widely accepted as antimicrobial prophylaxis in
hepato-bilio-pancreatic surgery. Microbial resistance to this drug is rapidly
increasing, nullifying the expected beneficial effects of its administration and
exposing patients to potentially severe SSIs.
Aim of this study is definition of an alternative prophylaxis schedule targeted
on bile cultures and validation of its efficacy on SSIs incidence among patients
undergoing pancreatic surgery in a referral centre.
METHODS: Between Jan-2010 and Oct-2013 we performed 222
consecutive pancreatic resections requiring bile contamination (203
pancreaticoduodenectomies and 19 total pancreatectomies). We routinely
performed culture on bile samples obtained intra-operatively and we
prospectively recorded SSIs development. Analyzing antimicrobial susceptibility of
detected germs, we introduced from Mar-2013 ampicillin-sulbactam as alternative
to standard cefazolin for perioperative prophylaxis; we therefore realized a
comparison between patients receiving standard (n=170) and new (n=52) schedule.
RESULTS: Analyzing the standard group, 56% of patients had positive bile cultures;
the great majority of microbes belonged to Enterococcus Spp. (E. Faecalis 29%, E.
Facium 18%). In 47% of patients a preoperative biliary stent was present: it was
strongly associated with bile infection (100% vs 17%, p<0,001); bile infection was
associated with higher morbidity both in patients with (72% vs 56%, p=0,037) or
without stent (87% vs 56%, p=0,026), as well as with higher SSIs rate (63% vs 37%,
p=0,113). 49,5% of infected bile samples harbored microbes resistant to cefazolin:
in these patients postoperative global SSIs were higher (71% vs 30%, p=0,023) as
well as superficial SSIs, deep SSIs and organ-space SSIs. Since we administered
ampicillin-sulbactam as perioperative prophylaxis, we observed a significant
decrease of superficial (20,6% vs 3,8%, p=0,005) and deep (8,8% vs 0, p=0.025)
SSIs, while we noted no difference in organ/space SSIs.
CONCLUSION: Bile infection in pancreatic surgery is related to a significant
increase of postoperative morbidity. The choice of ampicillin-sulbactam
prophylaxis, based on bile-cultures results, seems useful in reducing SSIs.
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S058 IT IS QUALITY AND QUANTITY: A SINGLE INSTITUTION’S EXPERIENCE
IN QUALITY MEASURES OF PANCREATIC CANCER CARE M
elanie Ongchin, MD,
Jennifer Steve, BS, David Bartlett, MD, Kenneth Lee, MD, Haroon Choudry, MD,
Wallis Marsh, MD, Allan Tsung, MD, Zureikat Amer, MD, Zeh Herbert, MD, Hogg
Melissa, MD, University of Pittsburgh, Pittsburgh, US
BACKGROUND: Despite extensive analysis of the management of pancreatic cancer
care, outcomes vary among institutions. Bilimoria et al developed a set of 50 quality
indicators (QI) addressing 5 domains in pancreatic cancer care. We examined our
institution’s compliance with these cancer care quality indicators, hypothesizing that
tracking these measures would be feasible and would assure high compliance.
METHODS: In 2011, we developed a database for a Pancreatic Quality
Improvement Project prospectively maintained to track these QI. We examined
patients from April 2011 to July 2012 with pancreatic adenocarcinoma.
RESULTS: 570 patients were captured, 322 had pancreatic adenocarcinoma. Of
those patients, 125 were resectable, 25 locally advanced, and 197 metastatic. 26%
of patients enrolled in one of our 11 clinical trials. We were >90% compliant with 42
of 43 of the validated QI. Compliance on QI #26 was 86% (table). Median time from
diagnosis to surgery was 24 days. 67% received neoadjuvant therapy; median time
to treatment (MTTT) was 22 days. 74% received adjuvant therapy; MTTT was 51
days. Of patients who received treatment more than 60 days from diagnosis, 55%
were stage 4 deciding on therapy vs hospice. Surgical outcomes tracked include:
2.2% peri-operative mortality, 85% R0 resection, 20.5 median lymph nodes, 350cc
median EBL, 459min median OR time, and 34% readmission rate. Our composite
score was 9 out of 10 compared to a median of 4 in Bilimoria’s study. One person
maintains this database, averaging 8hrs/wk.
CONCLUSION: We adhere to 98% of the validated indicators. Time maintaining
this database is minimal and prospectively tracks our performance in pancreatic
cancer care. Institutions performing pancreatic surgery should track these
indicators as part of their outcomes.
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S059 MOBILE RISK CALCULATOR APP FOR OPERATIVE AND ONCOLOGIC
OUTCOMES IN PATIENTS CONSIDERING PANCREADICODUODENECTOMY
FOR PANCREATIC ADENOCARCINOMA Pragatheeshwar Thirunavukarasu, MD,
Kristopher Attwood, Steven Nurkin, MD, Roswell Park Cancer Institute, Buffalo, US
INTRODUCTION: Accurate assessment of surgical risk prior to
pancreaticoduodenectomy is difficult. Procedure-specific and patient related
factors such as age and comorbid status make the prediction of operative
outcomes subjective, and often inaccurate. Oncological outcomes also depend
upon various tumor-specific factors. Use of elaborate scoring systems and
nomograms are time consuming and impractical for quick instant use. Tools to
provide reliable quantitative information on short and long-term outcomes, as
well as risks patients may expect with treatment, may help them deal with these
difficult life changing decisions. We aimed to develop a web and mobile application
for rapid point-of-care surgical risk and oncological outcome assessment.
METHODS: Using the 1998-2011 National Cancer Database Participant Use File
(NCBD-PUF), we identified individual patient and cancer specific variables to
risk stratify patients who underwent pancreaticoduodenectomy for pancreatic
adenocarcinoma. In a separate analysis, we used the National Surgical Quality
Improvement Project of the American College of Surgeons (ACS-NSQIP) database
(2005-2012) to extract data on demographic, clinical, operative and postoperative
outcome variables on all patients undergoing pancreaticoduodenectomy for
cancer. Statistical analyses were performed using a combination of univariate
associations and multivariate analyses associated with assessed outcomes.
Combining these robust databases and using appropriate statistical validation,
we generated user friendly, point of care, clinical calculators to predict risk of
operative morbidity and long-term oncologic survival. We then developed webbased mobile apps to make this calculator convenient and user friendly for clinical
use.
RESULTS: A mobile application was developed as shown in the attached screen
shot. It generates instant output to display surgical risk such as mortality, overall
morbidity and serious morbidity (sMorbidity). The application also analyzed stored
NSQIP data to calculate the accurateness of the generated predicated outcomes.
In a separate calculator (not shown), 1 and 3 year survival data is calculated based
on individual clinicopathologic variables.
CONCLUSION: This Point-of-Care Operative and Oncologic Risk Calculator for
pancreaticoduodenectomy is a combined NSQIP-NCDB based, easy-to-use
application and is compatible with widely used personal and corporate mobile
devices. It enables the surgeon to provide patients and families an objective,
immediate, point-of-care operative risk assessment, with the accompanied
predicted oncologic survival benefit. This would help the surgeon in setting
realistic expectations to patients considering surgery, and strengthen the process
of informed consent. Our next step would be to prospectively validate the use of
this application in the clinical setting.
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S060 PREDICTORS OF EARLY READMISSION AFTER PANCREATECTOMY
Jeffrey T Tosoian, MD, MPH, Caitlin W Hicks, MD, MS, Vicente Valero III, MD,
John L Cameron, MD, Martin A Makary, MD, MPH, Kenzo Hirose, MD, Frederic
E Eckhauser, MD, Nita Ahuja, MD, Timothy M Pawlik, MD, MPH, Matthew J
Weiss, MD, Christopher L Wolfgang, MD, Department of Surgery, Johns Hopkins
University School of Medicine, Baltimore, MD 21287, Baltimore, US
Introduction:/BACKGROUND: There are limited data exploring readmission
associated with complex surgical diagnoses. Existing studies frequently
underestimate readmission rates because not all patients present to the index
hospital where their procedure was performed. We studied the detailed pattern
and characteristics of readmission following pancreatectomy at a single institution
using a statewide database to improve readmission capture.
METHODS: Using a prospectively-collected institutional database in conjunction
with Maryland statewide data, we reviewed pancreas resections performed at the
Johns Hopkins Hospital between 2005 and 2010. Only Maryland residents were
included in order to capture readmissions to any Maryland hospital.
RESULTS: Of 595 subjects eligible for early readmission, 134 (22.5%) were
readmitted to either our institution (n=105, 78.4%) or an outside institution
(n=29, 21.6%). The majority (54.5%) of patients were readmitted due to
surgical complications, including abdominal abscess, pancreatic fistula,
gastrointestinal bleed, urinary tract infection, or respiratory failure. Other
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common reasons for readmission were failure to thrive (11.2%), abdominal pain
(9.7%), and gastrointestinal obstruction (6.0%). Patients readmitted for surgical
complications were more likely to present to our institution (Fisher’s exact
test, P=0.001), while the site of readmission did not differ significantly among
other readmission diagnoses. On multivariate analysis, factors associated with
readmission included age ≥65, baseline chronic liver disease, undergoing distal
pancreatectomy, post-operative intravenous antibiotics, and post-operative
drain placement (Table). On Kaplan-Meier analysis, readmitted subjects
demonstrated shorter median survival than those who were not readmitted
(20.3 versus 23.1 months, log-rank test P=0.011).
DISCUSSION/CONCLUSION: Early readmission after pancreatectomy is common
and a significant predictor of decreased overall survival. Specific patient-level
factors may identify patients at increased risk of readmission. Whether high-risk
patients could be targeted for risk-reduction strategies that .would decrease
readmissions and possibly lower hospital costs deserves further consideration.
S061 HIGH-VOLUME SURGEONS VERSUS HIGH-VOLUME HOSPITALS: ARE
BEST OUTCOMES MORE DUE TO WHO OR WHERE? P
aul G Toomey, MD, Sharona
B Ross, Amanda E Igartua, Michael DeGori, Anthony F Teta, Kenneth Luberice,
Prashant B Sukharamwala, MD, Alexander S Rosemurgy, MD, Florida Hospital
Tampa, Tampa, US
INTRODUCTION: High-volume hospitals are purported to provide ‘best’ outcomes.
High-volume hospitals and high-volume surgeons are inextricably related. We
undertook this study to evaluate the outcomes after pancreaticoduodenectomy
when high-volume surgeons relocate to a low-volume hospital.
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METHODS: Outcomes after the last 50 pancreaticoduodenectomies at a
high-volume hospital in 2012 were compared to the outcomes after the
first 50 pancreaticoduodenectomies undertaken at a low-volume (i.e., no
pancreaticoduodenectomies in >5 years) hospital in 2012-13; all operations were
undertaken by the same surgeons. Data are presented as median (mean ± SD).
RESULTS: Patients undergoing pancreaticoduodenectomies at a high-volume vs.
a low-volume hospital were not different relative to sex and age (Table). Patients
operated upon at the low-volume hospital had lower ASA class, had shorter
operations with less blood loss, spent less time in the ICU, and had shorter length
of stay (p < 0.05 for each, Table); 30-day mortality and 30-day readmission rates
were not different (Table).
CONCLUSIONS: The salutary benefits of being a high-volume hospital for
pancreaticoduodenectomy are transferred to a low-volume hospital when highvolume surgeons relocate. The ‘best’ outcomes associated with high-volume
hospitals may be primarily due to the high-volume surgeons who work there, and
the ‘best’ results follow the high-volume surgeons. The ‘best’ results seem to be
related more to who does the pancreaticoduodenectomy rather than where the
pancreaticoduodenectomy is undertaken.
S062 WHAT ARE THE FINANCIAL IMPLICATIONS OF CENTERS FOR REGIONAL
HEALTHCARE? A
lexander S Rosemurgy, MD, Richard L Klein, Carrie E Ryan, MS,
Prashant B Sukharamwala, MD, Thomas W Wood, MD, Sharona B Ross, MD,
Florida Hospital Tampa, Tampa, US
INTRODUCTION: Financial implications on regionalization of healthcare and
programmatic development are not often considered. We undertook this
study to evaluate and compare hospital cost of care and income with a
common operation (laparoscopic cholecystectomy) versus an operation often
associated with HPB programmatic development and healthcare regionalization
(pancreaticoduodenectomy).
METHODS: The charges and reimbursements of all laparoscopic cholecystectomies
(n=201) and pancreaticoduodenectomies (n=44) at one hospital undertaken from
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June 2012 to June 2013 were determined. Comparisons were undertaken using
ANOVA with significance accepted at p ≤ 0.05. Data are reported as median data
or as median (mean ± SD).
RESULTS: Pancreaticoduodenectomy, relative to laparoscopic cholecystectomy,
had greater time in the operating room (283 min vs. 93 min), hospital charges
($108,040.87 vs. $25,055.85), and hospital costs ($15,482.15 vs. $3,453.78)
(p<0.0001 for each), but generated similar income ($2,480.23 vs. $3,058.83,
p=0.88).
CONCLUSIONS: Pancreaticoduodenectomy requires more resource allocation
and costs hospitals more but leads to no more income. Many hospitals invest
great effort and resources to build programs and centers for regional healthcare.
However, their accounting systems are not based on cost accounting, but rather
on complex formulas of cost allocation. Consequently, these accounting systems
have great, and possibly inappropriate, impact on perceived income associated
with care. Considering these systems, it seems hospitals derive more return on
investment from commonly undertaken operations than those often associated
with regionalization of healthcare and programmatic development. Accounting
systems need to reflect actual costs to allow determinations of actual income to
better allocate healthcare resources and to seek appropriate compensation for
hospital care.
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S063 THE INCIDENCE OF PANCREATOGENIC DIABETES AFTER MAJOR PARTIAL
PANCREATIC RESECTION MAY BE GREATER THAN YOU THINK Richard A
Burkhart, MD, Susan M Gerber, MD, Renee M Tholey, MD, Kathleen Lamb, MD,
Anitha Somasundaram, MD, Caitlin McIntyre, Eliza Fradkin, Annie Ashok, Robert
Felte, MD, Jaya Mehta, Ernest Rosato, MD, Harish Lavu, MD, Serge A Jabbour,
MD, Charles J Yeo, MD, Jordan M Winter, MD, Department of Surgery, Jefferson
Pancreas, Biliary, and Related Cancer Center, Thomas Jefferson University,
Philadelphia, PA; Department of Endocrinology, Thomas Jefferson University
Hospital, Philadelphia, PA, Philadelphia, US
BACKGROUND: The number of pancreatic resections performed each year in the
US estimated at 5000 patients and growing. With many performed for benign
disease, many patients will experience prolonged survival (>2 years), yet the
long-term risk of pancreatogenic (type III) diabetes remains unknown. Previous
estimates from small studies outside the U.S. suggest a risk of developing diabetes
between 10-20%.
METHODS: A total of 1107 patients underwent pancreatectomy at Thomas
Jefferson University between 2005 and 2012. After IRB approval, attempts were
made to contact all living patients by telephone. Pre- and postoperative diagnoses
of diabetes mellitus (DM) were confirmed by verbal questionnaire. Individuals who
completed the diabetes-focused survey were included.
RESULTS: Telephone calls were made to 691 living patients who underwent partial
pancreatectomy. Diabetes-specific information was successfully obtained for 257
patients (representing 23% of the total cohort), including 179 who underwent
pancreaticoduodenectomy (PD) and 78 who underwent distal pancreatectomy
(DP). The median follow-up time after resection was 2.1 years.
In the PD group: 44 (25%) patients reported having DM prior to resection (median
7 years prior, range 0.1 to 30), with 10 (6%) reporting onset within 1 year. Of the
group carrying a pre-operative diagnosis of DM, 3 (7%) had improved glucose
control after resection (dose reduction in diabetes medicines), while 21 (48%)
required escalated management. Out of 135 patients without preoperative DM, 24
(18%) were newly diagnosed with DM postoperatively (median onset 7.5 months
postoperatively, range 1-64).
In the DP group: 23 patients (29%) had DM preoperatively, with just 4 having
onset within 1 year of resection (5%). No patients had improved glucose control
after resection, while 6 (26%) patients carrying a preoperative diagnosis of DM
had worse control after resection. Out of 55 patients without preoperative DM, 17
(31%) developed new onset DM after resection (median 6 months, range 0-60).
In the total cohort after partial pancreatectomy, 26% either experienced worse
glucose control (27 of 67 with preop DM, 40%) or a new diagnosis of DM (41 of 190
without preop DM, 22%). A high preoperative HgbA1C level (>6%) was associated
with an increased risk of developing new-onset DM post-resection (38% in the >6%
HgbA1C group vs. 11%, p<0.02).
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CONCLUSIONS: Twenty-two percent of patients undergoing partial
pancreatectomy experience new onset DM and 40% of patients experience
worsening DM after resection, a higher percentage of patients than previously
reported. These figures likely underestimate the true lifetime risk of
pancreatogenic diabetes, in light of the short follow-up time in this patient cohort
(2.1 years). An elevated preoperative HgbA1C (>6%) identifies patients at highest
risk for developing new onset DM after resection.
S064 EFFECT OF HIGH-DOSE PANCREATIC ENZYME REPLACEMENT THERAPY
ON THE DEVELOPMENT OF NON-ALCOHOLIC FATTY LIVER DISEASE AFTER
PANCREATICODUODENECTOMY, PAYING ATTENTION TO ETIOLOGY OF
DISEASES AND THE REMNANT PANCREATIC VOLUME R
ie Sato, Masashi
Kishiwada, Yasuhiro Murata, Akihiro Tanemura, Naohisa Kuriyama, Yashinori
Azumi, Shugo Mizuno, Masanobu Usui, Hiroyuki Sakurai, Masami Tabata, Shuji
Isaji, Hepatobiliary Pancreatic and Transplant Surgery, Mie University School of
Medicine, Tsu Mie, JP
BACKGROUND: Conventional nonalcoholic fatty liver disease (NAFLD) and
nonalcoholic steatohepatitis (NASH) are characterized by two steps of intrahepatic
lipid accumulation and inflammatory progression to fibrosis. The high incidence of
NAFLD after pancreaticoduodenectomy (PD) has been recently known, suggesting
the effect of malnutrition due to pancreatic exocrine deficiency (Kato H, Isaji S, J
Hepatobiliary Pancreat Sci 2010). The aim of this study is to investigate whether
high-dose pancreatic enzyme replacement therapy can prevent the development
of NAFLD after PD, paying attention to etiology of diseases and the remnant
pancreatic volume(RPV) measured by CT volumetry.
PATIENTS AND METHODS: Among the consecutive 183 patients who underwent
PD from April 2007 to March 2013, we retrospectively reviewed the charts of 144
patients who had been followed up more than 6 months after PD. The indication
of PD was pancreatic carcinoma(n=77), IPMN(n=26), bile duct carcinoma (n=12),
ampullary carcinoma (n=9), other neoplasm (n=9) and others (n=11). From October
2011, we have performed high-dose pancreatic enzyme replacement therapy
from early postoperative days using enteric-coated, delayed-release pancrelipase
(1800mg/day), and the subjects could be classified into the two periods: early
period (from April 2007 to September 2011, n=93) and late period (from October
2011 to March 2013, n=51). In early period, mean dose of pancreatic enzyme was
pancreatine 6.43g/day at 1 month after PD.
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RESULTS: NAFLD was found in 54 patients (37.5%), 83% of whom developed it
within 3 months after operation. Chronological data (preoperative and at 1, 3, 6
and 12 months after PD) of serum albumin were 3.6, 3.1, 3.4, 3.6 and 3.6 g/dl in
early period and 3.9, 3.4, 3.7, 3.8 and 3.9 g/dl in late period, showing significantly
higher levels at 1, 3 and 12month in late period (p<0.05). Total cholesterol levels did
not differ significantly. The incidence of NAFLD was lower in late period (29.4%)
than in early period (41.9%), not showing significant difference (p=0.138). In the
patients with pancreatic carcinoma (n=77: mean RPV of 10.03ml), the incidence of
NAFLD was not significantly different between the two periods: 42.0% vs. 39.0%
(p=0.815), while, in the patients without pancreatic carcinoma (n=67: meanRPV
of 22.07ml), the incidence of NAFLD is significantly lower in late period than in
early period: 41.9% vs.17.4% (P=0.045). In the patients with pancreatic carcinoma,
the incidence of diarrhea in postoperative day 30 is extremely high, showing no
significant difference between the two periods: 56.0% vs. 66.7% (p=0.362), while,
in the patients without pancreatic carcinoma, the incidence of diarrhea was much
lower in late period compared to early period: 32.6% vs. 13.0% (p=0.084). By
multivariate analysis including perioperative various factors, female, postoperative
diarrhea and age were selected as the independent risk factor for NAFLD.
CONCLUSION: High-dose pancreatic enzyme replacement therapy after PD
significantly prevented the development of NAFLD after PD, especially in the
patients without pancreatic adenocarcinoma. The significantly higher incidence of
diarrhea in the patients with pancreatic carcinoma, which was due to nerve plexus
dissection around SMA and smaller remnant pancreatic volume, was considered to
disturb the effect of high-dose enzyme therapy.
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2014 MEMBERSHIP ROSTER
A. Saavedra, Juan R., MD
INACTIVE | 2011
Cleveland Clinic Foundation
Email: [email protected]
Abbasi, Ammara, MD
RESIDENT | 2014
Beth Israel Deaconess Medical Center
Address: 110 Francis St., Suite 9B
Boston, MA 02215
Abbott, Daniel E., MD
ACTIVE | 2014
Univ. of Cincinnati
Surgery
Address: 3156 Wolf Run Ct.
Cincinnati, OH 45244
Abood, Gerard, MD
ACTIVE | 2013
Loyola Univ. Medical Center
Address: 2160 S. First Ave.
Maywood, IL 60153
Abraham, Anasooya, MD
INACTIVE | 2011
Univ. of Minnesota
Adam, Ulrich, MD
ACTIVE | 2014
Vivantes Humbolt Klinikum Berlin
Dept. of General and Vascular Surgery
Address: Am Nordgraben 2
Berlin, 13509 Germany
Adams, David, MD
ACTIVE | 2014
MUSC Medical Center
Dept. of Surgery
Address: 25 Courtenay Dr., MSC 290
Charleston, SC 29425
Ahmad, Syed A., MD
ACTIVE | 2014
Univ. of Cincinnati Medical Center
Surgical Oncology
Address: 231 Albert Sabin Way, ML 0772
Ahmed, Shuja, MD
RESIDENT | 2014
Wake Forest Baptist Medical Center
Dept. of Surgery
Address: Medical Center Blvd.
Winston Salem, NC 27157
Ahmed Ali, Usama, MD
RESIDENT | 2014
AMC Amsterdam
Address: Meibergdreef 9,
Amsterdam, 1105 AZ Netherlands
Ahn, Young Joon, MD, PhD
ACTIVE | 2014
Johns Hopkins Medical Institute
Address: 17 Mica Court
Baltimore, MD 21209
Ahuja, Nita, MD
ACTIVE | 2014
Johns Hopkins Univ.
Surgical Oncology
Address: 600 Wolfe St.
Baltimore, MD 21287
Albagli, Rafael, MD
ACTIVE | 2013
National Cancer Institute of Brazil
Address: Munig Baruto 396 11002
Rio de Janeiro, Brazil
Ali, Naoman, MD
INACTIVE | 2011
Beaumont Hospital
Allen, Peter J., MD
INACTIVE | 2010
Memorial Sloan-Kettering Cancer Center
Allendorf, John, MD
ACTIVE | 2014
Winthrop
Address: 120 Mineola Blvd.
Mineola, NY 11501
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2014 Membership Roster
Alrefaie, Waddah, MD
INACTIVE | 2011
Univ. of Minnesota
Alsfasser, Guido, MD
ACTIVE | 2014
Univ. of Rostock
Dept of Surgery
Address: Schillingallee 35
Rostock, 18057 Germany
Amini, Albert
RESIDENT | 2014
Medical College of Wisconsin
Address: 9200 W Wisconsin Ave.
Milwaukee, WI 53226
Andersen, Dana, MD
ACTIVE | 2014
Digestive Disease Division / NIDDK / NIH
Address: 6707 Democracy Blvd., Rm 659
Bethesda, MD 20892
Androutsopoulos, Vasiliki
INACTIVE | 2009
Angst, Eliane, MD
INACTIVE | 2009
Antiporda, Michael, MD
RESIDENT | 2014
Mayo Clinic Jacksonville
Address: 4500 San Pablo Rd.
Jacksonville, FL 32224
Arafat, Hwyda, MD, PhD
INACTIVE | 2010
Thomas Jefferson Univ.
Aranha, Gerard, MD
ACTIVE | 2014
Dept. of Surgery
Address: 2160 S First Ave.
Maywood, IL 60523
Arcangeli, Annarosa, MD, PhD
ACTIVE | 2013
Univ. of Florence
Experimental Pathology and Oncology
Address: Viale G.B. Morgagni 50
Firenze, 50134 Italy
Arcerito, Massino, MD
RESIDENT | 2013
Univ. of Michigan
Surgery
Address: 1500 E Medical Center Dr.,
SPC 534
Ann Arbor, MI 48109-5343
Arimoto, Jun, MD
RESIDENT | 2013
Yokohama City Univ.
Address: Kinko-cho 8-1-1004
Yokohama City, Japan
Arnoletti, Pablo, MD
ACTIVE | 2013
Florida Hospital
Address: 2415 N Orange Ave., Suite 400
Orlando, FL 32714
Arous, Edward, BS
INACTIVE | 2011
Univ. of Massachusetts Medical School
Arrangoiz, Rodrigo
INACTIVE | 2012
Arrese, David, MD
INACTIVE | 2012
Riverside Methodist Hospital
Asai, Kengo, MD
RESIDENT | 2014
Mayo Clinic
Address: 200 First St. SW,
Rochester, MN 55901
Asano, Takedhe, MD
INACTIVE | 2009
Teikyo Univ. SOM
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Asbun, Horacio, MD
ACTIVE | 2014
Mayo Clinic
Dept. of Surgery
Ashley, Stanley, MD
ACTIVE | 2013
Brigham & Women’s Hospital
Dept. of Surgery
Address: 75 Francis St.
Boston, MA 02115
Assifi, Mura, MD
RESIDENT | 2013
Atkinson, Donald, MD
ACTIVE | 2013
Allegheny General Hospital
Dept. of Surgery
Address: 420 E. North Ave., Suite 304
Pittsburgh, PA 15212
Atwal, Tegpal, MD
RESIDENT | 2013
Mayo clinic, Rochester
Gastroenterology
Address: 93 Grande Isle Ave. SW, Unit 2513
Rochester, MN 55902
Avery, Nathan, MD
RESIDENT | 2014
Virginia Mason Medical Center
Address: 1105 Spring St., Apt. 1302
Seattle, WA 98104
Azih, Lilian
INACTIVE | 2012
Babicky, Michele
INACTIVE | 2012
Baker, Marshall S., MD, MBA
ACTIVE | 2014
NorthShore Univ. Health System
Dept. of Surgery
Address: Walgreen’s Building 2nd Floor
2650 Ridge Ave.
Evanston, IL 60201
Bakker, Olaf, MD
INACTIVE | 2010
Univ. Medical Center Utrecht
Ball, Chad, MD, MSc, FRCSC, FACS
ACTIVE | 2014
Univ. of Calgary
Surgery
Address: 3538 - 8th Ave. N.W.
Calgary, AB T2N 1C9 Canada
Ballehaninna, Umashankar, MD
RESIDENT | 2013
Maimonides Medical Center
Surgery
Address: 4802 10th Ave., 4th Fl.
Brooklyn, NY 11219
Bang, Ji Young, MD, MPH
RESIDENT | 2013
Univ. of Alabama at Birmingham
Birmingham, AL
Banks, Peter A., MD
ACTIVE | 2014
Clinical Gastroenterology
Boston, MA 02115
Barboza, Eduardo, MD
ACTIVE | 2013
Clinica San Felipe
Surgery
Address: Gregorio Escobedo 676, 411 4th Fl.
Lima, 00011 Peru
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Barnett, Jr., Carlton C., MD
INACTIVE | 2010
Denver Health/Univ. of Colorado
Barringer, Jennifer, MS, PA-C
INACTIVE | 2011
UPMC
Barron, Morgan, MD
RESIDENT | 2013
Indiana Univ. School of Medicine
Address: 545 Barnhill Drive, EH-125
Indianapolis, IN 46202
Barry, Linda, MD
INACTIVE | 2010
Univ. of South Florida
Barton, Joshua, MD
INACTIVE | 2012
Mayo Clinic
Baschnagel, Andrew, MD
RESIDENT | 2014
William Beaumont Hospital
Address: 3601 W 13 Mile Rd.
TROY, MI 48073
Bass, Barbara, MD
INACTIVE | 2009
Bassi, Claudio, MD
ACTIVE | 2014
University of Verona
Surgery and Oncology
Address: Hospital G.B. Rossi
Verona, 37134 Italy
Baumgartner, Joel, MD
INACTIVE | 2011
Univ. of Pittsburgh Medical Center
Bausch, Dirk, MD
ACTIVE | 2014
UK-SH, campus Lübeck
General & Visceral Surgery
Address: Ratzeburger Allee 160
Lübeck, 23538 Germany
Beane, Joal, MD
INACTIVE | 2011
Indiana Univ.
Behrman, Stephen, MD
ACTIVE | 2014
Univ. of Tennessee, Memphis
Dept. of Surgery
Address: 910 Madison Ave. #208
Memphis, TN 38163
Behrns, Kevin E., MD
ACTIVE | 2014
Univ. of Florida
Dept. of Surgery Chairman
Address: PO Box 100286,
1600 SW Archer Rd., Room 6174
Gainesville, FL 32607
Benarroch-Gampel, Jaime
INACTIVE | 2012
Benson, Douglas, MD
INACTIVE | 2010
Univ. of Colorado
Bentrem, David J., MD
INACTIVE | 2011
Northwestern Univ. Medical School
Berger, Adam
INACTIVE | 2009
Berri, Richard, MD
INACTIVE | 2010
MD Anderson Cancer Center
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Besselink, Marc, MD, MSc, PhD
ACTIVE | 2014
Academic Medical Center Amsterdam
Address: Meibergdreef 9, Room G4.196
Amsterdam, 1105 AZ Netherlands
Bever, Katherine, MD
Boggi, Ugo, MD
ACTIVE | 2014
Oredale Di Cisanello
Divisione Di Chirurgia General
Address: Via Paradisa, 2
Pisa, 56124 Italy
INACTIVE | 2010
Univ. of Maryland
Boja-Cacho, Daniel
Bey, Eric PhD
Bold, Richard J., MD
INACTIVE | 2009
Biehl, Thomas, MD
INACTIVE | 2012
Bildzukewicz, Nikolai, MD
INACTIVE | 2009
Thomas Jefferson Univ. Hospital
Binkley, Charles E., MD
ACTIVE | 2013
Kaiser Permanente San Francisco Medical
Center
Surgery
Address: 2238 Geary Blvd.
San Francisco, CA 94115
Bliss, Lindsay, MD
RESIDENT | 2014
Address: 330 Brookline Ave., Stoneman 9
Attn: Jennifer Tseng
Boston, MA 02215
Bloomston, Mark, MD
INACTIVE | 2009
Ohio State Univ.
Bock, Eileen BE
INACTIVE | 2011
INACTIVE | 2009
INACTIVE | 2011
UC Davis Cancer Center
Bollen, Thomas, MD
INACTIVE | 2009
St. Anthonys Hospital
Bolton, Nathan, MD
RESIDENT | 2014
Ochsner Clinic Foundation
Address: 1542 Jefferson Highway
New Orleans, LA 70121
Bonwense, Stefan
INACTIVE | 2012
Boone, Brian, MD
RESIDENT | 2014
Address: 1409 4th St.
Booy, Stephanie Msc
RESIDENT | 2013
Erasmus MC
Internal Medicine and Surgery
Rotterdam, Netherlands
Borzomati, Domenico, MD, PhD,
FACS
INACTIVE | 2013
Policlinico Universitario Campus Biomedico
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Boutros, Cherif, MD, MSc
Brody, Jonathan, MD
Bouvet, Michael, MD
Broniatowski, Sharon
Boyd, Casey, MD
Broughan, Thomas A., MD
ACTIVE | 2014
Univ. of Maryland School of Medicine
General and Oncologic Surgery
Address: 22 S Greene St., Room S4B12
Baltimore, MD 21201
ACTIVE | 2013
Univ. of California, San Diego
Moores Cancer Center
Address: 3855 Health Sciences Drive
La Jolla, CA 92093-0987
INACTIVE | 2012
Univ. of Texas Medical Branch
Bradley, III, Edward, MD
INACTIVE | 2011
Florida State Univ. College of Medicine
Brat, Gabriel, MD
INACTIVE | 2009
Johns Hopkins Hospital
Brentnall, Teresa, MD
HONORARY/SPEAKER | 2012
Univ. of Washington
Address: 1959 NE Pacific St., Box 356424
Seattle, WA 98195
Bressan, Alexsander, MD
RESIDENT | 2014
Foothills Medical Centre - Univ. of Calgary
Address: 2010, Ulster Rd. NW, Unit 308
Calgary, AB T2N2T9 Canada
Brijbassie, Alan A., MD
INACTIVE | 2012
Univ. of Virginia
Brisinda, Giuseppe, MD
ACTIVE | 2013
Catholic Univ. Hospital “Agostino Gemelli”
Surgery
Address: Largo Agostino Gemelli 8
Rome, 00168 Italy
ACTIVE | 2013
Jefferson Medical College
Dept. of Surgery
Address: 1025 Walnut St., Suite 623
Philadelphia, PA 19107
ACTIVE | 2014
Cleveland Clinic
General Surgery
Address: 2646 Fairmont Blvd.
Cleveland, OH 44106
INACTIVE | 2011
Inova Fairfax Hospital
Brousert, Peter
RESIDENT | 2013
Institute of Pathology
Address: Breisachesstrasse 115a
Freiburg, 79106 Germany
Broussard, Brett, MD
RESIDENT | 2013
Address: 3509 Woodruff Circle
Birmingham, AL 35216
Browder, William, MD
INACTIVE | 2009
East Tennessee State Univ.
Brown, Erin, MD
INACTIVE | 2011
UC Davis
Brown, Kimberly, MD
ACTIVE | 2014
Address: 301 Univ. Blvd.
Galveston, TX 77555-0541
Brunicardi, F. Charles, MD
INACTIVE | 2010
Methodist Hospital
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Bruno, Morgan L. MS
ACTIVE | 2014
M.D. Anderson Cancer Center
Surgical Oncology
Address: 1515 Holcombe Blvd.
Houston, TX 77030
Buchler, Markus W., MD
INACTIVE | 2009
Univ. of Heidelberg
Burke, Erin, MD
RESIDENT | 2014
Univ. of Minnesota
Dept. of Surgery
Address: 420 Delaware St. SE MMC 195
Minneapolis, MN 55455
Burkhart, Richard, MD
RESIDENT | 2013
Address: 1015 Walnut St., Suite 611A
Email: richard.burkhart@jeffersonhospital.
org
Butler, James, MD
RESIDENT | 2014
Indiana Univ.
Address: Emerson Hall - Room 202
545 Barnhill Dr.
Butte, Jean, MD
RESIDENT | 2014
Univ. of Calgary
Address: 716 34th St., Basement
Calgary, AB T2N 2Y2 Canada
Byrd, David R., MD
INACTIVE | 2009
Univ. of Washington
Callery, Mark, MD
INACTIVE | 2012
Cameron, John L., MD
ACTIVE | 2013
Address: 1800 Orleans St., Blalock 679
Baltimore, MD 21287
Cappelli, Carla, MD, PhD
ACTIVE | 2013
Univ. of Pisa
Diagnostic and Interventional Radiology
Address: via Paradisa 2
Pisa, 56126 Italy
Cardona, Kenneth, MD
INACTIVE | 2012
Emory Univ. School of Medicine
Carroll, Jr., James E., MD
INACTIVE | 2010
Univ. of Massachussetts Medical School
Carter, Ross, MD
ACTIVE | 2013
Glasgow Royal Infirmary
West of Scotland Pancreatic Unit
Glasgow, G61 3BB UK
Carter, Timothy
INACTIVE | 2012
Cascini, Francesco Paulo
INACTIVE | 2011
Bio-Medico Campus, Univ. of Rome
Casey Bounds, Brenna, MD
INACTIVE | 2011
Massachusetts General Hospital
Castellanos, Jason, MD
RESIDENT | 2014
Vanderbilt Univ. Medical Center
Address: 4040 Woodlawn Dr. #12
Nashville, TN 37205
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Castello, Juliana, MD
INACTIVE | 2010
Cattaruzza, Fiore
INACTIVE | 2012
Cauley, Christy, BS
INACTIVE | 2011
Chau, Zeling
RESIDENT | 2013
Beth Israel Deaconess Medical Ctr.
Address: 330 Brookline Ave.
Boston, MA 02115
Chauhan, Shailendra, MD
INACTIVE | 2009
Univ. of S. Florida
Email: [email protected].
edu
Ceppa, Eugene, MD
Chen, Kathryn, MD
Cha, Charles, MD
Cherenfant, Jovenel, MD
ACTIVE | 2013
Address: 545 Barnhill Dr, EH 517
INACTIVE | 2009
Yale Univ. School of Medicine
Chabot, John, MD
ACTIVE | 2014
Columbia Univ. Medical Center
Address: 161 Fort Washington Ave.
New York, NY 10032
Chan, Carlos, MD
ACTIVE | 2014
National Institute of Medical Sciences
General Surgery
Address: Vasco de Quiroga 15, Tlalpan
Mexico, D.F. 15000 Mexico
Charnley, Richard M DM, FRCS
ACTIVE | 2014
Newcastle upon Tyne Hospitals
Surgery
Address: Freeman Hospital, Freeman Rd.
High Heaton Newcastle upon Tyne,
NE7 7DN UK
Chatterjee, Deyali, MD
INACTIVE | 2011
RESIDENT | 2013
Fox Chase Cancer Center
Address: 333 Cottman Ave.
ACTIVE | 2014
Franciscan Hammond Clinic
Surgery
Address: 9800 Valparaiso Dr.
Munster, IN 46321
Cho, Clifford S., MD
ACTIVE | 2014
Univ. of Wisconsin School of Medicine
Dept. of Surgery
Address: J4/703 CSC, 600 Highland Ave.
Madison, WI 53792
Chopin-Laly, Xavier, MD
INACTIVE | 2010
Choti, Michael, MD, MBA
ACTIVE | 2014
UT Southwestern Med Center
Dept. of Surgery
Address: 5323 Harry Hines Blvd.
Dallas, TX 75390-9031
Choung, Edward
INACTIVE | 2012
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Christein, John, MD
Clark, Whalen, MD
Christians, Kathleen, MD
Clegg, Carol MS
ACTIVE | 2014
Dept. of Surgery
Address: 1720 2nd Ave. S, KB429
Birmingham, AL 35294-0016
ACTIVE | 2014
Surgical Oncology
Address: 9200 W. Wisconsin Ave.
Milwaukee, WI 53214
Chugh, Rohit, MD
RESIDENT | 2013
Univ. of Minnesota
Address: 420 Deleware St. SE
Minneapolis, MN
RESIDENT | 2013
Dept. of Surgery
Address: 1001 S. Rome Ave., #2
Tampa, FL 33606
INACTIVE | 2011
Coelho, Ana Maria, MD, PhD
RESIDENT | 2013
Univ. of Sao Paulo
Address: R Joao Moura 690 #41
Sao Paulo, SP 5412001 Brazil
Coelho, Nelson Vieira, MD
INACTIVE | 2011
ACTIVE | 2013
Fundacao de Gastroenterologia
Endoscopy
Address: Silva So 255,
Porto Alegre, 90610-270 Brazil
Ciuffreda, Mauro
Contreras, Carlo, MD
Chun, Yun Shin, MD
INACTIVE | 2012
Clain, Jonathan, MD
INACTIVE | 2011
Mayo Clinic
Clancy, Thomas, MD
ACTIVE | 2014
Brigham & Women’s Hospital/Harvard
Medical School
Dept. of Surgery
Address: 75 Frances St.
Boston, MA 02043
Clark, Clancy, MD
ACTIVE | 2014
Wake Forrest Baptist Health
General Surgery-Surgical Oncology
Address: Medical Center Blvd.
Winston Salem, NC 27157
INACTIVE | 2010
Conway, W. Charles, MD
ACTIVE | 2014
Ochsner Medical Center
Surgery
Address: 1514 Jefferson Hwy., CT-8
Cooper, Amanda, MD
RESIDENT | 2014
Dept. of Surgical Oncgology
Address: 1400 Pressler St. Unit 1484
Houston, TX 77030
Cooper, Michol, MD, PhD
RESIDENT | 2013
Address: 600 N. Wolfe St., Halsted 610
Baltimore, MD 21287
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Coppola, Roberto, MD
ACTIVE | 2014
Univ. Campus Bio-Medico - Rome
General Surgery
Address: Via Alvaro del Portillo 200
Rome, 00128 Italy
Coppola, Alessandro
RESIDENT | 2014
Catholic Univ. of Sacred Heart
Address: largo A. Gemelli, 1
Rome, 00100 Italy
Correa, Camilo, MD
INACTIVE | 2009
Mass General Hospital
Crippa, Stefano, MD
INACTIVE | 2011
Policlinico GB Rossi Verona
Cui, Yunfeng, MD
INACTIVE | 2010
Johns Hopkins Bayview Medical Center
Cullen, Joseph J., MD
ACTIVE | 2014
Univ. of Iowa Hospitals and Clinics
Dept. of Surgery
Address: 200 Hawkins Drive, 1528 JCP
Iowa City, IA 52242
Cunha, Jose Eduardo, MD
ACTIVE | 2013
Sao Paulo Univ. Medical School
Associate Professor of Surgery
Address: Rua Oquira 116
Cunningham, Steven, MD
ACTIVE | 2013
Saint Agnes Hospital
Address: 900 Caton Ave.
Baltimore, MD 21229
Dale, Jonas, MD
INACTIVE | 2010
Haukeland Univ. Hospital
Daouadi, Mustapha
INACTIVE | 2012
Datta, Jashodeep, MD
RESIDENT | 2014
Univ. of Pennsylvania
Address: 3400 Spruce St.
De Campos, Tercio, MD
INACTIVE | 2012
Santa Casa School of Medicine
De Jesus-Monge, Wilfredo, MD, MSc
INACTIVE | 2011
de la Fuente, Sebastian, MD
ACTIVE | 2013
Florida Hospital Orlando and Univ. Central
Florida
Address: 2415 N. Ornage Ave., Suite 400
Orlando, FL 32804
Del Chiaro, Marco, MD, PhD
ACTIVE | 2014
Karolinska Instutitet
Address: Division of Surgery K53
Karolinska Univ. Hospital Huddinge
Stockholm, 14186 Sweden
Delitto, Daniel, MD
RESIDENT | 2014
Univ. of Florida
Address: 5011 NW 1st Pl.
Demeure, Michael J., MD, MBA
ACTIVE | 2014
Translational Genomics Research Institute
Integrated Cancer Genomics
Address: 9475 E Ironwood Square, Suite 102
Scottsdale, AZ 85258
TABLE OF CONTENTS
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Demirjian, Aram N., MD
ACTIVE | 2014
Univ. of California-Irvine
Hepatobiliary and Pancreas Surgery
Address: 333 City Boulevard West, Suite 1205
Orange, CA 92868
Dominguez, Ismael, MD
INACTIVE | 2009
Institute Nacional de Medicine
Donahue, Timothy, MD
INACTIVE | 2011
Univ. of Tennessee Health Science Center
ACTIVE | 2014
UCLA David Geffen School of Medicine
Surgery
Address: 10833 Le Conte Ave., 72-256 CHS
Los Angeles, CA 90095-6904
Desai, Rajendra, MS, DNB, MCh, FRCS
Downs-Canner, Stephanie, MD
Denbo, Jason, MD
ACTIVE | 2014
Kamineni Hospital Ltd
HPB Surgery and Liver Transplantation
Address: 3-6-261, Himayatnagar, Flat 303,
3rd Floor, Tirumala Apartments
Hyderabad, 500029 India
Desaki, Ryosuke
RESIDENT | 2014
Deziel, Daniel, MD
INACTIVE | 2010
Univ. Surgeons
Dholakia, Avani, BS
RESIDENT | 2013
Johns Hopkins Univ. School of Medicine
Address: 401 N. Broadway
Baltimore, MD 21231
DiNorcia, Joe
INACTIVE | 2012
Distler, Marius, MD
RESIDENT | 2013
Univ. of Dresden
Address: Fetscher Str. 74
Dresden, 01307 Germany
Dixon, Elijah, MD
ACTIVE | 2014
Univ. of Calgary
Dept. of Surgery & Oncology
Address: 108 Solace Ridge Place
Calgary, AB T3Z 3M9 Canada
RESIDENT | 2014
Address: 200 Lothrop St., Room 679 PUH
Dudeja, Vikas, MD
RESIDENT | 2014
Memorial Sloan-Kettering Cancer Center
Address: Program1275 York Ave.
New York, NY 10065
Duff, Michelle, DPT
INACTIVE | 2010
Pancreatic Cancer Action Network
(PanCAN)
Duncan, Casey, MD
RESIDENT | 2013
Univ. of Texas Medcal Branch
Address: 301 Univ. Blvd.
Duncan, Mark, MD
INACTIVE | 2009
Johns Hopkins Bayview
Duque, Marvin, MD
RESIDENT | 2013
Tufts Medical Center
Address: 800 Washington St., #245
Boston, MA 02111
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Duxbury, Mark, MA, DM, FRCSEd
ACTIVE | 2013
Glasgow Royal Infirmary
Address: Alexandra Parade
Glasgow, G31 2ER UK
Dwinell, Michael, PhD
INACTIVE | 2011
Edil, Barish, MD
ACTIVE | 2014
University of Colorado Hospital
Address: 1665 Aurora Court, Rm. 3337,
MS F-703
Aurora, CO 80045
Egawa, Shinichi, MD
INACTIVE | 2009
Tohoku Univ.
Epelboym, Irene, MD
RESIDENT | 2013
Surgery; Pancreas Center
Address: 161 Fort Washington Ave., 8th Fl.
New York, NY 10032
Erdmann, Joris, MD
RESIDENT | 2013
Erasmus MC
Rotterdam, Netherlands
Evans, Douglas B., MD
ACTIVE | 2014
Dept. of Surgery
Address: 9200 W. Wisconsin Ave.,
Suite 3510
Milwaukee, WI 53226
Evans, Anna, MD
INACTIVE | 2009
David Geffen School of Medicine at UCLA
RESIDENT | 2014
Yale New Haven Hospital
Address: 313 Mansfield St., Apt 2
New Haven, CT 06511
Einersen, Peter, BA
Falconi, Massimo, MD
Eibl, Guido, MD
RESIDENT | 2013
Address: 161 Ft. Washington Ave.
New York, NY 10032
El-Hayek, Kevin M., MD
ACTIVE | 2014
Cleveland Clinic
General Surgery
Address: 9500 Euclid Ave.
Cleveland, OH 44195
ACTIVE | 2014
Universiti Politecnica dlel Marche
Clinica Chirurgia del pancreas
Address: Ospedali Riuniti, Via Conca 71
Ancona-Torrette, 60126 Italy
Fan, Katherine
RESIDENT | 2013
Farkas, Jr., Gyula Andras, MD, PhD
Ellison, Trevor, MD
ACTIVE | 2014
Univ. of Szeged
Surgery
Address: Szokefalvi-Nagy Gyula u.6
Szeged, 06720 Hungary
Engebretson, Anitra, BS
Farnell, Michael B., MD
INACTIVE | 2010
Johns Hopkins Medical Center
ACTIVE | 2014
Pancreatic Cancer Action Network (PanCAN)
Patient Services
Address: 1500 Rosecrans Ave., Suite 200
Manhattan Beach, CA 90260
ACTIVE | 2014
Mayo Clinic
Dept. of Surgery
Address: 200 First St. NW
Rochester, MN 55905
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Farrell, James, MD
Fisher, William E., MD
Fatima, Javairiah, MD
Fleming, Jason B., MD
ACTIVE | 2014
Yale Univ.
Address: 333 Cedar St.
New Haven, CT 06520
INACTIVE | 2009
Mayo Clinic College of Medicine
Feng, Zizhen, MD, PhD
RESIDENT | 2013
Fergusson, James, MD
INACTIVE | 2011
The Canberra Hospital
Fernandez-Cruz, Laureano, MD,
FRCS(Ed)
INACTIVE | 2011
Univ. of Barcelona
Fernandez-del Castillo, Carlos, MD
ACTIVE | 2014
Surgery
Address: 15 Parkman St., ACC 460
Boston, MA 02114
Ferrara, Michael, MS
INACTIVE | 2012
Mayo Clinic
Ferrone, Cristina, MD
ACTIVE | 2014
Mass Gen Hospital
Address: 15 Parkman St., Wang 460
Boston, MA 02108
Fischer, Craig, MD
INACTIVE | 2012
The Methodist Hospital
Fisher, Alex, MS
RESIDENT | 2014
Address: 3526 Pape Ave., #2
ACTIVE | 2014
Baylor College of Medicine
Address: 6620 Main St., Suite 1450
Houston, TX 77030
ACTIVE | 2014
Univ. of Texas, MD Anderson Cancer Center
Division of Surgical Oncology
Address: 1400 Pressler St., Unit 1484,
PO Box 301402
Houston, TX 77030-1402
Flint, Gregg, BS
RESIDENT | 2013
Address: 1304 West Targee St.
Boise, ID 83706
Fong, Zhi Ven, MD
RESIDENT | 2014
Surgery
Address: 55 Fruit St., GRB 425
Boston, MA 02114
Franco, Jan, MD, PhD
ACTIVE | 2014
Mercy Medical Ctr - DSM
Address: 411 Laurel St.,
Des Moines, IA 50314
Frederick, Wayne A. I., MD
INACTIVE | 2010
Howard Univ.
Frey, Charles, MD
INACTIVE | 2012
Fronza, Jeffrey, MD
INACTIVE | 2009
Northwestern Univ. School of Medicine
Fuchshuber, Pascal, MD, PhD
INACTIVE | 2012
The Permanente Medical Group, Inc.
Walnut Creek Medical Ctr.
TABLE OF CONTENTS
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Fujimoto, Jiro, MD, PhD
ACTIVE | 2014
Hyogo College of Medicine
Dept. of Surgery
Address: 1-1 Mukogawa-cho
Nishinomiya, Hyogo 663-8501 Japan
Fujinaga, Kazuhisa
RESIDENT | 2014
Japan
Funel, NIccola, PhD
ACTIVE | 2013
Dept. of Translational Research on New
Technologies
Address: via paradisa, 2
pisa, 56124 Italy
Gamarra, Roberto, MD
INACTIVE | 2011
Ganai, Sabha, MD, PhD
ACTIVE | 2014
Southern Illinois Univ.
Address: Simmons Cancer Institute,
315 W Carpenter St.
Springfield, IL 62702
Gao, Qingshen, MD
ACTIVE | 2013
NorthShore Univ. HealthSystem
Address: 1001 Univ. Place
Evanston, IL 60201
Gareer, Haytham, MD
RESIDENT | 2014
National Cancer Institute, Cairo Univeristy
Address: Fom El Khaleg
Cairo, Egypt
Gaujoux, Sebastien, MD
INACTIVE | 2013
AP-HP Hôpital Beaujon
Gauvin, Jeffrey, MD
INACTIVE | 2011
UC Davis
Gawlas, Irmina, BA
RESIDENT | 2013
Address: 161 Fort Washington Ave.
New York, NY 10032
Gecelter, Gary, MD
INACTIVE | 2012
Gelrud, Andres, MD
INACTIVE | 2009
Univ. of Pittsburgh
Gilbert, Erin, MD
ACTIVE | 2014
Oregon Health & Science Univ.
General Surgery
Address: 3181 SW Sam Jackson Park Rd.,
L223A
Portland, OR 97239
Giovannetti, Elisa, MD, PhD
ACTIVE | 2014
Univ. of Pisa
Address: Via Roma 55
Pisa, 56100 Italy
Girelli, Roberto, MD
INACTIVE | 2010
Casa Di Cura Dott. Pederzoli
Glasgow, Robert, MD
INACTIVE | 2011
Univ. of Utah
Go, Vay Liang, MD
ACTIVE | 2014
UCLA
Digestive Diseases
Address: 900 Veteran Ave, Warren Hall
13-146
Los Angeles, CA 90095
Godoy, Renato, MD
INACTIVE | 2011
Faculdade de Medicina USP
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Goldberg, Ross, MD
Grundfest-Broniatowski, Sharon, MD
Golkar, Farhaad, MD
Guglielmo, Nicola, MD
INACTIVE | 2010
INACTIVE | 2011
Tampa General Hospital
Goni, Elisabetta, MD
RESIDENT | 2013
San Raffaele Scientific Institute
Gastroenterology
Address: Via Olgettina 58
Milan, 20132 Italy
Gonzalez, Carlos, MD
RESIDENT | 2013
Address: 13829 Black Canyon CT
Fishers, IN 46038
Gooszen, Hein, MD
INACTIVE | 2010
UMC Utrecht
Goyal, Kush, MD
INACTIVE | 2009
Univ. Hospitals Case Medical Center
Grady, Eileen F., PhD
INACTIVE | 2011
UCSF
Greenblatt, David Yu, MD, MSPH
INACTIVE | 2011
Univ. of Wisconsin
Grignol, Valene
INACTIVE | 2009
Gruetzmann, Robert, MD
ACTIVE | 2013
Dresden Univ.
Germany
INACTIVE | 2009
Cleveland Clinic A80
RESIDENT | 2013
Sapienza
Paride Stefanini
Address: Via Genzano 87
Rome, 00179 Italy
Gupta, Rajesh MBBS, MS, M Ch
ACTIVE | 2014
PGIMER
Surgical Gastroenterology Div.,
Dept. of General Surgery
Address: Sector 12
Chandigarh, 160012 India
Gusani, Naraj, MD
INACTIVE | 2009
Penn State Hershey Medical Center
Gust, Shannon
INACTIVE | 2009
Guzzetta, Angela
INACTIVE | 2012
Gvozdenović, Miomir S., MD
ACTIVE | 2013
Clinical Center of Serbia
Emergency Center
Address: Pasterova 8
Belgrade, 11000 Serbia
Haglund, Ulf, MD
INACTIVE | 2009
Uppsala Univ. Hospital
Hamilton, Nicholas, MD
INACTIVE | 2009
Washington Univ.
Hao, Disi
INACTIVE | 2012
TABLE OF CONTENTS
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Hardacre, Jeffrey, MD
ACTIVE | 2014
Univ. Hospitals Case Medical Ctr.
Dept of Surgery
Cleveland, OH 44106
Hari, Danielle, MD
INACTIVE | 2009
NIH
Harper, Megan, BS
INACTIVE | 2012
UC San Diego Moores Cancer Center
Hashimoto, Yasushi, MD
RESIDENT | 2013
Hiroshima Univ. Hospital
Address: 1-2-3 Kasumi, Minami-ku
Hiroshima, 734-8551 Japan
Hassanain, Ehab, MD
INACTIVE | 2009
SUNY Downstate Medical Center
Hatcher, Thomas S., MD
INACTIVE | 2011
Univ. of Mississippi Medical Center
Hawkins, William G., MD
Heneghan, Rachel, MD
RESIDENT | 2013
Address: 1100 9th Ave., H8-GME
Seattle, WA 98101
Hermeneit, Sonja, MD
INACTIVE | 2009
Universit Rastock
Hernandez, Jonathan, MD
INACTIVE | 2011
USF
Herrera-Caceres, Jaime O., MD
RESIDENT | 2013
Address: Moctezuma 56 interior 3
Ciudad de Mexico, 14050 Mexico
Hewitt, Kelly, MD
RESIDENT | 2013
Univ. of Utah
Address: 1950 Circle of Hope,
Ste. HCH N-6405
Salt Lake City, UT 84132
Heywood, Glenroy, MD
INACTIVE | 2011
Hill, Joshua, MD
ACTIVE | 2014
Washington Univ. School of Medicine
Dept. of Surgery
Address: 660 S. Euclid Ave.,
Campus Box 8109
St. Louis, MO 63110
INACTIVE | 2009
Univ. of Massachusetts
He, Jin, MD, PhD
Hirono, Seiko, MD
INACTIVE | 2011
Helling, Thomas S., MD
INACTIVE | 2010
Univ. of Mississippi Medical Center
Hines, Joe, MD
INACTIVE | 2012
UCLA School of Medicine
ACTIVE | 2014
Wakayama Medical Univ.
Second Dept. of Surgery
Address: 811-1 Kimiidera,
Wakayama, 641-8510 Japan
Hirose, Kenzo, MD
INACTIVE | 2010
Johns Hopkins Univ.
TABLE OF CONTENTS
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Hodul, Pamela, MD
ACTIVE | 2014
H. Lee Moffitt Cancer Center & Research
Institute
Dept. of Gastrointestinal Oncology
Address: 12902 Magnolia Drive, FOB-2
Tampa, FL 33612
Hoffman, John P., MD
ACTIVE | 2014
Surgery
Hogg, Melissa, MD
ACTIVE | 2014
Pittsburgh, PA
Holbrook, Ryan, MD
INACTIVE | 2010
Cancer Care Northwest
Honselmann, Kim, MD
RESIDENT | 2014
Univ. Medical Center Schleswig-Holstein,
Campus Luebeck
Address: Ratzeburgerallee 160
Luebeck, 23538 Germany
Hopt, Ulrich T., MD
ACTIVE | 2014
Univ. of Freiburg
Surgery
Address: Hugstetter Str. 55,
Freiburg, D 75106 Germany
Hornick, John, MD
INACTIVE | 2010
Horvath, Karen, MD
INACTIVE | 2011
Univ. of Washington
Hotz, Hubert, MD
INACTIVE | 2009
Charite School of Medicine Campus Ben
Franklin
House, Michael, MD
ACTIVE | 2014
Address: 545 Barnhill Drive, EH 529
Howard, Thomas, MD
INACTIVE | 2012
Indiana Univ. Medical Center
Hruban, Ralph H., MD
ACTIVE | 2014
John Hopkins Univ. SOM
Pathology
Address: 401 N. Broadway, Weinberg 2242
Baltimore, MD 21231
Huang, Qi
INACTIVE | 2012
Hughes, Steven J., MD
ACTIVE | 2014
Uf Health Shands
General Surgery
Address: 1600 SW Archer Rd., Po Box
100109
Hurtuk, Michael
INACTIVE | 2012
Huss, Harold T., DO
ACTIVE | 2014
CTCA Illinois
Surgical Onology
Address: 2520 Elisha Ave.
Zion, IL 60203
TABLE OF CONTENTS
124
Hwang, Rosa F., MD
ACTIVE | 2014
UT – MD Anderson Cancer Center
Surgical Oncology
Address: PO Box 301402, Unit 1484
Houston, TX 77230-1402
Iacobuzio, Christine, MD, PhD
INACTIVE | 2009
Johns Hopkins Medical Institution
Ideno, Noboru, MD
ACTIVE | 2013
Kyushu Univ.
Dept. Surgery and Oncology
Address: 3-1-1 Maidashi, Higashi-ku
Fukuoka, 812-8582 Japan
Isaji, Shuji, Prof.
ACTIVE | 2014
Mie Univ. Graduate School of Medicine
Hepatobiliary Pancreatic and Transplant
Surgery
Address: 2-174, Edobashi
Tsu, Mie 514-8507 Japan
Ito, Hiromichi, MD, FACS
ACTIVE | 2014
Michigan State Univ.
Dept. of Surgery
Address: 1200 E Michigan Ave., Suite 655
East Lansing, MI 48823
Jackson, Patrick G., MD
INACTIVE | 2009
Georgetown Univ. Medical Center
Jacobs, Michael J., MD
ACTIVE | 2014
St John Providence Hospital
Surgery
Address: 820 Puritan Ave.
Birmingham, MI 48009
Jamieson, Nigel, MRCS, PhD
RESIDENT | 2013
West of Scotland Pancreatic Unit
Address: Glasgow Royal Infirmary,
Glasgow, Lanarkshire G31 2ER UK
Jang, Jin-Young, MD, PhD
ACTIVE | 2014
Seoul Nat’l Univ. Hosptial
Dept. of Surgery
Address: Yongon-dong 28, Chongno-gu
Seoul, Korea
Jensen, Eric H., MD
ACTIVE | 2014
Univ. of Minnesota
Surgical Oncology
Address: 420 Delawaare St. SE, MC195
Joehl, Raymond J., MD
RETIRED/HONORARY | 2014
Hines VA Hospital
Surgical Service (112)
Address: 5th Ave. & Roosevelt Rd.
Hines, IL 60141
Johnson, Mike, MD
INACTIVE | 2009
Cleveland Clinic
Johnston, Cory, MD
INACTIVE | 2011
Univ. of Utah
Juhani, Sand, MD, PhD
ACTIVE | 2013
Tampere Univ. Hospital
Address: Tersbondie 35,
Tampere, 33521 Finland
Jukemura, José, MD
INACTIVE | 2012
Univ. of Sao Paulo
TABLE OF CONTENTS
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Jury, Robert P., MD
ACTIVE | 2014
Royal Oak Surgical Associates
Address: 3535 W. 13 Mile Rd. #205
Royal Oak, MI 48073
Kadera, Brian, MD
RESIDENT | 2013
Univ. of California - Los Angeles
Surgery
Address: 10833 LeConte Ave, 72-235 CHS
Kalish, Brian
INACTIVE | 2012
Kato, Hiroyuki, MD
INACTIVE | 2011
Mie Graduate School of Medicine
Katz, Matthew, MD
ACTIVE | 2014
Surgical Oncology
Address: 1400 Pressler St., Unit 1484
Houston, TX 77030
Kavuturu, Srinivas, MD
INACTIVE | 2011
Milton S Hershey Medical Center & College
of Medicine
Kawaguchi, Kei, MD, PhD
ACTIVE | 2014
Tohoku Univ. Graduate School of Medicine
Address: 1-1, Seiryo-machi, Aoba-ku
Sendai, Miyagi 980-8574 Japan
ac.jp
Kawai, Manabu, MD, PhD
ACTIVE | 2014
Address: Kimiidera 811-1
Wakayama, 641-8510 Japan
Kazantsev, George, MD
ACTIVE | 2014
Kaiser Foundation Hospital
Surgery
Address: 3600 Broadway, Third Floor
Oakland, CA 94611
Keck, Tobias, MD
ACTIVE | 2014
Univ. Hospital of Schleswig Holstein,
Campus Lübeck
Dept. of Surgery
Lüebeck, 23568 Germany
Keim, Rebecca, MD
ACTIVE | 2014
St. Peter’s Health Partners Medical
Associates
General Surgery
Address: 319 S. Manning Blvd., Suite 305
Albany, NY 12208
Keith, Roger G., MD
INACTIVE | 2010
Royal Univ. Hospital
Kelly, Kaitlyn
INACTIVE | 2012
Kelly, Tracy, MD
INACTIVE | 2011
Kendrick, Michael, MD
ACTIVE | 2014
Mayo Clinic
Divison of GI and General Surgery
Address: 200 First St., SW
Rochester, MN 55905
Kennedy, Eugene, MD
ACTIVE | 2013
Address: 80 Horseshoe Pt.
Phoenixville, PA 19460
TABLE OF CONTENTS
126
Kent, Tara, MD
ACTIVE | 2013
Dept. Surgery
Address: 330 Brooklyn Ave. Suite 9
Boston, MA 02115
Khan, Saboor, MBBS, PhD
INACTIVE | 2010
Mayo Clinic
Kim, Michael, MD
INACTIVE | 2011
King, Jonathan
INACTIVE | 2012
Kirkwood, Kimberly S., MD
ACTIVE | 2014
Univ. of California - San Francisco
General Surgery
Address: 521 Parnassus Ave.
Room C-341, Box 0790
San Francisco, CA 94143
Kishiwada, Masashi, MD, PhD
ACTIVE | 2014
Mie Univ.
Address: yumegaoka, Tsu
Mie, 514-0116 Japan
Kiswani, Vandhana
INACTIVE | 2012
Kitagawa, Hirohisa, MD
ACTIVE | 2014
Kanazawa Univ.
Address: 13-1 Takaramachi,
Kanazawa, 920-8641 Japan
Kitagawa, Yuichi, MD
ACTIVE | 2014
National Center for Geriatrics & Gerontology
Dept. of Surgery
Address: 35 Morioka Gengo,
Obu, Japan
Klar, Ernst, MD
ACTIVE | 2014
Univ. of Rostock
Dept. of Surgery
Address: Chirurgische Klinik und Poliklinik
Schillingallee 35
Rostock, 18057 Germany
Kleiner, Daniel, MD
RESIDENT | 2013
Washington Univ. in St. Louis
Address: 2454 Ivy Springs Lane,
Charlottesville, VA 22901
Kline, Jessica M., BS
INACTIVE | 2009
Kluger, Michael D., MD, MPH
ACTIVE | 2014
Columbia College of Physicians and
Surgeons
Surgery
Address: 161 Fort Washington Ave.,
8th Floor
New York, NY 10032
Koay, Eugene, MD, PhD
RESIDENT | 2013
Address: 1220 Holcombe, MS 97
Houston, TX 77030
Kobayashi, Hironori, MD
INACTIVE | 2012
Hiroshima Univ.
Kobayashi, Motoyuki
INACTIVE | 2012
ac.jp
Kok, Niels, MD, PhD
ACTIVE | 2013
Erasmus MC
Address: PO Box 2040,
Rotterdam, 3000 CA Netherlands
TABLE OF CONTENTS
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Kolarczyk, Aleksandra, Ms
Kuehn, Florian, MD
Kondo, Naru, MD
Kuroda, Nobukazu, MD, PhD
Kondo, Yuichi, MD, PhD
Kusnierz, Katarzyna, MD, PhD
RESIDENT | 2013
Medical Univ. of Silesia, Katowice Poland
Address: Jastrzebia 8/3,
Sosnowiec, - 41-209 Poland
RESIDENT | 2014
Hiroshima Univ.
Dept. of Surgery
Address: Kasumi, Minami-Ku
Hiroshima, 7328551 Japan
INACTIVE | 2011
Konstantinidis, Ioannis, MD
INACTIVE | 2010
Korotkov, Sergey
RESIDENT | 2013
9th Minsk Municipal Hospital
emergency abdominal surgery
Address: Semashko 8
Minsk, 220116 Belarus
Kosaka, Hisashi, MD, PhD
ACTIVE | 2014
Surgery
Address: 1-1 Mukogawa-tyou
Nishinomiya, Hyogo 663-8501 Japan
Krantz, Seth, MD
INACTIVE | 2011
Northwestern Univ.
Krepline, Ashley
RESIDENT | 2014
Milwaukee, WI 53226
Kubat, Eric, MD
INACTIVE | 2011
Univ. of California, San Francisco
RESIDENT | 2014
Univ. of Rostock
Address: Schillingallee 35
Rostock, 18057
ACTIVE | 2013
Dept. of Surgery
Address: 1-1, Mukogawa-cho,
Nishinomiya, Hyogo 6638501 Japan
ACTIVE | 2013
Medical Univ. of Silesia
Dept. of Gastroenterology
Address: Medykow 14
Katowice, 40-752 Poland
Kutlu, Onur C., MD
RESIDENT | 2013
Texas Tech Univ. Health Sciences Center
General Surgery
Address: 3601 4th St, MS8312
Lubbock, TX 79430
Kwon, David, MD
ACTIVE | 2014
Henry Ford Health System
Surgery
Address: 2799 W. Grand Blvd., K-8 Surgery
Detroit, MI 48202
Lamont, Jeffrey, MD
INACTIVE | 2009
Baylor Univ. Medical Center
Lampe, Pawel, MD, PhD
INACTIVE | 2012
Medical Univ. of Silesia
Lapshyn, Hryhoriy, PhD
RESIDENT | 2014
Univ. Hospital Freiburg
Address: Hugstetterstr. 55
TABLE OF CONTENTS
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Larvin, Michael, MD
ACTIVE | 2013
Univ. of Limerick
Address: GEMS Room 3-021
Limerick, Ireland
Laukkarinen, Johanna, MD, PhD
Lee, Jeffrey E., MD
ACTIVE | 2014
UT, MD Anderson Cancer Center
Dept. of Surgical Oncology
Address: 1400 Pressler St., Unit 1484
Houston, TX 77030
ACTIVE | 2014
Tampee Univ. Hospital
Dept of Gastroenterology and Alimentary
Tract surgery
Address: Teiskontie 35
Tampere, 33520 Finland
Lee, Kenneth K.W., MD
Lavu, Harish, MD
Lennon, Anne Marie, MD
ACTIVE | 2014
Surgery
Address: 1025 Walnut St., College Bldg,
Suite 605
Lazar, Melissa, MD
INACTIVE | 2010
Le, Maithao, MD
INACTIVE | 2011
City of Hope
Lee, Christina, MD
RESIDENT | 2014
Univ. of Wisconsin
Address: 600 Highland Ave.
Madison, WI 53792
Lee, Grace Clara, BS
RESIDENT | 2014
Dept. of Surgery
Address: 10 Emerson Place, Apt. 15H
Boston, MA 02114
ACTIVE | 2014
Univ. of Pittsburgh School of Medicine
Dept. of Surgery
Address: 497 Scaife Hall
INACTIVE | 2012
Johns Hopkins Univ.
Lesslie, III., Donald P., DO
ACTIVE | 2014
Univ. of Texas - Houston
Surgery
Address: 6431 Fannin St., MSB 4.164
Houston, TX 77030
Leung, Dennis MS
INACTIVE | 2011
Evanston NorthShore Univ. HealthSystem
Levenson, Victor, MD
INACTIVE | 2011
Lewis, Russell
RESIDENT | 2014
Perelman School of Medicine,
Univ. of Pennsylvania
Liang, Tao
INACTIVE | 2012
Lillemoe, Keith D., MD
ACTIVE | 2014
Dept. of Surgery
Address: 55 Fruit St., WHT 506
Boston, MA 02114
TABLE OF CONTENTS
129
Linnebacher, Michael
MacKenzie, Shawn
Liss, Andrew
Magge, Deepa, MD
INACTIVE | 2012
INACTIVE | 2012
Loux, Tara, MD
INACTIVE | 2011
Lowy, Andrew A., MD
ACTIVE | 2014
UC San Diego Moores Cancer Center
Surgery
Address: 3855 Health Sciences Dr. ML 0987
La Jolla, CA 92093-0987
Luffarelli, Paolo, MD
RESIDENT | 2014
Campus Bio-Medico Univ.
Address: via Alvaro del Portillo, 200
Rome, 00128 Italy
Ly, Quan P., MD
ACTIVE | 2014
Univ. of Nebraska Medical Center
Surgery
Address: 986345 Nebraska Medical Center
Omaha, NE 68198-4030
Lyo, Victoria, BA
INACTIVE | 2010
UCSF
Lyu, Heather, BA
RESIDENT | 2013
Address: 1110 South Kenwood Ave.
Baltimore, MD 21224
Machado, Marcel C.C., MD
ACTIVE | 2014
Univ. of Sao Paulo
Faculty of Medicine
Address: Peixoto Gomide 515 #134
INACTIVE | 2010
Virginia Piper Cancer Institute
INACTIVE | 2011
Magnuson, Thomas, MD
ACTIVE | 2013
Johns Hopkins
Dept. of Surgery
Address: 4940 Eastern Ave., A558
Baltimore, MD 21224
Mahvi, David, MD
INACTIVE | 2009
Northwestern Univ.
Maithel, Shishir Kumar, MD
ACTIVE | 2013
Emory Univ.
Surgery, Division of Surgical Oncology,
Winship Cancer Institute
Address: 1365C Clifton Rd., NE, Building C,
2nd Floor
Atlanta, GA 30322
Makary, Martin
INACTIVE | 2009
Johns Hopkins
Makoto, Satake, MD, PhD
ACTIVE | 2014
Hyogo College of Medicine, Sasayama
Med. Ctr.
Dept. of Surgery
Address: 5 Kurooka
Sasayama, Hyogo 6692-321 Japan
Makowiec, Frank, MD
ACTIVE | 2014
Univ. of Freiburg
Dept. of Surgery
Address: Hugstetter Strasse 55
Freiburg, D-79106 Germany
TABLE OF CONTENTS
130
Malleo, Giuseppe, MD
INACTIVE | 2012
Pioliclinico GB Rossi Verona
Email: giuseppe.malleo@
ospedaleuniverona.it
Mammen, Joshua, MD
INACTIVE | 2009
Manos, Lindsey, PA-C
RESIDENT | 2014
Johns Hopkins Medicine
Dept. of Surgery
Address: 600 North Wolfe St., Halsted 600
Baltimore, MD 21287
Mansour, John
ACTIVE | 2014
Address: 5323 Harry Hines Blvd.
Dallas, TX 75390-8548
Marchegiani, Giovanni, MD
RESIDENT | 2014
MGH - Harvard Medical School
Address: 55 Fruit St.
Boston, MA 02114
Marcus, Stuart, MD
INACTIVE | 2011
St. Vincent’s Medical Center
Marks, William H., MD, PhD
INACTIVE | 2009
Swedish Medical Center
Martin, Ronald, MD
ACTIVE | 2013
Marshfield Clinic
Address: 1000 North Oak Ave.
Marshfield, WI 54449
Martin II., Robert C. G., MD, PhD
ACTIVE | 2014
Univ. of Louisville School of Medicine
Surgery/Surgical Oncology
Address: 315 E. Broadway (M10)
Louisville, KY 40202
Martinie, John, MD
ACTIVE | 2014
Carolinas Medical Center
Surgery
Address: 1025 Morehead Medical Dr., #300
Charlotte, NC 28204
Mathur, Abhishek, MD
RESIDENT | 2013
Indiana Univ.
Address: 345 Bayshore Blvd., Apt. 409
Tampa, FL 33606
Matrisian, Lynn, PhD, MBA
ACTIVE | 2014
Research and Scientific Affairs
Address: 1500 Rosencrans Ave., Suite 200
Manhattan Beach, CA 90260
Matsubayashi, Hiroyuki, MD, PhD
ACTIVE | 2013
Shizuoka Cancer Center
Endoscopy
Address: 1007, Shimonagakubo, Nagaizumi
Suntogun, Shizuoka 411-8777 Japan
Matthews, Jeffrey B., MD
ACTIVE | 2014
The Univ. of Chicago
Dept. of Surgery
Address: 5841 S. Maryland Ave., MC 5029
Chicago, IL 60637
Maupin, George Capt.
INACTIVE | 2009
Mazzini, Guilherme, MD
ACTIVE | 2014
Universidade Federal do Rio Grande do Sul
Address: Ramiro Barcelos 2600, anexo
Porto Alegre, RS 90035 Brazil
McAuliffe, John
INACTIVE | 2012
TABLE OF CONTENTS
131
McDonald, Douglas R., MD
RESIDENT | 2014
ETSU
Surgery
Address: 66 Glory Court,
Jonesborough, TN 37659
McDowell, Dena, MS, RD
INACTIVE | 2011
Froedtert Hospital
McKenzie, Shawn, MD
INACTIVE | 2009
City of Hope National Medical Center
McMillan, Matthew
RESIDENT | 2014
Univ. of Pennsylvania School of Medicine
Address: 3400 Spruce St, 4 Silverstein
Menon, Vijay, MD
RESIDENT | 2013
Cedars-Sinai Medical Center
Address: 8635 W. Third St., Suite 590W
Merchant, Nipun, MD
ACTIVE | 2014
Address: 2220 Pierce Ave
597 Preston Research Building
Nashville, TN 37232-6860
Mesleh, Marc, MD
ACTIVE | 2014
Advocate Christ Medical Center
Address: 4400 W 95th St., Suite 413
Oak Lawn, IL 60453
Metildi, Cristina, MD, MAS
RESIDENT | 2013
UC San Diego Health System
Address: 3990 Centre St., Unit 102
San Diego, CA 92103
Meyer, Alberto
INACTIVE | 2011
USP
Mezhir, James J., MD
ACTIVE | 2014
Univ. of Iowa Hospitals and Clinics
Surgical Oncology
Address: 200 Hawkins Drive, 4642 JCP
Iowa City, IA 52242
Michelassi, Fabrizio, MD
INACTIVE | 2011
Weill Medical College of Cornell Univ.
Mier, Fernando, MD
INACTIVE | 2009
ABC Medical Center
Mier, Juan, MD
ACTIVE | 2014
Centro Medico ABC
Surgery
Address: Paseo de la Reforma 2608-1215
Mexico City, DF 11950 Mexico
Miller, Benjamin, BA
RESIDENT | 2013
Mino-Kenudson, Mari, MD
ACTIVE | 2014
Massachusetts General Hospital & Harvard
Medical School
Pathology
Address: Warren 122, 55 Fruit St.
Boston, MA 02114
Mizuno, Shugo, MD
ACTIVE | 2014
Mie Univ.
Address: 2-174 Edobashi
Tsu City, Mie 514-0001 Japan
Mohammed, Somala, MD
RESIDENT | 2014
Baylor College of Medicine
Address: 7675 Phoenix Dr. #834
Houston, TX 77030
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Moningi, Shalini
RESIDENT | 2014
Johns Hopkins School of Medicine
Address: 640 N. Calvert St., Apt. A
Baltimore, MD 21202
Email:
Muilenburg, Diego, MD
INACTIVE | 2009
Univ. of California at Davis
Mulvihill, Sean J., MD
ACTIVE | 2014
Univ. of Milan
Address: Via Manzoni 56, Rozzano
Milano, 20089 Italy
ACTIVE | 2014
Univ. of Utah Medical Group
Dept. of Surgery
Address: 175 N Medical Drive East, Room
5223
Salt Lake City, UT 84132-2301
Moody, Frank G., MD
Murata, Yasuhiro, MD
Montosori, Marco, MD
ACTIVE | 2014
UT Houston Medical School
Dept. of Surgery
Address: 6431 Fannin St., MSB 4.130
Houston, TX 77030
Morgan, Katy, MD
ACTIVE | 2014
Medical Univ. of South Carolina
Dept of Surgery
Address: 25 Courtenay Dr., Suite 710,
MSC 290
INACTIVE | 2012
Mie Univ.
Murr, Michel M., MD
ACTIVE | 2014
USF- Tampa General Hospital Bariatric
Center
Dept. of Surgery
Address: 5 Tampa General Circle, Suite 410
Tampa, FL 33606
Muscarella, II, Peter, MD
INACTIVE | 2011
Universitätsklinikum Rostock
ACTIVE | 2014
Ohio State Univ.
Surgery
Address: N711 Doan Hall, 410 West 10th Ave.
Columbus, OH 43210
Moriya, Toshiyuki, MD, PhD
Nadeau, Laura, MD
Moritz, Katharina, Dr.
ACTIVE | 2014
Okitama Public General Hospital
Address: 2000 Nishi-Otsuka
Kawanishi-Machi, Yamagata 992-0601
Japan
Moser, Arthur James, MD
ACTIVE | 2014
BIDMC
Surigical Oncology
Address: 330 Brookline Ave
Boston, MA 02215
INACTIVE | 2011
Nagorney, David M., MD
ACTIVE | 2014
Mayo Clinic College of Medicine
Subspecialty General Surgery
Address: 200 First St. SW
Rochester, MN 55905
Nakagawa, Naoya, MD
RESIDENT | 2013
Hiroshima Univ.
Address: 1-2-3 Kasumi, MInami-ku
Hiroshima, Hiroshima 734-8551 Japan
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Nakamura, Masafumi, MD, PhD
ACTIVE | 2013
Address: Matsushima 577, 701-0192
Kurashiki, Japan
Nakashima, Akira, MD
INACTIVE | 2010
Hiroshima Univ.
Nakeeb, Attila, MD
ACTIVE | 2014
Dept. of Surgery
Address: 539 Emerson Hall
Nappo, Gennaro, MD
RESIDENT | 2014
Univ. Campus Bio-Medico di Roma
General Surgery
Address: Via Alvaro Del Potillo, 200
Rome, 00128 Italy
Narra, Vinod, MD
INACTIVE | 2009
Henry Ford Hospital
Naru, Kondo, MD
INACTIVE | 2010
Hiroshima Univ.
Nathan, Hari, MD
INACTIVE | 2009
Johns Hopkins Univ.
Nealon, William H., MD
ACTIVE | 2014
Vanderbilt Univ. School of Medicine
General Surgery
Address: 1161 Medical Center Dr., D5203
MCN
Neeff, Hannes P., MD
ACTIVE | 2014
Univ. Hospital Freiburg
General and Digestive Surgery
Address: Hugstetterstr. 55
Newhook, Timothy, MD
RESIDENT | 2014
Univ. of Virginia
Dept. of Surgery
Address: PO Box 800679
Nguyen, Andrew
RESIDENT | 2014
UCLA
Address: 1730 Sawtelle Blvd. #307,
Nguyen, Katherine, MD
INACTIVE | 2009
Nguyen, Trang, MD
RESIDENT | 2014
Univ. of Pittsburgh
Address: 425 N. Neville St., Apt 102
Niccola, Funel
INACTIVE | 2012
Nicholl, Michael B., MD
ACTIVE | 2014
Univ. of Missouri
Dept. of Surgery
Address: One Hospital Drive, MC 520E
Columbia, MO 65212
Nichols, R. Charles, MD
ACTIVE | 2014
UF Proton Therapy Institute
Radiation Oncology
Address: 2015 North Jefferson St.
Nijmeijer, Rian
INACTIVE | 2009
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134
Nikfarjam, Mehrdad, MD, PhD,
FRACS
ACTIVE | 2014
Univ. of Melbourne, Austin Health
Surgery
Address: LTB 8, 145 Studley Rd. Heidelberg
Melbourne, VIC 3084 Australia
Nissen, Nicholas, MD
ACTIVE | 2013
Cedars-Sinai Medical Center
Dept. of Surgery
Address: 8635 W. Third St., Suite 590
Nubuoka, Yu, MD
INACTIVE | 2009
Mie Univ. Graduate School of Medicine
Nussbaum, Michael S., MD
ACTIVE | 2014
Univ. of Florida COM
Dept. of Surgery
Address: 653 W. 8th St., 3rd Floor
Faculty Clinic
Okada, Toshihiro, MD, PhD
INACTIVE | 2011
Okuda, Yoshihiro, MD
RESIDENT | 2014
Olino, Kelly, MD
INACTIVE | 2010
The Johns Hopkins Hospital
Onetti Muda, Andrea, MD
ACTIVE | 2013
Campus Bio-Medico Univ. of Rome
Dept. of Pathology
Address: Via Alvaro del Portillo, 200,
Rome, 00128 Italy
Ongchin, Melanie, MD
RESIDENT | 2014
Orr, Shannon, MD
INACTIVE | 2011
Osvaldt, Alessandro, MD, PhD
ACTIVE | 2014
Hospital de Clinicas de Porto Alegre
Address: Cristovao Colombo, 3060,
Porto Alegre, RS 90035-170 Brazil
Otsuka, Takao, MD, PhD
ACTIVE | 2014
Kyushu Univ.
Dept. of Surgery and Oncology
Address: 3-1-1 Maidashi, Higashi-ku
Ouellet, Jean-Francois
INACTIVE | 2012
Ouellette, James DO
INACTIVE | 2009
Wright State Univ.
Ovrebo, Kjell, MD
INACTIVE | 2010
Haukeland Univ. Hospital
Paniccia, Alessandro
INACTIVE | 2012
Panni, Roheena, MD
RESIDENT | 2014
St. Louis, MO 63108
Papalezova, Katia, MD
INACTIVE | 2010
Duke Univ. Medical Center
Papavasiliou, Pavlos, MD
INACTIVE | 2011
TABLE OF CONTENTS
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Pappas, Theodore N., MD
Partelli, Stefano, MD
Pappas, Sam, MD
Paulus, Elena, MD
INACTIVE | 2010
Duke Univ. Medical Center
ACTIVE | 2014
General Surgery
Address: 2160 S. First Ave.
Maywood, IL 60153
INACTIVE | 2011
Univ. of Verona
INACTIVE | 2011
Pawlik, Timothy, MD, PhD
INACTIVE | 2011
Univ. of New Mexico
ACTIVE | 2014
Johns Hopkins Univ.
Surgery
Address: 600 N. Wolfe St., Blalock 665
Baltimore, MD 21287
Parekh, Dilip, MD
Pek, Chulja
Parasher, Gulshan, MD
INACTIVE | 2009
Univ. of Southern California
Parikh, Alexander, MD
ACTIVE | 2014
Surgical Oncology
Address: 2220 Pierce Ave., 597 PRB
Nashville, TN 37232
Parikh, Purvi Y., MD
ACTIVE | 2014
Address: 7 Keats Common,
Slingerlands, NY 12159
Parikh, Janak, MD, MSHS
ACTIVE | 2014
St. John Providence
Address: 26850 Providence Parkway,
Suite 504
Novi, MI 48374
Park, Joo Kyung, MD
INACTIVE | 2009
Seoul National Univ. Hospital
Parmar, Abhishek, MD
RESIDENT | 2013
UCSF-East Bay, UTMB
Address: 2902 Chenevert St., Unit K
Houston, TX 77004
INACTIVE | 2009
Pellegrini, Carlos A., MD
Univ. of Washington
Dept. of Surgery
Address: 1959 NE Pacific St., Box 356410
Seattle, WA 98195-6410
Peng, June
RESIDENT | 2014
Cleveland Clinic
Cleveland, OH 44195
Penteado, Sonia, MD
ACTIVE | 2014
Hospital das Clinicas FM VSP
Gastroenterology
Address: rua Cristiano Viana 1089/11
Sao Paulo, 05411-002 Brazil
Perrone, Giuseppe, MD
ACTIVE | 2013
Campus Bio-Medico Univ.
Pathology
Address: Via Alvaro del Portillo, 200
Rome, 00128 Italy
TABLE OF CONTENTS
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Perrone, Vittorio Grazio, MD
INACTIVE | 2009
Chirurgia Univ.
Petzel, Maria, BS, RD
INACTIVE | 2012
Pham, Hung, PhD
INACTIVE | 2009
UCLA David Geffen School of Medicine
Pilgrim, Charles, MD, PhD
RESIDENT | 2013
Address: 9200 W Wisconsin Ave.
Milwaukee, WI 53226
Pimiento, Jose, MD
INACTIVE | 2012
Moffitt Cancer Center
Pineda, Danielle
INACTIVE | 2012
Pinson, C. Wright, MD
INACTIVE | 2009
Vanderbilt Univ.
Pitt, Henry, MD
ACTIVE | 2014
Temple Univ. School of Medicine
Dept. of Surgery
Address: 3509 N. BRd St., Boyer Pavilion
9th Floor Rm E938
Philadpelphia, PA 19140
Plichta, Jennifer, MD, MS
RESIDENT | 2014
General Surgery
Address:: 2160 S. First Ave., EMS Bldg
Maywood, IL 60153
Polanco, Patricio, MD
RESIDENT | 2014
Address: 507 Maryland Ave.
Pollina, Luca Emanuele, MD
INACTIVE | 2010
Hospital-Univ. of Pisa
Porpiglia, Andrea, MD
RESIDENT | 2014
Address: 333 Cottman Ave., H3-133
Postier, Russell, MD
ACTIVE | 2014
Univ. of Oklahoma College of Medicine
Dept. of Surgery
Address: PO Box 26901 - Williams Pavillion
Room 2140
Oklahoma City, OK 73126
Prejeant, Kristi, MD
INACTIVE | 2010
Univ. of Oklahoma Health Science Ctr.
Prinz, Richard A., MD
ACTIVE | 2014
Dept. of Surgery
Address: 2650 Ridge Ave. Walgreen 2507
Evanston, IL 60201
Pucci, Michael J., MD
ACTIVE | 2014
Jefferson Univ. Physicians
Dept. of Surgery
Address: 1100 Walnut St., Suite 500
Pupine, Aiste, MD
INACTIVE | 2011
Hospital of Lithuanian Univ. of Health
Sciences
TABLE OF CONTENTS
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Purich, Edward, PhD
Reber, Howard, MD
Que, Florencia G., MD
Reddy, Sanjay S., MD
ACTIVE | 2013
ChiRhoClin, Inc.
Address: 4000 Blackburn Lane, Suite 270
Burtonsville, MD 20866
ACTIVE | 2014
Mayo Clinic
Dept. of Surgery
Rochester, MN 55905
Rabiee, Atoosa, MD
INACTIVE | 2009
Johns Hopkins Bayview
Ragulin Coyne, Elizaveta, MD, MHS
INACTIVE | 2012
UMASS Medical School
Email: elizaveta.ragulincoyne@
umassmemorial.org
Raigani, Siavash, BA
RESIDENT | 2013
CWRU School of Medicine
Address: 2300 Overlook Rd., Apt. 717
Cleveland, OH 44106
Rao, Bettina, Prof.
INACTIVE | 2009
Univ. of Rostock
Raoof, Mustafa
INACTIVE | 2012
Raper, Steven E., MD
INACTIVE | 2009
Rasmussen, Ib C., MD, PhD
ACTIVE | 2014
Falun County Hospital
Dept. of Surgery
Address: Hurtigs gata 23 2tr
Falun, SE-79182 Sweden
ACTIVE | 2014
UCLA School of Medicine
Address: 10833 LeConte Ave.
ACTIVE | 2014
Reddy, Sushanth, MD
INACTIVE | 2010
Johns Hopkins Univ.
Reid Lombardo, Kaye M., MD
ACTIVE | 2014
Mayo Clinic
Dept. of Surgery
Rochester, MN 55905
Relles, Daniel, MD
RESIDENT | 2013
Jefferson
Address: 1015 Walnut St. Suite 620
Rezaee, Neda, MD
RESIDENT | 2014
Johns Hopkins Univ.
Address: 600 North Wolfe St., Blalock 1206
Baltimore, MD 21287
Riall, Taylor S., MD, PhD
ACTIVE | 2014
Dept. of Surgery
Address: 301 Univ. Blvd., JSA 6.110c
Richards, Nathan, MD
INACTIVE | 2010
TABLE OF CONTENTS
138
Richter, Harry, MD
ACTIVE | 2014
Stroger Hospital of Cook County
Dept. of Surgery
Address: 1901 W Harrison St.
Chicago, IL 60612
Rilo, Horacio, MD
INACTIVE | 2011
Univ. of Arizona
Rittenhouse, David, MD
INACTIVE | 2011
Robinson, Jamie, MD
RESIDENT | 2014
Dept of Surgery
Address: 1161 21st Ave. S, D-4314 MCN
Rocha, Flavio, MD
Rosati, Carlo M., MD
INACTIVE | 2011
Scuola Superiore Sant’Anna
Rosati, Lauren
RESIDENT | 2014
Address: 7709 Takoma Ave.
Takoma Park, MD 20912
Rose, J. Bart, MD, MAS
RESIDENT | 2013
GME
Address: 1100 9th Ave.
Seattle, WA 98101
Rosemurgy, Alexander S., MD
ACTIVE | 2014
Florida Hospital Tampa
Surgery
Address: 3000 Medical Park Drive #310,
Tampa, FL 33613
ACTIVE | 2013
Address: 1100 9th Ave.
Seattle, WA 98101
Rosen, Matthew Marc, MD
Rochefort, Matthew
Rosenberg, Lawrence, MD
INACTIVE | 2012
Roggin, Kevin, MD
INACTIVE | 2011
Univ. of Chicago
Roland, Christina, MD
RESIDENT | 2013
Ronnekleiv-Kelly, Sean, MD
RESIDENT | 2013
Univ. of Wisconsin Hospital and Clinics
Address: Dept. of Surgery,
600 Highland Ave.
Madison, WI 53792
INACTIVE | 2009
ACTIVE | 2014
Jewish General Hospital- McGill Univ.
Surgery
Address: 3755 Lote Sarinthe Catherine
Suite B-119
Montreal, QC H2T1E3 Canada
Rosenberg, Wade, MD
INACTIVE | 2010
Texas Surgical Associates
Ross, Sharona B., MD, FACS
ACTIVE | 2014
Surgery
Address: 3000 Medical Park Drive,
Suite 310
Tampa, FL 33613
TABLE OF CONTENTS
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Roy, Ishan
Salem, Ahmed Farouk, PhD
Royal, Richard E., MD
Salman, Bulent, MD
INACTIVE | 2011
ACTIVE | 2013
Address: 1400 Pressler Drive, Unit 1484
Houston, TX 77030
Rupp, Christopher, MD
INACTIVE | 2011
Univ. of NC Chapel Hill
Sachdeva, Ashwin
INACTIVE | 2009
Newcastle Univ.
Sagi, Sashidhar
INACTIVE | 2012
Sah, Raghuwansh
INACTIVE | 2011
Univ. of Minnesota
Saif, Wasif, MD, MBBS
ACTIVE | 2014
Tufts Univ. School of Medicine
Tufts Cancer Center
Address: 800 Washington St.
Suite 7099 7South
Boston, MA 02111
INACTIVE | 2009
Univ. of Pisa & Thomas Jefferson
ACTIVE | 2013
John Hopkins
Surgery
Address: 600 N. Wolfe St., 1206 Blalock
Baltimore, MD 21287
Saluja, Ashok K., PhD
ACTIVE | 2014
Univ. of Minnesota
Surgery, Basic & Translational Research
Address: 420 Delaware St. SE, MMC 195
Samuel, Isaac, MD
INACTIVE | 2011
Univ. of Iowa
Sanabria, Juan, MD, MSc, FRCSC
ACTIVE | 2014
Case Western Reserve Univ., Cancer
Treatment Centers of America
Surgery, Nutrtion & Preventive Medcine
Address: 3239 Bremerton Rd.
Pepper Pike, OH 44124
Sanchez, Norberto, MD
INACTIVE | 2011
Beth Isreal Deaconess MC
Sakabe, Ryutaro, MD
Sand, Juhani, MD, PhD
Sakata, Naoaki, MD, HD
Sanford, Dominic, MD
INACTIVE | 2011
Hiroshima Univ.
INACTIVE | 2009
Loma Linda Univ.
Saldinger, Pierre F., MD
ACTIVE | 2013
New York Hospital Queens
Surgery
Address: 56-45 Main St.
Flushing, NY 11355
INACTIVE | 2011
Tampere Univ. Hospital
RESIDENT | 2013
Address: 4531 Westminster Place
St. Louis, MO 63108
Santos Sousa, Hugo, MD, MSc
INACTIVE | 2012
Centro Hospitalar de São João
Univ. of Porto Faculty of Medicine
TABLE OF CONTENTS
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Sarmiento, Juan M., MD
ACTIVE | 2014
Emory Univ. Hospital
Dept. of Surgery
Address: 1365 Clifton Rd. NE, Suite A5039
Atlanta, GA 30322
Sarosiek, Konrad, MD
RESIDENT | 2013
Thomas Jefferson
Address: 201 N 8th St. Unit 314
Philadelphia, PA 19106-1011
Sarr, Michael G., MD
ACTIVE | 2014
Mayo Clinic
Gastroenterology Research Unit
Address: 200 1st St. SW
Rochester, MN 55905
Sasaki, Hayato, MD
RESIDENT | 2014
Hiroshima Univ.
Address: 1-2-3 Kasumi, Minami-ku
Hiroshima, 734-8551 Japan
Sassatani, Alexandre, MD
INACTIVE | 2009
Santa Casa Medical School
Sasson, Aaron R., MD
ACTIVE | 2014
Univ. of Nebraska Medical Center
Dept. of Surgery
Address: 986345 Nebraska Medical Center
Omaha, NE 68198-6345
Satoi, Sohei, MD, FACS
ACTIVE | 2014
Kansai Medical Univ.
Dept. of Surgery
Address: 2-5-1, Shin-machi, Hirakata
OSAKA, 573-1010 Japan
Scaife, Courtney, MD
ACTIVE | 2014
Univ. of Utah/ Huntsman Cancer Institute
General Surgery
Address: 1950 Circle of Hope, Suite N6405
Schellhaas, Elisabeth, MD
INACTIVE | 2009
Charite Medical School
Schiller, William R., MD
ACTIVE | 2014
Southern Illinois Univ. - SOM
Surgery
Address: 784 Aspen Compound,
Santa Fe, NM 87501
Schmidt, C. Max
ACTIVE | 2013
Address: 550 N Univ. Blvd.
Schneider, Patrick
INACTIVE | 2009
Penn State College of Medicine
Schulick, Richard, MD
INACTIVE | 2011
Schwandner, Frank
INACTIVE | 2011
Univ. of Rostock
Schwarz, Roderich, MD, PhD
ACTIVE | 2014
Indiana Univ. Health Goshen Center for
Cancer Care
Address: 200 High Park Ave
Goshen, IN 46526-4810
Schwesinger, Wayne H., MD
INACTIVE | 2009
The Univ. of Texas HSC at San Antonio
Sclabas, Guido, MD
INACTIVE | 2011
Mayo Clinic
Scognamiglio, Pasquale
RESIDENT | 2014
Campus Bio-Medico Univ. of Rome
Address: Via Alvaro del Portillo, 200
Rome, 00128 Italy
TABLE OF CONTENTS
141
Scow, Jeffrey S., MD
INACTIVE | 2010
Mayo Clinic
Seifert, Hans, MD
ACTIVE | 2013
Carl von Ossietzky Universität
Gastroenterology and Hepatology
Address: Rahel Straus Str. 10
Oldenburg, 26131 Germany
Serrano, Pablo, MD
ACTIVE | 2014
McMaster Univ.
Surgery
Address: 711 Concession St., B3-161
Hamilton, ON L8V1C3 Canada
Seshadri, Ramanathan, MD
RESIDENT | 2014
Carolinas Medical Center
Address: 1025 Morehead Medical Drive,
Suite 600
Huntersville, NC 28078
Sethi, Saurabh, MD, MPH
Sharp, Kenneth W., MD
ACTIVE | 2014
Dept. of Surgery
Address: D5203 MCN
Sharpe, Susan, MD
RESIDENT | 2014
Univ. of Chicago
Address: 5841 South Maryland Ave, MC6040
Chicago, IL 60637
Shaw, Christiana, MD
INACTIVE | 2010
Shea, Jill, MD, PhD
ACTIVE | 2013
Univ. of Utah
Dept. of Surgery
Address: 1950 Circle of Hope, Ste. HCH
N6405
INACTIVE | 2009
Wayne State Univ. Detroit MC
Shelton, Julia
Sewryn, Mariusz MSN
Sheppard, Brett C., MD
RESIDENT | 2013
Slielsian Medical Univ.
Address: Pck 10
Sosnowiec, 41-200 Poland
Shah, Paresh, MD
ACTIVE | 2013
Lenox Hill Hospital
Address: 186 east 76th St.
new york, NY 10075
Shah, Rupen, MD
INACTIVE | 2011
Henry Ford Hospital
INACTIVE | 2012
ACTIVE | 2014
Oregon Health & Sciences Univ.
Division of General Surgery
Address: 3181 SW Sam Jackson Park Rd
Mail Code: L223A
Portland, OR 97239
Sherman, Karen
INACTIVE | 2012
Shi, Jun
INACTIVE | 2012
Shimizu, Shuji, MD
INACTIVE | 2011
Kyushu Univ. Hospital
TABLE OF CONTENTS
142
Shin, Marcus PhD
ACTIVE | 2014
Forest Labs
Medical Affairs
Address: 6510 Ocean Crest Dr. Apt. C109
Rancho Palos Verdes, CA 90275
Shoup, Margo, MD
ACTIVE | 2014
Cadence Cancer Center at Warrenville
Surigical Oncology
Address: 4405 Weaver Parkway
Warrenville, IL 60555
Showalter, Shayna, MD
INACTIVE | 2009
Shuford, Betsy RN
ACTIVE | 2013
Address: 25 Courtenay Dr., Suite 7100 A
Shukla, Parul, MD
INACTIVE | 2009
TATA Memorial Hospital
Siecean, Andrada, MD, PhD
INACTIVE | 2009
Univ. of Medicine & Pharmacy
Siripurapu, Veeraiah, MD
INACTIVE | 2011
Fox Chase Medical Center
Smith, Kerrington D., MD
ACTIVE | 2014
Dartmouth Hitchcock Medical Center
Surgery
Address: One Medical Center Drive
Lebanon, NH 03756
Smith, Jillian K., MD, MPH
INACTIVE | 2011
Solorzano, Carmen C., MD
INACTIVE | 2009
Sylvester Cancer Center
Solotkin, Kathleen MSN
INACTIVE | 2011
Eli Lilly and Company
Soriano, Perry A., MD
INACTIVE | 2009
Everett Clinic
Spencer, Philip
INACTIVE | 2011
Spitzer, Austin
INACTIVE | 2012
Squires, Malcolm Hart, MD
RESIDENT | 2013
Emory Univ.
Dept. of Surgery, Div. of Surgical Oncology
Address: 865 Fraser St. SE
Atlanta, GA 30315
Stauffer, John, MD
ACTIVE | 2014
Mayo Clinic
Stein, Julie Ann, MD
INACTIVE | 2011
Stephens, Robert V., MD
Dept. of Surgery
Address: 2320 E. Marshall
Phoenix, AZ 85016
StLaudereas, Styestovia Yestee, PhD
INACTIVE | 2012
Methodist Hospital -Vascular Surgeries
Email: drstyestoviastlaudereas@yahoo.
com
TABLE OF CONTENTS
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Strasberg, Steven M., MD
Talamonti, Mark S., MD
Strohl, Madeleine
Talbott, Vanessa, MD
ACTIVE | 2014
Surgery
Address: 660 S Euclid Ave, Campus Box 8109
St. Louis, MO 63110
RESIDENT | 2014
Sugimoto, Motokazu, MD
RESIDENT | 2014
St. Luke’s Health System
Address: 100 East Idaho St., Suite 301
Boise, ID 83712
Sugiura, Teiichi, MD, PhD
INACTIVE | 2011
Shizuoka Cancer Center
Sutton, Jeffrey, MD
RESIDENT | 2014
Univ. of Cincinnati College of Medicine
Address: 231 Albert Sabin Way, ML 0558,
SRU 1588
Swanson, Richard S., MD
ACTIVE | 2014
Surgery
Address: 75 Francis St
Boston, MA 02115
Takaori, Kyoichi “Tony”, MD
ACTIVE | 2014
Kyoto Univ.
Dept. of Surgery
Address: 54 Kawara-cho, Shogoin, Sakyo-ku
Kyoto, Kyoto 606-8507 Japan
Talamini, Mark, MD
ACTIVE | 2013
Univ. of CA SD
Dept. of Surgery
Address: 200 W. Arbor Drive, MC 8400
San Diego, CA 92103-8400
ACTIVE | 2014
Address: 2650 Ridge Ave., Walgreen 2507
Evanston, IL 60201
INACTIVE | 2011
Talley, Anitra BS
INACTIVE | 2012
Tamirisa, Nina, MD
RESIDENT | 2014
Univ. of Texas Medical Branch in Galveston
Tanaka, Masao, MD, PhD
ACTIVE | 2014
Kyushu Univ.
Surgery and Oncology
Address: 3-1-1 Maidashi
Tanaka, Shoichiro, MD
RESIDENT | 2013
Address: 1514 Jefferson Hwy.
Tapper, Elliot, MD
INACTIVE | 2009
Beth Israel Deaconess
Thayer, Sarah, MD, PhD
INACTIVE | 2012
Theruvath, Tom, MD, PhD
INACTIVE | 2011
Tholey, Renee, MD
RESIDENT | 2013
Address: 1015 Walnut St
TABLE OF CONTENTS
144
Thomas, Ryan
INACTIVE | 2012
Thomay, Alan
INACTIVE | 2012
Thompson, Lee W., MD
ACTIVE | 2014
IMC-Cancer Surgery of Mobile, P.C.
Surgical Oncology
Address: 3 Mobile Infirmary Circle,
Suite 305
Mobile, AL 36607
Thompson, Geoffrey, MD
INACTIVE | 2011
Mayo Clinic
Toledo, Sergio, MD
ACTIVE | 2013
Oregon Health & Science Univ.
Address: 3181 SW Sam Jackson Park Rd.
Mail Code: L223A
Portland, OR 97239
Toomey, Paul, MD
RESIDENT | 2014
Univ. South Florida
Surgery
Address: 4246 53rd Ave. S
St Petersburg, FL 33711
Toste, Paul, MD
RESIDENT | 2014
UCLA
Address: 10833 Le Conte, 72-229 CHS
Tran Cao, Hop, MD
RESIDENT | 2014
U.T., MD Anderson Cancer Center
Address: 1400 Pressler St., FCT 17.5000
Houston, TX 77030
Traverso, William, MD
ACTIVE | 2014
St. Luke’s Hospital System
Center for Pancreatic Disease
Address: 100 East Idaho St., Suite 301
Boise, ID 83616
Trevino, Jose G., MD
ACTIVE | 2014
Univ. of Florida-Gainesville
Address: 1600 SW Archer Rd., Rm. 6164
Truty, Mark, MD, MSc
INACTIVE | 2012
Tsai, Susan, MD, MHS
ACTIVE | 2014
Address: 9200 W Wiscinsin Ave.
Milwaukee, WI 53226
Tseng, DSJ, MD
RESIDENT | 2013
Address: Heidelberglaen 100
Utrecht, Netherlands
Tseng, Jennifer F., BS, AB, MD, MPH
ACTIVE | 2014
Surgery
Address: 330 Brookline Ave., Stoneman Bldg
9th Floor, Room 913
Boston, MA 02115
Tseng, Warren, MD
INACTIVE | 2009
Univ. of California, Davis
Tsiotos, Gregory, MD
INACTIVE | 2011
Metropolitan Hospital
Tzeng, Ching-Wei, MD
ACTIVE | 2014
Univ. of Kentucky
Address: 800 Rose St., UKMC C212
Lexington, KY 40536
TABLE OF CONTENTS
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Uemura, Kenichiro, MD
ACTIVE | 2014
Hiroshima Univ.
Dept. of Surgery
Address: 1-2-3 Kasumi, Minamiku,
Nishikasumi
Hiroshima, 7348551 Japan
Ujiki, Michael, MD
INACTIVE | 2009
Northshore Health System
Valeri, Sergio, MD
INACTIVE | 2011
Univ. Campus Bio-Medico di Roma
Valero, III, Vicente, MD
RESIDENT | 2014
Johns Hopkins Univ.
Address: 314 Murdock Rd.
Baltimore, MD 21212
van Sanvoort, Hjalmar, MD
INACTIVE | 2009
Vanderveen, Kimberly, MD
INACTIVE | 2009
Mayo Clinic
VanLier Ribbink, Jeff, MD
INACTIVE | 2009
Scottsdale Healthcare
Varadarajulu, Shyam S., MD
ACTIVE | 2014
Florida Hospital
Center for Interventional Endoscopy
Address: 601 East Rollins St.
Orlando, FL 34786
Vege, Santhi S., MD
Valsangkar, Nakul, MD
ACTIVE | 2014
Mayo Clinic Foundation
Gastroenterology and Hepatology
Address: 200 First St. SW,
Rochester, MN 55905
Van Brunschot, Sandra, MD
Velanovich, Vic, MD
INACTIVE | 2012
INACTIVE | 2012
Radboud Univ. Nijmegen Medical Center
Van Buren, II, George, MD
ACTIVE | 2014
The Elkins Pancreas Center, Michael E.
DeBakey
Address: 6620 Main St, Suite 1350
Houston, TX 77030
Van Cott, Christine E., MD
ACTIVE | 2014
Dept. of Surgery
Address: One Tampa General Circle, F145
Tampa, FL 33606
Venkat, Raghunandan, MD, MPH
INACTIVE | 2011
Johns Hopkins Medical Institution
Verzaro, Roberto M., MD
ACTIVE | 2013
St. Vincents Medical Center
Dept. of Surgery/Oncology
Address: 2800 Main St., 3rd Floor Cancer
Center
Bridgeport, CT 06606
INACTIVE | 2011
Vannini Hospital Rome
Van Eijch, Casper, MD, PhD
Vietsch, Eveline E., MD
INACTIVE | 2012
Erasmus
Vickers, Selwyn, MD
INACTIVE | 2010
Univ. ofMN
INACTIVE | 2012
Georgetown Univ.
TABLE OF CONTENTS
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Villatoro, Edwardo, MD
INACTIVE | 2009
Queen’s Medical Center
Visser, Brendan C., MD
ACTIVE | 2014
Stanford Univ.
General Surgery
Address: 300 Pasteur Drive, H3680
Stanford, CA 94305-5655
Vlada, Adrian MB BCh
RESIDENT | 2013
Univ. of Florida
Address: 1600 SW Archer Rd.,
Vollmer, Charles M., MD
ACTIVE | 2014
Univ. of Pennsylvania School of Medicine
Dept. of Surgery
Address: 3400 Spruce St., Silverstein
Pavilion
Volpe, Carmine, MD
INACTIVE | 2011
Univ. of Florida-Jacksonville
von Holzen, Urs, MD
INACTIVE | 2009
Vyas, Ojas, MD
RESIDENT | 2014
Tufts
Address: 18 Bay State Ave. #1
Somerville, MA 02144
Wada, Keita, MD
ACTIVE | 2013
Teikyo Univ.
Dept. of Surgery
Address: 2-11-1 Kaga, Itabashi-ku
Tokyo, 165-0025 Japan
Walsh, R. Matthew, MD
ACTIVE | 2014
The Cleveland Clinic Foundation
Address: 9500 Euclid Ave. Desk A100,
Cleveland, OH 44195
Warshaw, Andrew L., MD
ACTIVE | 2014
Administration
Address: 55 Fruit St., BUL 370
Boston, MA 02114
Watson, Chris, MD
INACTIVE | 2010
Weaver, Donald W., MD
ACTIVE | 2014
Wayne State Univ.
Dept. of Surgery
Address: 3990 John R.
Detroit, MI 48201
Weber, Cynthia, MD
RESIDENT | 2013
Dept of Surgery
Address: 2160 S First Ave.
Maywood, IL 60153
Weber, Sharon, MD
ACTIVE | 2014
UW School of Medicine and Public Health
Dept. of Surgery
Address: 738 Oneida Place
Madison, WI 53711
Weiss, Matthew, MD
INACTIVE | 2009
Wellner, Ulrich, MD
RESIDENT | 2014
UKSH Campus Lübeck
Lübeck, 23562 Germany
TABLE OF CONTENTS
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Wey, Jane, MD
ACTIVE | 2013
Cleveland Clinic
General Surgery
Address: 9500 Euclid Ave., #A100
Beachwood, OH 44122
Whang, Edward, MD
INACTIVE | 2011
White, Patrick, MD
INACTIVE | 2011
White, Rebekah, MD
ACTIVE | 2013
Duke Univ.
Surgery
Address: DUMC Box 3247
Durham, NC 27710
Wiatrek, Rebecca, MD
INACTIVE | 2011
City of Hope
Wild, Aaron
INACTIVE | 2012
Williams, Sandra, MD
INACTIVE | 2010
Williard, Deborah, BSCHE
INACTIVE | 2009
ICVAMC Univ. of Iowa
Wilson, Stuart, MD
ACTIVE | 2014
Dept. of Surgery
Address: 9200 W. Wisconsin Ave.
Milwaukee, WI 53226
Windsor, John, MD
INACTIVE | 2012
Univ. of Auckland
Winner, Megan
INACTIVE | 2012
Winslow, Emily R., MD
ACTIVE | 2014
UW School of Medicine and Public Health
Dept. of Surgery
Address: 600 Highland Ave. K4/749
Madison, WI 53792
Winter, Jordan M., MD
ACTIVE | 2014
Surgery
Address: 1025 Walnut St., St. 605 College
Witkowski, Elan, MD
INACTIVE | 2012
UMass Medical School
Wolf, Andrea, MD
ACTIVE | 2013
Spectrum Health
Address: 145 Michigan St., NE
Grand Rapids, MI 49503
Wolf, Ron
INACTIVE | 2012
Wolfgang, Christopher, MD, PhD
ACTIVE | 2014
Johns Hopkins Univ.
Surgical Oncology
Address: 600 N Wolfe Street, 685 Blalock
Baltimore, MD 21287
Wong, Joyce, MD
ACTIVE | 2014
Penn State Milton S. Hershey Medical Center
Surgery
Address: 500 Univ. Dr., MC 11070
Hershey, PA 17033
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Wood, Thomas, MD
Yeo, Charles, MD
Worhunsky, David, MD
Yeo, Theresa, PhD
RESIDENT | 2014
Address: 3000 Medical Park Dr. Suite 310
Tampa, FL 33613
RESIDENT | 2013
Address: 300 Pasteur Drive, #H3591
Stanford, CA 94305
Xourafas, Dimitrios
INACTIVE | 2012
Yamaguchi, Junpei
INACTIVE | 2012
Yamaguchi, Koji, MD
INACTIVE | 2011
Univ. of Occupational and Environmental
Health
Yamanaka, Junichi, MD
INACTIVE | 2010
Yamaue, Hiroki, MD, PhD
ACTIVE | 2014
Dept. of Surgery
Address: 1015 Walnut St., Suite 620 Curtis
ACTIVE | 2014
Dept. of Surgery
Address: 1015 Walnut St, Suite 605B
College Bldg
Yeo, Dannel, PhD
ACTIVE | 2013
The Univ. of Melbourne
Dept. of Surgery
Address: Austin Health, Studley Rd
Heidelberg, VIC 3084 Australia
Yoon, Yoo-Seok, MD, PhD
ACTIVE | 2014
Seoul National Univ. Bundang Hospital
Surgery
Address: 82 Gumi-ro 173 Beon-gil,
Bundang-gu
Seongnam-si, South Korea
ACTIVE | 2014
Address: 811-1 Kimiidera
Wakayama, Wakayama 641-8510 Japan
Yoshida, Koji, MD, PhD
Yang, Anthony, MD
Yuan, Zuobiao, MD, PhD
Yeboah, Edward Kwasi, BSc, MB,
ChB, MRCS(Ire)
Zani, Sabino
INACTIVE | 2011
Seoul National Univ. Bundang Hospital
INACTIVE | 2012
Royal Perth Hospital
ACTIVE | 2013
Kawasaki Medical School
Address: 577, Matsushima
Kurashiki, Okayama 7000192 Japan
INACTIVE | 2009
Univ. of Iowa
INACTIVE | 2012
TABLE OF CONTENTS
149
Zaydfudim, Victor, MD, MPH
RESIDENT | 2014
Univ. of Virginia Health Systems
Address: PO Box 800709
Zdon, Michael J., MD
INACTIVE | 2009
The Chicago Medical School
Zea, Nicolas
INACTIVE | 2012
Zeh, Herbert, MD
ACTIVE | 2014
UPMC
UPMC Cancer Pavilion
Address: 5150 Centre Ave., Suite 417
Zenilman, Michael, MD
ACTIVE | 2014
John Hopkins Univ.
Address: 12009 Titan Way
Potomac, MD 20854
Zerbi, Alessandro, MD
ACTIVE | 2014
Humanitas Mirasole SpA
Address: Via manzoni 56, Rozzano
Milano, 20089 Italy
Zheng, Lei, MD, PhD
ACTIVE | 2014
Oncology and Surgery
Address: 1650 Orleans St., CRB1, Rm. 488
Baltimore, MD 21042
Zhiyun, He, MD
INACTIVE | 2010
Univ. of Oklahoma HSC
Zhvitiashvili, Igor
ACTIVE | 2013
SSMA
General Surgery
Address: Frunze St. 40
Smolensk, 214006 Russia
Ziegler, Kathryn, MD
INACTIVE | 2011
Indiana Univ.
Zimmermann, Carolin
INACTIVE | 2010
Univ. Hospital Dresden
Zinner, Michael, MD
ACTIVE | 2014
Dept. of Surgery
Boston, MA 02115
EMAIL: [email protected]
Zuberi, Kashif, MD
INACTIVE | 2009
Marshfield Clinic
Zureikat, Amer Harran, MD
ACTIVE | 2014
Address: 5150 Centre Ave., Suite 421
Zyromski, Nicholas, MD
ACTIVE | 2014
Dept. of Surgery
Address: 545 Barnhill Dr., EH, 5TH FLR
TABLE OF CONTENTS
150
PAST & FUTURE MEETINGS
SAVE THE DATE
49th Annual Pancreas Club Meeting
May 15-16, 2015
Washington DC
DATE & LOCATION
HOST
2013
WDW Swan & Dolphin Hotel, Orlando, FL
Pablo Arnoletti
2012
Hyatt Mission Bay, San Diego, CA
Mark Talamini
2011
Chicago, IL
2010
New Orleans, LA
2009
Chicago, IL
2008
San Diego, CA
2007
Children’s Medical Center, Washington, DC
2006
Los Angeles, CA
2005
Chicago, IL
2004
New Orleans, LA
Alton Ochsner
2003
Orlando, FL
Michael Murr
2002
San Francisco, CA
2001
Hilton Atlanta, Atlanta, GA
Aaron Fink
2000
University of California, SD, San Diego, CA
A.R. Moosa
1999
Peabody, Orlando, FL
1998
LSU, Tulane, New Orleans, LA
1997
University Health Sciences, Bethesda, MD
1996
Laurel Heights, UCSF, San Francisco, CA
1995
University of California, SD, San Diego, CA
1994
Tulane University, New Orleans, LA
1993
Massachusettes General Hospital, Boston, MA
Past & Future Meetings
Gerard Aranha, Mark Talamonti, David Bentrem
Gerard Aranha, Mark Talamonti, David Bentrem
Mark Talamini, Mike Bouvet
Dana Anderson
Howard A. Reber
Gerard V. Aranha, Richard Bell
Kimberly Kirkwood
Michael M. Murr, James G. Norman
J. Patrick O’Leary, Elmo Cerise
John W. Harmon
Sean Mulvihill
A.R. Moosa
Elmo Cerise, J. Patrick O’Leary
Andrew Warshaw
TABLE OF CONTENTS
151
PAST & FUTURE MEETINGS
1992
University of California, SF, San Francisco, CA
1991
LSU, Tulane, New Orleans, LA
1990
University of Texas, San Antonio, TX
1989
Washington Hilton
1988
Tulane University, New Orleans, LA
1987
University of Illinois, Chicago, IL
Phillip Donahue
1986
Ft. Miley VA, San Francisco, CA
Carlos Pellegrini
1985
Mt. Sinai Hospital, New York, NY
David Dreiling
1984
LSU Medical Center, New Orleans, LA
Francis Nance
1983
Washington Hilton, Washington, DC
1982
University of Chicago, Chicago, IL
1981
Alumni Hall, NYU, New York, NY
John Ranson
1980
Salt Lake City, UT
Frank Moody
1979
LSU Medical Center, New Orleans, LA
Isadore Cohn
1978
Jockey Club, Las Vegas, NV
Charles Frey
1977
Toronto, Canada
Roger Keith
1976
Doral on the Ocean, Miami, FL
1975
Univiversity of Texas, San Antonio, TX
1974
No Meeting
1973
1972
1971
Sheraton Hotel, Philadelphia, PA
John Howard
1970
University of Chicago, Chicago, IL
Edward Paloyan
1969
David Dreiling
1968
Leon Goldman
1967
Philadelphia, PA
1966
Northwestern, Evanston, IL
Carlos Pellegrini
Elmo Cerise, J. Patrick O’Leary
Bradley Aust
Gregory Bulkley, Frances Milligan, John Cameron
Elmo Cerise
Francis Milligan
A.R. Moosa
Robert Zeppa
Bradley Aust
David Dreiling
Englebert Dunphy
John Howard
Marion Anderson
TABLE OF CONTENTS
152
Past & Future Meetings
SAVE THE DATE
49 ANNUAL
MEETING
th
OF THE PANCREAS CLUB
May 15-16, 2015 in Washington, DC
www.pancreasclub.com

2014 Meeting Program

Transcription

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