Cancer research February / March 2008

Transcription

Buocher Höhe
(Stuttgart - Remshalden)
Medizin
ist
KEINE
Wissenschaft
Moderne
Krebsforschung
Brauchen wir mehr
Forschung?
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Kassel Km, Dodmane PR, Schulte NA, Toews ML
Lysophosphatidic acid induces rapid and sustained decreases in epidermal growth factor
binding via different signaling pathways in BEAS-2B airway epithelial cells.
J Pharmacol Exp Ther. 2008 Feb 28; [Epub ahead of print]
Nishioka C, Ikezoe T, Yang J, Miwa A, Tasaka T, Kuwayama Y, Togitani K, Koeffler HP,
Yokoyama A
Ki11502, a novel multi-targeted receptor tyrosine kinase inhibitor, induces growth arrest and
apoptosis of human leukemia cells in vitro and in vivo.
Blood. 2008 Feb 28; [Epub ahead of print]
Mokhtari D, Myers JW, Welsh N
The MAPK kinase kinase-1 is essential for stress-induced pancreatic islet cell death.
Endocrinology. 2008 Feb 28; [Epub ahead of print]
Han S, Witt RM, Santos TM, Polizzano C, Sabatini BL, Ramesh V
Pam (Protein associated with Myc) functions as an E3 Ubiquitin ligase and regulates
TSC/mTOR signaling.
Cell Signal. 2008 Feb 1; [Epub ahead of print]
E der K, Guan H, Sung HY, Francis SE, Crossman DC, Kiss-Toth E
LDL uptake by monocytes in response to inflammation is MAPK dependent but independent
of tribbles protein expression.
Immunol Lett. 2008 Jan 24; [Epub ahead of print]
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Li M, Zhang Y, Feurino LW, Wang H, Fisher WE, Brunicardi FC, Chen C, Yao Q
Interleukin-8 increases vascular endothelial growth factor and neuropilin expression and
stimulates ERK activation in human pancreatic cancer.
Cancer Sci. 2008 Feb 27; [Epub ahead of print]
Penolazzi L, Pocaterra B, Tavanti E, Lambertini E, Vesce F, Gambari R, Piva R
Human osteoclasts differentiated from umbilical cord blood precursors are less prone to
apoptotic stimuli than osteoclasts from peripheral blood.
Apoptosis. 2008 Feb 29; [Epub ahead of print]
Lee KB, Lee JS, Park JW, Huh TL, Lee YM
Low energy proton beam induces tumor cell apoptosis through reactive oxygen species and
activation of caspases.
Exp Mol Med. 2008 Feb 29;40(1):118-29.
Park MH, Lee DH
Endothelin 1 protects HN33 cells from serum deprivation-induced neuronal apoptosis
through Ca(2+)-PKCalpha-ERK pathway.
Exp Mol Med. 2008 Feb 29;40(1):92-7.
Goeldner C, Reiss D, Wichmann J, Meziane H, Kieffer BL, Ouagazzal AM
Nociceptin receptor impairs recognition memory via interaction with NMDA receptordependent mitogen-activated protein kinase/extracellular signal-regulated kinase signaling
in the hippocampus.
J Neurosci. 2008 Feb 27;28(9):2190-8.
W ang C, Li N, Liu X, Zheng Y, Cao X
A novel endogenous human CaMKII inhibitory protein suppresses tumor growth by
inducing cell cycle arrest via p27 stabilization.
J Biol Chem. 2008 Feb 27; [Epub ahead of print]
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Miyazawa M, Ito Y, Kosaka N, Nukada Y, Sakaguchi H, Suzuki H, Nishiyama N
Role of MAPK signaling pathway in the activation of dendritic type cell line, THP-1, induced
by DNCB and NiSO(4).
J Toxicol Sci. 2008 Feb;33(1):51-9.
J ia XW, Liu BC, Shi XL, Gao A, Ye M, Zhang FM, Liu HF, Jiao S
[ERK, JNK/AP-1 pathway was involved in silica-induced cell cycle changes.]
Zhonghua Lao Dong Wei Sheng Zhi Ye Bing Za Zhi. 2008 Jan;26(1):3-6. Chinese.
Song JH, Kim JH, Park S, Kang W, Kim HW, Kim HE, Jang JH
Signaling responses of osteoblast cells to hydroxyapatite: the activation of ERK and SOX9.
J Bone Miner Metab. 2008;26(2):138-42. Epub 2008 Feb 27.
Lafuente N, Matesanz N, Azcutia V, Romacho T, Nevado J, Rodríguez-Mañas L, Moncada
S, Peiró C, Sánchez-Ferrer CF
The deleterious effect of high concentrations of D-glucose requires pro-inflammatory
preconditioning.
J Hypertens. 2008 Mar;26(3):478-485.
Drake CJ, Fleming PA, Argraves WS
The genetics of vasculogenesis.
Novartis Found Symp. 2007;283:61-71; discussion 71-6, 238-41.
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Deming D, Geiger P, Chen H, Vaccaro A, Kunnimalaiyaan M, HolenK
ZM336372, A Raf-1 Activator, Causes Suppression of Proliferation in a Human
Hepatocellular Carcinoma Cell Line.
J Gastrointest Surg. 2008 Feb 26; [Epub ahead of print]
Lee JY, Rhee MH, Cho JY
Novel modulatory effects of SDZ 62-434 on inflammatory events in activated macrophagelike and monocytic cells.
Naunyn Schmiedebergs Arch Pharmacol. 2008 Feb 26; [Epub ahead of print]
Boutilier J, Ceni C, Pagdala PC, Forgie A, Neet KE, Barker PA
Proneurotrophins require endocytosis and intracellular proteolysis to induce TRKA
activation.
J Biol Chem. 2008 Feb 25; [Epub ahead of print]
S havit E, Beilin O, Korczyn AD, Sylantiev C, Aronovich R, Drory VE, Gurwitz D, Horresh
I, Bar-Shavit R, Peles E, ChapmanJ
Thrombin receptor PAR-1 on myelin at the node of Ranvier: a new anatomy and physiology
of conduction block.
Brain. 2008 Feb 25; [Epub ahead of print]
K rajcik R, Jung A, Hirsch A, Neuhuber W, Zolk O
Functionalization of carbon nanotubes enables non-covalent binding and intracellular
delivery of small interfering RNA for efficient knock-down of genes.
Biochem Biophys Res Commun. 2008 Feb 22; [Epub ahead of print]
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Wang C, Wu LL, Liu J, Zhang ZG, Fan D, Li L
Crosstalk between angiotensin II and platelet derived growth factor-BB mediated signal
pathways in cardiomyocytes.
Chin Med J (Engl). 2008 Feb 5;121(3):236-40.
W u H, Li H, Guo J
Spry2-mediated inhibition of the Ras/ERK pathway through interaction with Src kinase
following cerebral ischemia.
Brain Inj. 2008 Mar;22(3):275-81.
L ang SA, Brecht I, Moser C, Obed A, Batt D, Schlitt HJ, Geissler EK, Stoeltzing O
Dual inhibition of Raf and VEGFR2 reduces growth and vascularization of hepatocellular
carcinoma in an experimental model.
Langenbecks Arch Surg. 2008 Feb 23; [Epub ahead of print]
S imão S, Fraga S, Jose PA, Soares-da-Silva P
Oxidative stress and alpha(1)-adrenoceptor-mediated stimulation of the Cl(-)/HCO(3)(-)
exchanger in immortalized SHR proximal tubular epithelial cells.
Br J Pharmacol. 2008 Feb 25; [Epub ahead of print]
M eini A, Sticozzi C, Massai L, Palmi M
A nitric oxide/Ca(2+)/calmodulin/ERK1/2 mitogen-activated protein kinase pathway is
involved in the mitogenic effect of IL-1beta in human astrocytoma cells.
Br J Pharmacol. 2008 Feb 25; [Epub ahead of print]
• du Toit EF, Genis A, Opie LH, Pollesello P, Lochner A
• A role for the RISK pathway and K(ATP) channels in pre- and post-conditioning
induced by levosimendan in the isolated guinea pig heart.
• Br J Pharmacol. 2008 Feb 25; [Epub ahead of print]
• Means CK, Miyamoto S, Chun J, Brown JH
• S1P1 receptor localization confers selectivity for G{sub}i mediated cAMP and
contractile responses.
• J Biol Chem. 2008 Feb 24; [Epub ahead of print]
• Kim DI, Lee SJ, Lee SB, Park K, Kim WJ, Moon SK
• Requirement for Ras/Raf/ERK pathway in naringin-induced G1-cell cycle arrest via
p21WAF1 expression.
• Carcinogenesis. 2008 Feb 22; [Epub ahead of print]
• Schmid T, Jansen AP, Baker AR, Hegamyer G, Hagan JP, Colburn NH
• Translation Inhibitor Pdcd4 Is Targeted for Degradation during Tumor Promotion.
• Cancer Res. 2008 Feb 22; [Epub ahead of print]
• Emanuelli B, Eberlé D, Suzuki R, Kahn CR
• Overexpression of the dual-specificity phosphatase MKP-4/DUSP-9 protects
against stress-induced insulin resistance.
• Proc Natl Acad Sci U S A. 2008 Feb 22; [Epub ahead of print]
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Nielsen J, Hoffert JD, Knepper MA, Agre P, Nielsen S, Fenton RA
Proteomic analysis of lithium-induced nephrogenic diabetes insipidus: Mechanisms for
aquaporin 2 down-regulation and cellular proliferation.
Proc Natl Acad Sci U S A. 2008 Feb 22; [Epub ahead of print]
P arsa KV, Butchar JP, Rajaram MV, Cremer TJ, Tridandapani S
The tyrosine kinase Syk promotes phagocytosis of Francisella through the activation of Erk.
Mol Immunol. 2008 Feb 22; [Epub ahead of print]
Y u Y, Wang Y, Feng M
Human leukocyte antigen-G1 inhibits natural killer cytotoxicity through blocking the
activating signal transduction pathway and formation of activating immunologic synapse.
Hum Immunol. 2008 Jan;69(1):16-23. Epub 2007 Dec 26.
G lenn G, van der Geer P
Toll-like receptors stimulate regulated intramembrane proteolysis of the CSF-1 receptor
through Erk activation.
FEBS Lett. 2008 Feb 20; [Epub ahead of print]
Rath O, Park S, Tang HH, Banfield MJ, Brady RL, Lee YC, Dignam JD, Sedivy JM, Kolch
W, Yeung KC
The RKIP (Raf-1 Kinase Inhibitor Protein) conserved pocket binds to the phosphorylated Nregion of Raf-1 and inhibits the Raf-1-mediated activated phosphorylation of MEK.
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Nielsen J, Hoffert JD, Knepper MA, Agre P, Nielsen S, Fenton RA
Proteomic analysis of lithium-induced nephrogenic diabetes insipidus: Mechanisms for
aquaporin 2 down-regulation and cellular proliferation.
Proc Natl Acad Sci U S A. 2008 Feb 22; [Epub ahead of print]
P arsa KV, Butchar JP, Rajaram MV, Cremer TJ, Tridandapani S
The tyrosine kinase Syk promotes phagocytosis of Francisella through the activation of Erk.
Mol Immunol. 2008 Feb 22; [Epub ahead of print]
Y u Y, Wang Y, Feng M
Human leukocyte antigen-G1 inhibits natural killer cytotoxicity through blocking the
activating signal transduction pathway and formation of activating immunologic synapse.
Hum Immunol. 2008 Jan;69(1):16-23. Epub 2007 Dec 26.
G lenn G, van der Geer P
Toll-like receptors stimulate regulated intramembrane proteolysis of the CSF-1 receptor
through Erk activation.
FEBS Lett. 2008 Feb 20; [Epub ahead of print]
• Rath O, Park S, Tang HH, Banfield MJ, Brady RL, Lee YC, Dignam JD, Sedivy
JM, Kolch W, Yeung KC
• The RKIP (Raf-1 Kinase Inhibitor Protein) conserved pocket binds to the
phosphorylated N-region of Raf-1 and inhibits the Raf-1-mediated activated
phosphorylation of MEK.
• Cell Signal. 2008 Jan 24; [Epub ahead of print]
• PMID: 18294816 [PubMed - as supplied by publisher]
• T akamura H, Ichisaka S, Watanabe K, Toigawa M, Hata Y
• Effects of anesthesia on immunohistochemical detection of phosphorylated
extracellular signal-regulated kinase in cerebral cortex.
• J Neurosci Methods. 2008 Jan 17; [Epub ahead of print]
• PMID: 18294698 [PubMed - as supplied by publisher]
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• F avreau C, Delbarre E, Courvalin JC, Buendia B
• Differentiation of C2C12 myoblasts expressing lamin A mutated at a site
responsible for Emery-Dreifuss muscular dystrophy is improved by inhibition of the
MEK-ERK pathway and stimulation of the PI3-kinase pathway.
• Exp Cell Res. 2008 Feb 6; [Epub ahead of print]
• Nishioka C, Ikezoe T, Yang J, Miwa A, Tasaka T, Kuwayama Y, Togitani K, Koeffle
Ki11502, a novel multi-targeted receptor tyrosine kinase inhibitor, induces growth
arrest and apoptosis of human leukemia cells in vitro and in vivo.
• Li M, Zhang Y, Feurino LW, Wang H, Fisher WE, Brunicardi FC, Chen C, Yao Q.
Interleukin-8 increases vascular endothelial growth factor and neuropilin expression
and stimulates ERK activation in human pancreatic cancer.
• Wang C, Li N, Liu X, Zheng Y, Cao X.
A novel endogenous human CaMKII inhibitory protein suppresses tumor growth by
inducing cell cycle srrest via p27 stabilization.
• Deming D, Geiger P, Chen H, Vaccaro A, Kunnimalaiyaan M, Holen K.
ZM336372, A Raf-1 Activator, Causes Suppression of Proliferation in a Human
Hepatocellular Carcinoma Cell Line.
• Lang SA, Brecht I, Moser C, Obed A, Batt D, Schlitt HJ, Geissler EK, Stoeltzing O.
Dual inhibition of Raf and VEGFR2 reduces growth and vascularization of
hepatocellular carcinoma in an experimental model.
• Verstehen Sie das?
• Ki11502 is a novel multi-targeted receptor tyrosine kinase (RTK) inhibitor with
selectivity against platelet derived growth factor receptor alpha/beta (PDGFRalpha/
beta). Ki11502 (0.1-1 nM, 2 days) profoundly caused growth arrest, G0/G1 cell
cycle arrest, and apoptosis associated with downregulation of Bcl-2 family proteins
in the eosinophilic leukemia EOL-1 cells having the activated FIP1-like
1/PDGFRalpha fusion gene. Ki11502 decreased levels of p-PDGFRalpha and its
downstream signals including p-Akt, p-ERK, and p-STAT5 in EOL-1 cells. Of note,
Ki11502 was also active against imatinib-resistant PDGFRalphaT674I mutant. In
addition, Ki11502 inhibited proliferation of biphenotipic leukemia MV4-11 and
acute myelogeneous leukemia MOLM13 and freshly isolated leukemia cells having
activating mutations in FMS-like tyrosine kinase 3 (FLT3). This occurred in
paralleled with the drug inhibiting FLT3 and its downstream signal pathways, as
measured by fluorescence-activated cell sorting using the phospho-specific
antibodies. Also, Ki11502 totally inhibited proliferation of EOL-1 cells growing as
tumor xenografts in SCID mice without any noticeable adverse effects. Taken
together, Ki11502 has profound antiproliferative effects on select subsets of
leukemia including those possessing imatinib-resistant mutation.
• Oder das?
• Interleukin-8 (IL-8) is associated with tumorigenesis by promoting angiogenesis
and metastasis. Although up-regulation of IL-8 is indicated in many cancers, its
function in pancreatic cancer has not been well characterized. In this study we
examined the expression of IL-8 on pancreatic cancer cells and clinical tissue
specimens, and investigated the effect of exogenous IL-8 on gene expression, and
signaling in human pancreatic cancer cells. We found that pancreatic cancer cells
expressed higher amount of IL-8 mRNA than normal human pancreatic ductal
epithelium cells. IL-8 mRNA was also substantially overexpressed in 11 of 14
(79%) clinical pancreatic-adenocarcinoma samples compared with that in their
surrounding normal tissues. Exogenous IL-8 up-regulated the expression of vascular
endothelial growth factor(165), and neuropilin (NRP)-2 in BxPC-3 cells, one of
human pancreatic cancer cell lines. IL-8 expression was inducible by hypoxia
mimicking reagent cobalt chloride. In addition, IL-8 activated extracellular signalregulated kinase (ERK)1/2 signaling pathway in BxPC-3 cells. Our studies suggest
that IL-8 might be a malignant factor in human pancreatic cancer by induction of
vascular endothelial growth factor and NRP-2 expression and ERK activation.
Targeting IL-8 along with other antiangiogenesis therapy could be an effective
• Oder das?
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Calcium/calmodulin-dependent protein kinase II (CaMKII) regulates numerous physiological functions.
Inhibition of CaMKII activity, mostly by synthetic reagents, has been proved to suppress cell growth in
many cases. So far there's no report about the physiological functions and underlying mechanisms of
endogenous CaMKII inhibitory proteins in cell cycle progression. Here we report the characterization of a
novel human endogenous CaMKII inhibitor, hCaMKIINalpha (calcium/calmodulin-dependent protein
kinase II inhibitory protein alpha), which directly interacts with activated CaMKII and effectively inhibits
CaMKII activity. hCaMKIINalpha expression is negatively correlated with the severity of human colon
adenocarcinoma. Overexpression of hCaMKIINalpha inhibits colon adenocarcinoma growth in vitro and
in vivo by arresting cell cycle at the S phase through its conserved inhibitory region (27CIR), while
silencing of hCaMKIINalpha expression accelerates the tumor growth and cell cycle progression. We
found that the effect of hCaMKIINalpha on cell cycle is correlated with up-regulation of p27 expression,
which may be due to the inhibition of proteasome degradation but not transcriptional regulation of p27.
Moreover, hCaMKIINalpha de-activated MEK/ERK, which is prerequisite to the inhibition of T187
phosphorylation and subsequent proteasomal degradation of p27, causing the inhibition of S-phase
progression of cell cycle. The findings underscore a link between hCaMKIINalpha-mediated inhibition of
CaMKII activity and p27-dependent pathways in controlling tumor cell growth and cell cycle, and
implied a potential application of hCaMKIINalpha in the therapeutics of colon cancers.
• Oder das?
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Hepatocellular carcinoma has been described to exhibit characteristics similar to that of neuroendocrine
tumors (NETs). This includes similar anti-neoplastic responses to extracellular signal-regulated kinase
(ERK) activation. NET cells and HepG2 cells have both shown growth inhibition with ERK activation.
ZM336372, a Raf-1 activating agent, has been shown to cause growth inhibition and suppression of
hormone secretion in a neuroendocrine cell line. Here we examine treatment of the HepG2 cell line with
ZM336732 to determine if a similar anti-proliferative response will be obtained. HepG2 cells were treated
with ZM336372 or solvent (dimethyl sulfoxide). The resulting effect on the proliferation was measured
using the 3,4-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. Western blot
analysis was performed to examine the activation of the Raf-1/mitogen-activated protein kinase
kinase/ERK pathway, chromogranin A production, and p21(CIP1) level. Growth inhibition was observed
with ZM336372 in a dose-dependent fashion. Minimal baseline phosphorylation of ERK 1/2 was
observed; however, activation was observed after treatment with ZM336372. Chromogranin A secretion
was suppressed due to treatment with ZM336372. A dose-dependent up-regulation of p21(CIP1) was
observed in response to ZM336372 treatment. ZM336372 causes growth inhibition, suppression of
hormone secretion, and up-regulation of cell cycle inhibitors in a human hepatocellular carcinoma cell
line, similar to that previously seen in NETs.
• Oder das?
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BACKGROUND AND AIMS: Activation of the mitogen-activated protein kinaseextracellular-signal-regulated kinase (ERK) pathways plays an important role in the
progression of hepatocellular carcinoma (HCC). Importantly, Raf kinases are principal
effectors within this oncogenic signaling cascade. We hypothesized that concomitant
inhibition of Raf and vascular endothelial growth factor receptor 2 (VEGFR2) will affect
tumor growth and angiogenesis of HCC. MATERIALS AND METHODS: Human HCC cell
lines, endothelial cells (EC), and vascular smooth muscle cells (VSMC) were used. For
blocking Raf kinase and VEGFR2, the small molecule inhibitor NVP-AAL881 (Novartis,
USA) was used. Activation of signaling intermediates was assessed by Western blotting, and
changes in cell motility were evaluated in migration assays. Effects of NVP-AAL881 on
HCC growth were determined in a subcutaneous tumor model. RESULTS: NVP-AAL881
disrupted activation of ERK and STAT3 in HCC cells and reduced cancer cell motility. In
addition, the migration of ECs and VSMC was also significantly impaired. In ECs, HCCconditioned media-induced activation of STAT3 was diminished by NVP-AAL881 treatment.
In vivo, NVP-AAL881 significantly reduced tumor growth, CD31-vessel area, and numbers
of BrdU-positive proliferating tumor cells. CONCLUSIONS: Combined inhibition of Raf and
VEGFR2 disrupts oncogenic signaling and efficiently reduces tumor growth and
vascularization of HCC. Hence, this strategy could prove valuable for therapy of HCC.
58 von 79 Onkologen sagten,
dass sie niemals selber eine
Chemotherapie machen
würden!
Wissenschaftler des McGill Krebs Centers in den USA sandten einen
Fragebogen an 118 Onkologen und fragten diese, welche der 6 üblichen
Therapien sie bei sich selbst anwenden würden. 79 Ärzte reagierten und
hiervon sagten 64, dass sie niemals eine Therapie mit Cisplatin machen
würden – eine durchaus übliche Chemotherapie, deren Umsatz immerhin
über 100 Millionen Euro im Jahr beträgt. Viel schlimmer war jedoch, dass
58 der 79 Ärzte antworteten, dass sie niemals eine Chemotherapie
machen würden, weil sie erstens ineffektiv sei und zweitens viel zu
giftig.
Meine
onkologische Reise
Mutationstheorie
DNS
Mutationstheorie
Tumor
1. Krebszelle
1. Metastase
Mutationstheorie
Entartung oder Anpassung?
Nicht-Kleinzelliges Bronchialkarzinom
Mutationstheorie
WANN sieht ein Pathologe einen Tumor?
… oder nach 30 Zellteilungen
wenn der Tumor
Nach einer Zellteilung …
1.073.741.824 Zellen hat?
Mutationstheorie
Mutationstheorie
Mutationstheorie
Wie bösartig sind Tumore?
Mutationstheorie
Mutationstheorie
Mutationstheorie
15.02.1985
15.02.1994
17.07.1989
17.05.1998
02.01.2010
Mutationstheorie
Herzkrebs?
Mutationstheorie
Metastasen im Blut?
Stockholm 2007:
(Lancet 2007; 369: 1724-1730)
In 5 Jahren hatten 12.013 von
354.094 Blutspendern Krebs.
Ergebnis: In dieser Gruppe (auch
bei Leukämien und Lymphomen)
gab es KEINEN EINZIGEN
ZUSÄTZLICHEN KREBSFALL.
Mutationstheorie
1cm =
3
30 Verdoppelungen =
1.073.741.824 Zellen
Grundsatz:
Eine einzige
verstreute
Krebszelle erzeugt
einen neuen Tumor!
Mutationstheorie
Mutieren Krebszellen
auf ihrem Weg durch
das Blut?
Mutationstheorie
Teratome und Chimären (Karl Illmensee und Leroy Stevens 1974)
Mutationstheorie
DNA
DNA
McKinney (1969), Illmensee, Stevens, Mintz (1975), Seeger ...
Kein
Krebs
Krebs
Der große Irrtum =
der 8. Stein ist schuldig
Körper. / psych. / seel. / karm. Stress
Hormonverschiebungen (I-A-C)
Zellmembranänderungen
Störungen der Zellatmung
Enzymatische Störungen
Mileuanpassung (Entdifferenzierung)
Genveränderungen
1. Krebszelle & Tumor
Der große Irrtum
So viele Professoren auf der ganzen Welt
können sich doch nicht irren –
ODER?
Der große Irrtum
Bis vor wenigen Jahren haben alle
Professoren auf der Welt
unterrichtet:
Das menschliche Genom
hat 100.000 Gene!
Mitochondrientheorie
Krebsentstehung:
• Störung des Elektronenflusses
• Fehlmodulation der ATP
• Vermehrte Radikalenbildung
• Ausschaltung der Hämoxygenase
• NO Störungen
• ATMUNGSSTÖRUNG
Mitochondrientheorie
• Zellmembranspannung
Normal: 70mV – 90mV
DNS
Krebs: unter 20 mV
Ohne gesunde Mitochondrien ist kein Aufrechthalten der Zellspannung möglich!
Psyche & Krebs
Psychischer Konflikt
Psychischer Konflikt
Gehirn
Organ
(Sokrates, Plato,
Aristoteles über Freud,
Jung bis zu LeShan)
Organ
(Neue Medizin, MetaMedizin, Synergetik…)
Dr. Frydas
Adrenalintheorie
• Stress = Adrenalinausschüttung
• Zu viel Stress = zu wenig Adrenalin durch
Erschöpfung des chromaffinen Systems
• Krebskranke haben fast immer extrem niedrige
Adrenalinspiegel
Insulin
Adrenalin
Theorie der 2. Leber
Dr. Cousmine
Normal
Krebsvorstadium
Krebs mit Tumor
• Welche Gruppe hat das beste Immunsystem?
• Welche Gruppe kann man am leichtesten mit Gift töten?
Schlussfolgerungen:
Keine Operation des Tumors, sonst zusätzliche
Belastung der Entgiftungsorgane wie Leber und Lunge.
•
Keine Immunsteigerung mit Mistel, Thymus ...
(Nentsis/Russland und Dr. R.T.Prehn - Thymusforschung)
•
Nicht noch mehr Gift wie Chemotherapie ...
•
Oberstes Gebot: Entgiftung
Ist Krebs ein Problem des Immunsystems?
• Unser Immunsystem unterstützt Tumore durch Angiogenese
• Organ transplantierte Patienten haben nicht mehr Krebs
• Nentzis in Russland haben weniger Krebs
• Aids-Patienten haben nicht mehr Krebs (Ausnahme: Kaposi-Sarkom)
• Krebspatienten
mit Autounfälle sind kürzer in der Klinik
Simoncini Methode
Dr. Tullio Simoncini
Rom
Darm - Vorher
Tumore verhindern die Ausbreitung
gefährlicher Pilze im Körper.
Darm - Nachher
Weitere Theorien
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•
•
•
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Säure-Basen Theorie - Erich Rouka
Trichomonadentheorie - Lebedewa – Moskau
Parasitentheorie Clark / Lebedewa …
Wilhelm Reich - bioenergetische Abwehr
Rudolf Steiner - Ätherleib contra phys. Leib
TCM
Ayurveda ... und…
Theorie
&
Praxis
Erfolgreiche Therapien
Tumor zerstörende Therapien (konventionell):
• Operation
• Chemotherapien
• Bestrahlung
• Antikörper
• Angiogeneseblocker
• Gentherapien wie z. B. Gendicine
Erfolgreiche Therapien 1
Tumor zerstörende Therapien:
• Galvano
• Vitamin C i.V.
• Ukrain (Schöllkraut / mod. Thiotepa)
• Regionale & Systemische Hyperthermie
• Tierische Giftstoffe z. B. von Schlangen, Spinnen…
• Dr. Simoncini – Natriumbicarbonat Umspülung
Tumor zerstörende Therapien:
• Tumosteron (Hydroxycholesterin)
• Laetril – Vit. B17 – Amygdalin
• IPT (Insulin Potential Therapy)
• Carnivora
• Buserelin (Prof. Hackethal)
• Photodynamische Therapie
Immunsystem modulierende Therapien:
• VG 1000 - Prof. Govallo Moskau
• IAT – Lunge, Mesotheliom
• Transferfaktoren – Dr. G. Pizza Bologna
• Tallberg
• Kremer Therapie
• Nutri-Therapie – Gonzales (Pankreaskrebs)
• Fötale Therapien (Grundsatzfrage!)
• Tumorimpfungen (ASI, Dendrit. Zellen, Dr. Klehr)
• Antineoplastone (Phenylessigsäure, Dr. Burzynski/Texas)
• PapImi / Athen, Prof. Pappas
• Aqua Tilis / Eindhoven, Dr. Essaidi
• COD
• Moderate Hyperthermie
• Aktive Fiebertherapie (Coley / Newcastle Viren) &
• Homöopathie
• Tien Hsien Liquid (TianXian)
Ernährungstherapien:
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Budwig, Gerson
Makrobiotik, Breuß, Rohkost
Dries, Moermann, Brucker, Bircher-Benner
Ayurveda, 5 Elemente,
Metabolic Typing
Ursachen suchende Therapien:
• Synergetik (Bernd Joschko)
• Persönlichkeitsinformatik (Wolfgang Rother)
• Meta-Medizin (Dr. Bader)
• Psychoanalyse (Freud / Jung / Adler / Berne …)
Kausanetik (Lothar Hirneise)
Evolution = Überleben
Symptomeigendynamik
Das Hauptproblem der Schulmedizin:
Symptome werden nur am Ende der
Zeitlinie gesehen!
Hypertonie (Bluthochdruck)
• Bessere Organdurchblutung
• Bessere Kapillardurchblutung
• Höhere Entgiftungsleistung
• Bessere Muskeltätigkeit
• Verhinderung von Arterienverkalkung
durch Proteinabbau in den
Gefäßwänden uvm.
Herzinfarkt
Schlaganfall
Tumorerkrankungen
* Verbrennt vermehrt Zucker
* Blockiert und verbrennt Giftstoffe
• Blockiert und verkapselt Pilze
• Zeigt auf der psychischen Ebene
an, dass es Zeit für Änderungen
ist…
Kachexie
Tod
Ernährung - Entgiftung - Energie
Gerson Therapie
Dr. Max Gerson
13 frisch gepresste Säfte
6 Kaffeeeinläufe
Kalium / Fette
Ziel:
Ausgleich Natrium/Kalium
Öl-Eiweiß Kost
Öl-Eiweiß-Kost
• Transfettsäuren im Tumor
• Cytochromoxydase raus =
Elektronenübertragung blockiert
und dadurch entsteht eine
Dr. Johanna Budwig
& Lothar Hirneise
Störung der Zellatmung
Öl-Eiweiß Kost
7 Uhr
8 Uhr
10-11 Uhr
12.00 Uhr
12.15 Uhr
15.00 Uhr
15.30 Uhr
18.00 Uhr
20.30 Uhr
1 Glas Sauerkrautsaft.
Linomel / Leinöl / Quark Müsli
Frisch gepresste Säfte
(1 Esslöffel Linomel, 1 Glas Sekt)
Vorspeise + Hauptgericht + Nachtisch
Linomel, Sekt oder /und Saft
Linomel, 1 - 3 Gläser Muttersaft
Suppe (Buchweizen…)
(Evtl. 1 Glas Rotwein)
Entgiftung - Raus
• Darmsanierung (Colon-Hydro, Einläufe –
Kaffee/Natron)
•
•
•
•
Säure/Basen Ausgleich (Natron-Bäder…)
Zähne (Wurzelkanäle, Amalgam, Metalle ...)
Hitze (von Kneipp bis Ardenne)
Atemtherapien
Entgiftung – nichts mehr rein
•
•
•
•
•
Ernährung
Kosmetika (& Shampoo, Deos ...)
Immer vermeiden: Aluminium
Zahnpasta (Fluoride)
EMF (Netzfreischalter, keine Mikrowellen, keine
Matratzen mit Metallfedern…)
• Wasser (Filter, Destillation, Verwirbler…)
Energie
Liebe
Glaube
Sexualität
Egobefriedigung
(z. B. mit Geld)
Essen
+
Angst
Energie
Liebe
Angst
Glauben
Glaube
Appetit
Sexualität
Ego /
Geldgier
Energie
Kein Platz in der
„modernen“ Medizin!
Der Arzt weiß was Sie haben und
warum Sie krank sind!
Fragen sind nicht notwendig!
Vorteil:
Der Arzt kann „Ihren Tumor“ behandeln
und muss sich nicht mit Ihnen abgeben.
Energie (mental & spirituell)
•
•
•
•
Systemsprünge
Future History – Simonton?
Niemals WIE, sondern WARUM
Mentales Arbeiten (positives Denken, Lachen,
Erwartungshaltung, Entscheidungen treffen ...)
• Spirituelle Begleitung (Kirche, Guru ...)
• Tumorvertrag
Und
jetzt?
Studie:
3E-Programm in
Kombination mit
Papimi anstatt
einer palliativen
Intervention
Outcome nach 23 Monaten:
Patientengruppe: 67 Patienten mit einer Lebenserwartung von
durchschnittlich sechs Monaten (alle von Ärzten dokumentiert).
36 Überlebende (53%)
8 Patienten waren nach 23 Monaten TUMORFREI
15 Patienten hatten eine Stable Disease
2 Patienten waren im PET negativ
Studie: 3E-Programm in Kombination mit
Papimi anstatt einer palliativen Intervention
Download der Studie:
www.krebstherapien.de/3e-studie.pdf
Alle Symptome, auch Tumore, haben einen Sinn und sind
ZUERST EINMAL gut und wichtig für das ÜBERLEBEN
des einzelnen Menschen!
Keine Heilung ohne Änderung der Ursachen möglich
Fokus auf Antistress Therapien für Geist und Körper
Je kränker Sie sind, desto mehr Disziplin benötigen Sie um
gesund zu werden - und desto größer sind meistens die
notwendigen Lebensänderungen
Sie benötigen ein Minimalverständnis für Krankheiten
Tumore müssen nicht immer sofort zerstört werden
Krebs ist so lange heilbar, so lange Sie in der Lage sind den
notwendigen Schalter zurück ins Leben zu finden.
It's another day in paradise
PF 1205* 71394 Kernen
07151-910217 * 07151-910218
www.krebstherapien.de
[email protected]

Cancer research February / March 2008

Transcription

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