AA. Gastric C I 06. ppt - Università degli studi di Pavia

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Model for development of hereditary diffuse gastric cancer * gastric mucosa in CDH1 (E - cadherin gene) germline mutation carriers is normal until second CDH1 allele is inactivated or repressed (second hit) by transcriptional downregulation; [- promoter hypermethylation is one mechanism for downregulation (transcription factor mediated events also play a role, including environmental and physiological factors such as diet, carcinogen exposure, ulceration and gastritis)]; - since downregulation may occur in multiple cells, multifocal tumors develop; - tumor expands slowly until additional genetic events, possibly combined with an altered microenvironment → clonal expansion and disease progression; [- because second hit does not involve somatic, irreversible, mutation of second CDH1 allele, it is possible that early stage lesions is reversible]
RECEPTOR TYROSINE KINASE AND PROLIFERATION AND TISSUE EXPANSION * receptor tyrosine kinases (RTKs) = main positive regulators of proliferation and tissue expansion (through downstream pathways including ras - MAPK and PI3K / Akt cascade); * RTKs negatively act on E - cadherin function → disassembly of adherens junctions; - downstream elements of RTK signalling interact and activate Rho family GTPases (Rac, Rho, Cdc42) system that interfere with cadherin - mediated adhesion through changes in actin cytoskeleton; * catenin p120 acts as regulator of cadherin function either promoting or repressing E - cadherin - dependent adhesion
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Università degli Studi di Pavia AA
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GASTRIC ADENOCARCINOMA
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GASTRIC ADENOCARCINOMA (Cancer Stat
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* age - adjusted cancer death rates
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RISK FACTORS AND PATHOGENESIS
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GASTRIC ADENOCARCINOMA Etiology. I.
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GASTRIC ADENOCARCINOMA Etiology. II
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NATURAL HISTORY OF HELICOBACTER PYL
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NATURAL HISTORY OF HELICOBACTER PYL
Page 19 and 20: Pathogen - host interactions in pat
Page 21 and 22: Pathogen - host interactions in pat
Page 23 and 24: GASTRIC ADENOCARCINOMA Etiology. II
Page 25 and 26: GASTRIC CANCER Pathology. I. * 85%
Page 27 and 28: GASTRIC CANCER Pathology. III. Leio
Page 30 and 31: GASTRIC ADENOCARCINOMA Pathology. V
Page 32 and 33: GASTRIC ADENOCARCINOMA Pathology. V
Page 34 and 35: GASTRIC ADENOCARCINOMA Pathology. I
Page 37 and 38: GASTRIC ADENOCARCINOMA Pathology. X
Page 47 and 48: “EARLY” GASTRIC CANCER
Page 55 and 56: GENETICS
Page 57 and 58: GASTRIC ADENOCARCINOMA Genetics. II
Page 59 and 60: GENETIC STEPS OF INTESTINAL TYPE GA
Page 61 and 62: GASTRIC ADENOCARCINOMA Genetics. II
Page 63 and 64: Schematic structure of telomere - r
Page 65 and 66: * adenoma → carcinoma sequence in
Page 67 and 68: GASTRIC ADENOCARCINOMA Genetics. VI
Page 69: GASTRIC ADENOCARCINOMA Genetics. VI
Page 73 and 74: SCHEMA TO GUIDE THE MANAGEMENT OF F
Page 75 and 76: GASTRIC ADENOCARCINOMA Genetics. VI
Page 77 and 78: CLINICAL FEATURES
Page 79 and 80: GASTRIC ADENOCARCINOMA Clinical fea
Page 81 and 82: GASTRIC ADENOCARCINOMA Clinical fea
Page 83: GASTRIC ADENOCARCINOMA Clinical fea
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AA. Gastric C I 06. ppt - Università degli studi di Pavia

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