Genetic Alterations and Polymorphisms in Gastric Cancer

胃癌的基因變化及基因多形性

吳明賢(Ming-Shiang Wu) ； 陳建仁(Chien-Jen Chen) ； 林肇堂(Jaw-Town Lin)

《Journal of the Formosan Medical Association》 102卷7期 (2003/07) Pp. 447-458

https://doi.org/10.29828/JFMA.200307.0002

並列摘要

The etiology of gastric cancer (GC) is multifactorial, and is likely to involve the actions of genes multiple levels along the multistage carcinogenesis process. This article reviews the considerable progress that has been achived in understanding the genetics of GC. The genetic effects consist of inherited genetic factors that predispose to GC, and the genetic targets of neoplastic progression that confer altered growth capacity to neoplastic cells. Inherited genotypes include germline mutations of high-penetrance genes directly associated with hereditary GC syndromes and genetic polymorphisms that indirectly affect the susceptibility to GC after exposure to carcinogens or Helicobacter pylori infection. Based on accumulation of different oncogenes or tumor suppressor genes alterations, 2 broad classes of genetic pathways called suppressor and mutator phenotypes are defined that participate in the development and progression of GC. Examples of genes involved in pathogenesis of GC include p53, adenomatous polyposis coli (APC), ß-catenin, E-cadherin, transforming growth factor (TGF)-ßRII, and hMLH1. Delineating genes involved in different subtypes of GC can reflect the heterogeneity and biologic characteristics of GC. Elucidation of the role of inherited genotypes and genetic alterations at different stages of gastrocarcinogenesis may provide a more coherent picture of the mechanism of this devastating disease and facilitate the development of novel approaches to effective prevention and intervention. Advances in high throughput technologies and functional genomics have rapidly increased our understanding of gene structure and function and its role in disease.

並列關鍵字

Genetic predisposition to disease ； Genetic research ； Polymorphism ； genetics ； Review ； Stomach neoplasms