Stomach - Genetic and epigenetic alterations of preneoplastic and neoplastic lesions

被引：20

作者：

David, Stefan ^{[1
]}

Meltzer, Stephen J. ^{[1
,2
]}

机构：

[1] Johns Hopkins Univ, Sch Med, Dept Med, Div Gastroenterol, Baltimore, MD 21205 USA

[2] Johns Hopkins Univ, Sch Med, Dept Oncol, Sidney Kimmel Comprehens Canc Ctr, Baltimore, MD 21205 USA

来源：

CANCER BIOMARKERS | 2011年 / 9卷 / 1-6期

关键词：

Gastric cancer; genetics; epigenetics; microsatellite instability chromosomal instability; mutation; deletion; translocation; methylation; oncogene; tumor suppressor gene; EPSTEIN-BARR-VIRUS; HELICOBACTER-PYLORI-INFECTION; CPG ISLAND HYPERMETHYLATION; TUMOR-RELATED GENES; E-CADHERIN GENE; COMPARATIVE GENOMIC HYBRIDIZATION; SPORADIC GASTRIC CARCINOMAS; POLYMERASE-CHAIN-REACTION; DIFFERENTIATED-TYPE ADENOCARCINOMAS; MISMATCH REPAIR GENES;

D O I：

10.3233/CBM-2011-0169

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 [肿瘤学];

摘要：

Gastric cancer is one of the most common neoplasias in the world and remains an important cause of cancer-related mortality. Vast resources have been invested in the study of the molecular events driving the development and progression of gastric tumors. Gastric cancer is known to result from an interaction between host and environmental factors. The present review will discuss the most how genetic and epigenetic changes contribute to gastric carcinogenesis and their potential for developing novel diagnostic and therapeutic tools.

引用

页码：493 / 507

页数：15

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