Department of Preclinical and Clinical Pharmacology, University of Florence, Florence 50139, Italy.
World J Gastroenterol. 2011 Jan 21;17(3):290-9. doi: 10.3748/wjg.v17.i3.290.
Gastric cancer is one of the leading causes of cancer-related deaths worldwide, although the incidence has gradually decreased in many Western countries. Two main gastric cancer histotypes, intestinal and diffuse, are recognised. Although most of the described genetic alterations have been observed in both types, different genetic pathways have been hypothesized. Genetic and epigenetic events, including 1q loss of heterozygosity (LOH), microsatellite instability and hypermethylation, have mostly been reported in intestinal-type gastric carcinoma and its precursor lesions, whereas 17p LOH, mutation or loss of E-cadherin are more often implicated in the development of diffuse-type gastric cancer. In this review, we summarize the sometimes contradictory findings regarding those markers which influence the progression of gastric adenocarcinoma.
胃癌是全球癌症相关死亡的主要原因之一，尽管在许多西方国家，其发病率已逐渐下降。有两种主要的胃癌组织学类型，肠型和弥漫型，已被确认。尽管在这两种类型中都观察到了大多数描述的遗传改变，但已经假设了不同的遗传途径。包括 1q 杂合性丢失（LOH）、微卫星不稳定性和高甲基化在内的遗传和表观遗传事件，主要在肠型胃癌及其前体病变中报道，而 17p LOH、突变或 E-钙黏蛋白缺失更常涉及弥漫型胃癌的发生。在这篇综述中，我们总结了这些标志物在影响胃腺癌进展方面有时相互矛盾的发现。
