Genetic and epigenetic changes in stomach cancer

被引:81
作者
Yokozaki, H [1 ]
Yasui, W [1 ]
Tahara, E [1 ]
机构
[1] Hiroshima Univ, Sch Med, Dept Pathol 1, Hiroshima 7348551, Japan
来源
INTERNATIONAL REVIEW OF CYTOLOGY - A SURVEY OF CELL BIOLOGY, VOL 204 | 2001年 / 204卷
关键词
gastric cancer; genetic alteration; epigenetic alteration; human carcinogenesis;
D O I
10.1016/S0074-7696(01)04003-7
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Genetic and epigenetic alterations of multiple cancer-related genes and molecules are implicated in the development and progression of human gastric carcinomas. Reactivation of telomerase, inactivation of p53 tumor suppressor gene, overexpression of cyclin E, and reduced expression of p27KIP1 by disorganized degradation in proteasome are common events of both well-differentiated and poorly differentiated gastric adenocarcinomas. Inactivation of hMLH1 mismatch repair gene by CpG hypermethylation resulting in microsatellite instability, amplification of c-erb B2 oncogene, inactivation of APC tumor suppressor gene, and K-ras mutations are preferentially associated with well-differentiated gastric cancer. Conversely, reduction or loss of E-cadherin and catenins by both mutation and CpG hypermethylation and K-sam and c-met oncogene amplification are necessary for the development and progression of poorly differentiated or scirrhous gastric carcinomas. Interaction between cancer cells expressing c-met and hepatocyte growth factor from stromal cells is implicated in morphogenesis of gastric cancer. © 2001 Academic Press.
引用
收藏
页码:49 / 95
页数:47
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