期刊
ANNUAL REVIEW OF PATHOLOGY-MECHANISMS OF DISEASE
卷 4, 期 -, 页码 399-415出版社
ANNUAL REVIEWS
DOI: 10.1146/annurev.pathol.4.110807.092202
关键词
hepatocellular carcinoma; p53; retinoblastoma; cell-cycle checkpoint; aneuploidy
类别
资金
- National Institute of Allergy and Infectious Diseases [U19-AI40035]
- NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [U19AI040035] Funding Source: NIH RePORTER
Hepatitis C virus (HCV) is the only known RNA virus with an exclusively cytoplasmic life cycle that is associated with cancer. The mechanisms by which it causes cancer are unclear, but chronic immune-mediated inflammation and associated oxidative chromosomal DNA damage probably play a role. Compelling data suggest that the path to hepatocellular carcinoma in chronic hepatitis C shares some important features with die mechanisms of transformation employed by DNA tumor viruses. Interactions of viral proteins with key regulators of the cell cycle, the retinoblastoma-susceptibility protein, p53, and possibly DDX5 and DDX3 lead to enhanced cellular proliferation and may also compromise multiple cell-cycle checkpoints that maintain genomic integrity, thus setting the stage for carcinogenesis. Dysfunctional DNA damage and mitotic spindle checkpoints resulting from these interactions may promote chromosomal instability and leave the hepatocyte unable to control DNA damage caused by oxidative stress mediated by HCV proteins, alcohol, and immune-mediated inflammation.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据