Feitelson M
Department of Pathology and Cell Biology, Jefferson Medical School, Thomas Jefferson University, Philadelphia, Pennsylvania 19107.
Clin Microbiol Rev. 1992 Jul;5(3):275-301. doi: 10.1128/CMR.5.3.275.
For many years, epidemiological studies have demonstrated a strong link between chronic hepatitis B virus (HBV) infection and the development of primary hepatocellular carcinoma (PHC). Other hepatocarcinogens such as hepatitis C virus and aflatoxin also contribute to hepatocarcinogenesis either in conjunction with HBV infection or alone. Cellular and molecular biological studies are providing explanations for the HBV-PHC relationship, and models are now being formulated to further test the relative importance of various factors such as viral DNA integration, activation of oncogenes, genetic instability, loss of tumor suppressor genes, and trans-activating properties of HBV to the pathogenesis of PHC. Further research will probably define more than a single mechanism whereby chronic HBV infection results in PHC.
多年来,流行病学研究已证明慢性乙型肝炎病毒(HBV)感染与原发性肝细胞癌(PHC)的发生之间存在密切联系。其他致癌因素,如丙型肝炎病毒和黄曲霉毒素,也可与HBV感染协同作用或单独导致肝癌发生。细胞和分子生物学研究正在为HBV与PHC的关系提供解释,目前正在构建模型,以进一步检验病毒DNA整合、癌基因激活、基因不稳定、肿瘤抑制基因缺失以及HBV的反式激活特性等各种因素在PHC发病机制中的相对重要性。进一步的研究可能会确定慢性HBV感染导致PHC的机制不止一种。