Block Timothy M, Mehta Anand S, Fimmel Claus J, Jordan Robert
Department of Molecular Pharmacology and Biochemistry, Jefferson Center for Biomedical Research of Thomas Jefferson University, 700 East Butler Ave., Doylestown, PA 18901, USA.
Oncogene. 2003 Aug 11;22(33):5093-107. doi: 10.1038/sj.onc.1206557.
Hepatocellular carcinoma (HCC) is the fifth most common cancer, but the third leading cause of cancer death, in the world, with more than 500,000 fatalities annually. The major etiology of HCC/liver cancer in people is hepatitis B virus (HBV), followed by hepatitis C virus infection (HCV), although nonviral causes also play a role in a minority of cases. Recent molecular studies confirm what was suspected: that HCC tissue from different individuals have many phenotypic differences. However, there are clearly features that unify HCC occurring in a background of viral hepatitis B and C. HCC due to HBV and HCV may be an indirect result of enhanced hepatocyte turnover that occurs in an effort to replace infected cells that have been immunologically attacked. Viral functions may also play a more direct role in mediating oncogenesis. This review considers the molecular and cellular mechanisms involved in primary hepatocellular carcinoma, using a viral perspective.
肝细胞癌（HCC）是全球第五大常见癌症，但却是癌症死亡的第三大主要原因，每年有超过50万人死亡。人类HCC/肝癌的主要病因是乙型肝炎病毒（HBV），其次是丙型肝炎病毒感染（HCV），尽管非病毒原因在少数病例中也起作用。最近的分子研究证实了之前的怀疑：不同个体的HCC组织存在许多表型差异。然而，在乙型和丙型病毒性肝炎背景下发生的HCC显然有一些共同特征。由HBV和HCV引起的HCC可能是肝细胞更新增强的间接结果，这种更新是为了替换受到免疫攻击的感染细胞。病毒功能在介导肿瘤发生过程中也可能发挥更直接的作用。本综述从病毒角度探讨原发性肝细胞癌所涉及的分子和细胞机制。
