Chen C J, Yu M W, Liaw Y F
Graduate Institute of Epidemiology, College of Public Health, National Taiwan University, Taipei, Republic of China.
J Gastroenterol Hepatol. 1997 Oct;12(9-10):S294-308. doi: 10.1111/j.1440-1746.1997.tb00513.x.
Hepatocellular carcinoma (HCC) is one of the major cancers in the world. There is a striking variation in HCC incidence rates between various countries, with a highest-to-lowest ratio of 112.5 for males and 54.7 for females. The high-risk populations are clustered in sub-Saharan Africa and eastern Asia. The male-to-female ratio for HCC ranges from < 1 to 6.4 and mostly from 2 to 4. There exist significant variations in the incidence of HCC among different ethnic groups living in the same area and among migrants of the same ethnic groups living in different areas. The age curves of HCC are significantly different in various countries, suggesting variability in exposure to risk factors. Chronic carriers of hepatitis B and C viruses (HBV and HCV, respectively) have an increased risk of HCC. The relative and attributable HCC risk of HBV and HCV carrier status varies in different countries. There exists a synergistic interaction on HCC between the two viruses. Aflatoxin exposure, cigarette smoking, heavy alcohol consumption, low vegetable intake, inorganic arsenic ingestion, radioactive thorium dioxide exposure, iron overload and the use of oral contraceptives and anabolic steroids have been documented as HCC risk factors. Recent molecular epidemiological studies have shown that low serum retinol levels as well as elevated serum levels of testosterone, neu oncoprotein and aflatoxin B1-albumin adduct are associated with an increased HCC risk. There is a synergistic interaction on HCC between chronic HBV infection and aflatoxin exposure. Familial aggregation of HCC exists and a major susceptibility gene of HCC has been hypothesized. Patients of some genetic diseases are at an increased risk of HCC. The genetic polymorphisms of cytochrome P450 2E1 and 2D6 and arylamine N-acetyltransferase 2 are associated with the development of HCC. A dose-response relationship between aflatoxin exposure and HCC has been observed among chronic HBV carriers who have null genotypes of glutathione S-transferase M1 or T1, but not among those who have non-null genotypes. Human hepatocarcinogenesis is a multistage process with the involvement of a multifactorial aetiology. Gene-environment interactions are involved in the development of HCC in humans.
肝细胞癌（HCC）是全球主要癌症之一。不同国家之间的HCC发病率存在显著差异，男性的最高发病率与最低发病率之比为112.5，女性为54.7。高危人群集中在撒哈拉以南非洲和东亚地区。HCC的男女比例范围从小于1到6.4，多数在2到4之间。生活在同一地区的不同种族群体以及生活在不同地区的同一种族移民中，HCC发病率存在显著差异。不同国家HCC的年龄曲线差异显著，这表明风险因素暴露存在变异性。乙型和丙型肝炎病毒（分别为HBV和HCV）的慢性携带者患HCC的风险增加。HBV和HCV携带者状态导致的HCC相对风险和归因风险在不同国家有所不同。两种病毒在HCC发生上存在协同相互作用。黄曲霉毒素暴露、吸烟、大量饮酒、蔬菜摄入量低、无机砷摄入、放射性二氧化钍暴露、铁过载以及口服避孕药和合成代谢类固醇的使用已被证明是HCC的风险因素。最近的分子流行病学研究表明，血清视黄醇水平低以及血清睾酮、神经癌蛋白和黄曲霉毒素B1 -白蛋白加合物水平升高与HCC风险增加有关。慢性HBV感染与黄曲霉毒素暴露在HCC发生上存在协同相互作用。HCC存在家族聚集现象，并且推测存在一个主要的HCC易感基因。一些遗传疾病患者患HCC的风险增加。细胞色素P450 2E1和2D6以及芳胺N -乙酰转移酶2的基因多态性与HCC的发生有关。在谷胱甘肽S -转移酶M1或T1无基因型的慢性HBV携带者中，观察到黄曲霉毒素暴露与HCC之间存在剂量反应关系，但在有非无基因型的携带者中未观察到这种关系。人类肝癌发生是一个多阶段过程，涉及多因素病因。基因 - 环境相互作用参与了人类HCC的发生。
