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原发性肝癌的遗传流行病学研究
引用本文:孟炜,陆鸿雁,蔡如琳,江峰,姜庆五,林文尧,沈福民.原发性肝癌的遗传流行病学研究[J].中华流行病学杂志,2002,23(6):438-440.
作者姓名:孟炜  陆鸿雁  蔡如琳  江峰  姜庆五  林文尧  沈福民
作者单位:1. 200032,上海,复旦大学公共卫生学院流行病学教研室
2. 江苏省海门市卫生防疫站
基金项目:国家自然科学基金资助项目 (3 993 0 160 )
摘    要:目的 研究原发性肝癌的遗传模式 ,探讨本病的遗传与环境的交互作用。方法 采用Penrose法、简单分离分析和Falconer法对乙型肝炎表面抗原 (HBsAg)阳性队列中的 10 0例原发性肝癌家系资料进行遗传流行病学研究。先证者样本来自同地区 9万名 8年随访队列人群 ,分析遗传模式并将队列中家系样本发病情况分别与队列人群和一般人群的发病情况进行比较 ,计算遗传度。结果 先证者家系一级亲属肝癌发生率为 4 .0 % ,高于一般人群发生率 (0 .4 4 % ) ,也高于队列人群的肝癌发生率 (1.0 3% )。HBsAg阳性在先证者家系中存在聚集 ,且HBsAg阳性与肝癌的发生有强相关(OR =8.4 4 ,95 %CI :3.37~ 2 0 .0 6 ,P <0 .0 0 1) ;应用Penrose法计算 ,同胞肝癌发生率 一般人群肝癌发生率 (s q)接近 1 q1 2 ;简单分离分析提示不符合单因子遗传模式 ;与一般人群遗传度相比 (5 9%±7% ) ,队列人群遗传度h2 =4 2 %± 6 % ,P <0 .0 5。在控制了HBsAg后 ,一般人群遗传度下降为4 7%± 7% ,队列人群遗传度下降为 2 9%± 8%。结论 肝癌不符合单基因遗传模式 ,为一多因子疾病 ,受遗传与环境的综合影响。

关 键 词:发病率  分离分析  乙型肝炎表面抗原  原发性肝癌  遗传流行病学
收稿时间:2002/3/21 0:00:00
修稿时间:2002年3月21日

A study on the genetic epidemiology of hepatocellular carcinoma
MENG Wei,LU Hongyan,CAI Rulin,JIANG Feng,JIANG Qingwu,LIN Wenyao and SHEN Fumin.A study on the genetic epidemiology of hepatocellular carcinoma[J].Chinese Journal of Epidemiology,2002,23(6):438-440.
Authors:MENG Wei  LU Hongyan  CAI Rulin  JIANG Feng  JIANG Qingwu  LIN Wenyao and SHEN Fumin
Institution:The Department of Epidemiology, Public Health School of Fudan University, Shanghai 200032, China.
Abstract:OBJECTIVE: To explore the interaction between inheritance and environment with the aid of research on the genetic modes of hepatocellular carcinoma (HCC). METHODS: A genetic epidemiological study of HCC was conducted based on the methods of Penrose, simple segregation and Falconer for 100 proband pedigrees from HBsAg positive cohort. The proband samples came from a cohort of 90,00 people who were followed for 8 years. Analyses on genetic modes were carried out and heritability was calculated through the comparison of the proband pedigrees incidence frequency with incidence frequencies of the cohort and general population. RESULTS: The incidence frequency of first-degree relatives was 4.0%, higher than what was seen in the general population incidence frequency (0.44%) and the cohort (1.03%). A familial aggregation of HBsAg carriers and a strong positive correlation between HBsAg carrier status and HCC were noticed (OR = 8.44, 95% CI: 3.37-20.06, P < 0.001). A ratio of the incidence frequency among siblings to the incident frequency among general population (s/q) approached 1/q(1/2) by Penrose method, but simple segregation did not show agreement with single-gene inheritance. The heritability from positive cohort was 42% +/- 6% (P < 0.05), compared with the heritability (59% +/- 7%) of general population. When the effect of the HBsAg was under control, the heritability from positive cohort turned to be 29% +/- 8% (P < 0.05), compared with the heritability (47% +/- 7%) of general population. CONCLUSION: Our findings suggested that HCC followed a multifactorial mode rather than single inheritance. An interaction effect of inheritance and environment on HCC was also noticed.
Keywords:Hepatocellular carcinoma  Segregation analysis  Heretibility  
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