- 现金
- 62111 元
- 精华
- 26
- 帖子
- 30437
- 注册时间
- 2009-10-5
- 最后登录
- 2022-12-28
|
<http://onlinelibrary.wiley.com/doi/10.1111/j.1872-034X.2010.00732.x/abstract>
Combined pre-S deletion and core promoter mutations related to hepatocellular
carcinoma: A nested case-control study in China
Li-Shuai Qu1,†, Tao-Tao Liu1,†, Fei Jin1, Yan-Mei Guo1, Tao-Yang Chen2,
Zheng-Pin Ni2, Xi-Zhong Shen1,*Article first published online: 25 OCT 2010
DOI: 10.1111/j.1872-034X.2010.00732.x
© 2010 The Japan Society of Hepatology
Issue
Abstract
Aim: To investigate the roles of biomedical factors, hepatitis B virus (HBV)
DNA levels, genotypes, and specific viral mutation patterns on the progression
of hepatocellular carcinoma (HCC) in Qidong, China.
Methods: A total of 2387 males (aged 20–65 years) who were seropositive for
the hepatitis B surface antigen (HBsAg), but had not been diagnosed with HCC,
were recruited to a community-based HCC screening study from August, 1996.
Evaluation of virological parameters at recruitment was determined for 196 HCC
patients during 10 years of follow-up and 323 controls.
Results: After adjustment for age at recruitment, history of cigarette
smoking and alcohol consumption, alanine aminotransferase (ALT) elevation,
alpha-fetoprotein (AFP) levels >20 ng/mL, hepatitis B e antigen positive, HBV
DNA levels ≥4.00 log10 copies/mL, pre-S deletion, T1653 mutation, T1762/A1764
double mutations, and T1766 and/or A1768 mutations were associated with
subsequent risk of HCC. A significant biological gradient of HCC risk by HBV DNA
levels from less than 2.69 log10 copies/mL to 6.00 log10 copies/mL or greater
was observed. HBV with a complex mutation combination pattern (pre-S deletion,
T1762/A1764 double mutations, and T1766 and/or A1768 mutations) rather than a
single mutation was associated with the development of HCC. The longitudinal
observation demonstrated a gradual combination of pre-S deletion, T1762/A1764
double mutations, and T1766 and/or A1768 mutations during the development of
HCC.
Conclusions: AFP levels >20 ng/mL, high HBV DNA levels, pre-S deletion, and
T1762/A1764 double mutations at recruitment were independent risk factors of
HCC. Combination of pre-S deletion and core promoter mutations increased the
risk of HCC.
联合预- S的缺失和核心启动子突变与肝癌
癌:巢式病例对照研究在中国
Li-Shuai Qu1,†, Tao-Tao Liu1,†, Fei Jin1, Yan-Mei Guo1, Tao-Yang Chen2,
Zheng-Pin Ni2, Xi-Zhong Shen1
,*条第一发表时间:2010年10月25日
分类号:10.1111/j.1872-034X.2010.00732.x
© 2010日本文化协会的杂志发行
摘要
目的:探讨生物医学因素,乙型肝炎病毒(HBV)的角色
DNA水平,基因型,和具体的进展病毒突变模式
启东肝癌,中国(肝癌)。
方法:2387总男性(年龄20-65岁)谁是为阳性
乙型肝炎表面抗原(HBsAg),但没有被诊断为肝癌,
被招募到以社区为基础的肝癌从1996年8月筛选研究。
在招聘病毒学指标综合评价,确定196肝癌
患者在10年的后续行动和控制323年。
结果:在调整了年龄在招聘,香烟的历史
吸烟和饮酒,谷丙转氨酶(ALT)升高,
α-甲胎蛋白(AFP)水平“20毫微克/毫升,B型肝炎e抗原阳性,乙肝病毒
DNA水平≥4.00 log10拷贝/毫升,前- S的缺失,T1653突变,T1762/A1764
双突变,T1766和/或A1768突变与
随后肝癌的风险。一个重要的生物梯度肝癌风险乙型肝炎病毒DNA
从不到2.69 log10拷贝数/毫升至6.00 log10拷贝/ ml或以上
进行了观察。乙肝病毒变异与复杂组合模式(预S缺失,
T1762/A1764双突变,T1766和/或A1768突变),而不是一
单基因突变与肝癌的发展。纵向
观察表现出了前- S的缺失,T1762/A1764渐进融合
在发展双突变,T1766和/或A1768突变
肝癌。
结论:AFP水平“20毫微克/毫升,HBV DNA水平高,前- S的删除,
T1762/A1764双突变在招聘的独立危险因素
肝癌。前- S的缺失和核心启动子突变组合增加
肝癌的风险。
|
|