Suppr超能文献

STAT4 变异体在慢性乙型肝炎诱导的肝细胞癌中的微小作用。

A trivial role of STAT4 variant in chronic hepatitis B induced hepatocellular carcinoma.

机构信息

Institute of Tropical Medicine, University of Tübingen, Germany.

出版信息

Infect Genet Evol. 2013 Aug;18:257-61. doi: 10.1016/j.meegid.2013.05.025. Epub 2013 Jun 6.

Abstract

Two polymorphisms in the STAT4 and HLA-DQ loci were more recently reported to associate with chronic hepatitis B (CHB) induced hepatocellular carcinoma (HCC). We utilised an independent Vietnamese cohort of clinically classified HBV patients of chronic hepatitis B carriers (n=206), liver cirrhosis (n=222) and hepatocellular carcinoma (n=239) and assessed the influence of the reported variants. The STAT4 variant (rs7574865) was marginally associated with HCC susceptibility in CHB carriers in allelic and recessive genetic models (OR=0.84, 95%CI=0.7-0.99, P=0.048 and OR=0.7, 95%CI=0.5-0.99, P=0.047). No significant association between the studied variant with several clinical parameters such as liver enzymes (ALT, AST), total and direct bilirubin, AFP, HBV genotype and viral loads were observed. Our study highlights the reported variant to be a trivial factor and possibly other confounding factors may regulate STAT4 expression during HCC development.

摘要

两个 STAT4 和 HLA-DQ 基因座的多态性最近被报道与慢性乙型肝炎 (CHB) 诱导的肝细胞癌 (HCC) 相关。我们利用一个独立的越南队列,对临床分类的 HBV 患者进行研究,包括慢性乙型肝炎携带者 (n=206)、肝硬化 (n=222) 和肝细胞癌 (n=239),并评估了报告的变异体的影响。STAT4 变异体 (rs7574865) 在等位基因和隐性遗传模型中与 CHB 携带者的 HCC 易感性呈边缘相关 (OR=0.84,95%CI=0.7-0.99,P=0.048 和 OR=0.7,95%CI=0.5-0.99,P=0.047)。在研究的变异体与几种临床参数之间没有观察到显著的相关性,如肝酶 (ALT、AST)、总胆红素和直接胆红素、AFP、HBV 基因型和病毒载量。我们的研究强调了报告的变异体是一个微不足道的因素,可能还有其他混杂因素可能在 HCC 发展过程中调节 STAT4 的表达。

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验