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首页> 外文期刊>Lung cancer: Journal of the International Association for the Study of Lung Cancer >Elevated risk of squamous-cell carcinoma of the lung in heavy smokers carrying the variant alleles of the TP53 Arg72Pro and p21 Ser31Arg polymorphisms.
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Elevated risk of squamous-cell carcinoma of the lung in heavy smokers carrying the variant alleles of the TP53 Arg72Pro and p21 Ser31Arg polymorphisms.

机译:鳞状细胞癌的风险升高在重度吸烟者肺部携带的基因变异的等位基因TP53 Arg72Pro p21和Ser31Arg多态性。

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摘要

Alterations in cell cycle regulation and apoptosis leading to malignant transformation could be caused by common genetic variants in tumor suppressor genes. The effects of the TP53 polymorphism Arg72Pro on lung cancer risk have been investigated in numerous studies with, however, conflicting results. In many studies, important risk modifiers such as smoking or tumor histology were not taken into account. We therefore investigated the combined effects of polymorphisms in TP53 (Arg72Pro) and p21/CDKN1A (Ser31Arg) and smoking on lung cancer risk. Our case-control study consisted of 405 patients with lung cancer, mainly squamous-cell carcinoma (185) and adenocarcinoma (177) and 404 unmatched tumor-free hospital controls. Multivariate regression analysis showed a moderate but statistically significant risk of lung cancer overall and especially of squamous-cell carcinoma (OR, 1.65; CI, 1.10-2.47) for TP53 72Pro allele carriers. The risk was markedly increased in heavy smokers (>20 pack-years) with squamous-cell carcinoma (OR, 2.80 in patients homozygous for 72Pro; CI, 1.19-6.58), but not in light smokers (
机译:改变细胞周期调控和细胞凋亡导致恶性转变常见的基因变异引起的肿瘤抑制基因。多态性Arg72Pro肺癌风险在大量研究与调查,然而,冲突的结果。吸烟或肿瘤等重要风险修饰符组织学没有考虑。因此调查的综合影响多态性在TP53 (Arg72Pro)和p21 / CDKN1A(Ser31Arg)和吸烟对肺癌的风险。病例对照研究包括405例肺癌,主要是鳞状细胞癌(185)和腺癌(177)和404无与伦比的患肿瘤医院控制。回归分析显示一个温和但统计上显著的肺癌的风险的整体,特别是鳞状细胞癌(前,1。65;运营商。重度吸烟者(> 20久)鳞状细胞癌患者(或2.80纯合子72专业版;(< = 20久)。Ser31Arg多态性建议31爵士是一个有中等等位基因为鳞状细胞癌。两者的联合效应的分析多态性高或透露TP53 72 pro运营商p21 31 ser的纯合子比72 pro航空公司一般;明显与鳞状细胞重度吸烟者癌(OR, 3.84;表明,TP53 Arg72Pro多态性鳞状细胞癌的风险增加主要是在重度吸烟者。与吸烟是生理上的,72 pro p53变体,减少细胞凋亡扩展G1细胞周期阻滞后报告致癌物质暴露。通过进一步的分子流行病学研究是十分必要的。

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