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The programmed cell death 6 interacting protein insertion/deletion polymorphism is associated with non-small cell lung cancer risk in a Chinese Han population.

机译:在中国汉族人群中,程序性细胞死亡6相互作用的蛋白质插入/缺失多态性与非小细胞肺癌风险有关。

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摘要

It has been proposed that genetic factors contribute to the susceptibility of non-small cell lung cancer (NSCLC). The programmed cell death 6 interacting protein (PDCD6IP) encodes for a protein that has been known to bind to the products of the PDCD6 gene, a required protein in apoptosis. The aim of this study is to investigate the relationship between PDCD6IP insertion/deletion (I/D) polymorphism (rs28381975) and NSCLC risk in a Chinese population. A population-based case-control study was conducted in 449 NSCLC patients and 512 cancer-free controls. The genotype of the PDCD6IP gene was determined by using a polymerase chain reaction assay. The promoter activity was analyzed by luciferase reporter assay in A549 and H1299 cells. Statistically significant difference was observed when the patients and controls were compared according to ID + II versus DD (OR?=?1.72, 95 % CI 1.29-2.31, P?
机译:已经提出遗传因素有助于非小细胞肺癌(NSCLC)的易感性。程序性细胞死亡6相互作用蛋白(PDCD6IP)编码一种已知与PDCD6基因产物结合的蛋白,PDCD6基因是凋亡中必需的蛋白。这项研究的目的是调查中国人群中PDCD6IP插入/缺失(I / D)多态性(rs28381975)与NSCLC风险之间的关系。在449名NSCLC患者和512名无癌对照中进行了基于人群的病例对照研究。通过使用聚合酶链反应测定法确定PDCD6IP基因的基因型。通过荧光素酶报告基因分析在A549和H1299细胞中分析启动子活性。当根据ID + II与DD比较患者和对照组时,观察到统计学上的显着差异(OR≥1.72,95%CI 1.29-2.31,P≤0.01)。 I等位基因与NSCLC风险显着相关(OR≥1.41,95%CI 1.18-1.69,P <0.01)。与TNM I + II期相比,PDCD6IP I / D多态性显着增加了晚期NSCLC风险(OR≥2.06,95%CI 1.30-3.26,P <0.01)。在A549和H1299细胞中,携带I等位基因的启动子报告基因结构显示出比D等位基因显着更高的启动子活性(P≥0.001)。这项研究的结果表明,PDCD6IP I / D多态性可能与中国汉族人群的NSCLC易感性有关。

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