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首页> 外文期刊>British Journal of Cancer >Mdm2-SNP309 polymorphism in prostate cancer: no evidence for association with increased risk or histopathological tumour characteristics
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Mdm2-SNP309 polymorphism in prostate cancer: no evidence for association with increased risk or histopathological tumour characteristics

机译：Mdm2-SNP309多态性在前列腺癌：没有证据与增加的风险或组织病理学肿瘤特征相关

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The search for inherited cancer susceptibility factors is a major focus of epidemiologic cancer studies. Analyses of single-nucleotide polymorphisms (SNP) in a variety of genes revealed a correlation between a specific allele variant and cancer predisposition. Human mouse double-minute 2 protein (Mdm2) is a cellular E3 ligase capable of ubiquitination and degradation of p53. Therefore, Mdm2 is a crucial factor of cell cycle control and cell survival. The Mdm2 promoter SNP309 was shown to increase Mdm2 expression and can, thereby, inhibit the p53 pathway. This SNP was found to be associated with increased risk and early onset of various malignancies. For prostate cancer no studies are reported to date. In a case–control study we determined the distribution of the Mdm2 SNP309 in 145 male subjects with prostate cancer and in 124 male controls without any malignancy using RFLP analysis. Cases and controls showed a similar distribution of the SNP (P=0.299). Genotype distribution showed neither an association with histopathological characteristics of the tumours nor with prognosis. Age at disease onset was also not modified by the SNP. This first study of the Mdm2 SNP309 in prostate cancer patients suggests no correlation between a certain allelic variant and an increased cancer risk.
机译：寻找遗传的癌症易感因素是流行病学癌症研究的主要重点。对多种基因中的单核苷酸多态性（SNP）进行的分析揭示了特定等位基因变异与癌症易感性之间的相关性。人鼠两分钟2蛋白（Mdm2）是一种能够将p53泛素化和降解的细胞E3连接酶。因此，Mdm2是细胞周期控制和细胞存活的关键因素。 Mdm2启动子SNP309显示增加Mdm2表达，并因此可以抑制p53途径。发现该SNP与各种恶性肿瘤的风险增加和早期发作有关。对于前列腺癌，迄今为止尚无研究报道。在一项病例对照研究中，我们使用RFLP分析确定了Mdm2 SNP309在145名患有前列腺癌的男性受试者和124名无任何恶性肿瘤的男性对照中的分布。病例和对照显示SNP的分布相似（P = 0.299）。基因型分布既不与肿瘤的组织病理学特征相关，也不与预后相关。 SNP也未改变发病年龄。前列腺癌患者中Mdm2 SNP309的首次研究表明，某些等位基因变异与增加的癌症风险之间无相关性。

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