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DNA 修复基因中的遗传变异与 CDKN2A 突变阳性/阴性易患皮肤恶性黑色素瘤家族中皮肤恶性黑色素瘤的风险。

Genetic variants in DNA repair genes and the risk of cutaneous malignant melanoma in melanoma-prone families with/without CDKN2A mutations.

机构信息

Division of Cancer Epidemiology and Genetics, NCI/NIH, Bethesda, MD, USA.

出版信息

Int J Cancer. 2012 May 1;130(9):2062-6. doi: 10.1002/ijc.26231. Epub 2011 Aug 9.

Abstract

Cutaneous malignant melanoma (CMM) is an etiologically heterogeneous disease with genetic, environmental (sun exposure) and host (pigmentation/nevi) factors and their interactions contributing to risk. Genetic variants in DNA repair genes may be particularly important since their altered function in response to sun exposure-related DNA damage maybe related to risk for CMM. However, systematic evaluations of genetic variants in DNA repair genes are limited, particularly in high-risk families. We comprehensively analyzed DNA repair gene polymorphisms and CMM risk in melanoma-prone families with/without CDKN2A mutations. A total of 586 individuals (183 CMM) from 53 families (23 CDKN2A (+), 30 CDKN2A (-)) were genotyped for 2964 tagSNPs in 131 DNA repair genes. Conditional logistic regression, conditioning on families, was used to estimate trend p-values, odds ratios and 95% confidence intervals for the association between CMM and each SNP separately, adjusted for age and sex. p-Values for SNPs in the same gene were combined to yield gene specific p-values. Two genes, POLN and PRKDC, were significantly associated with melanoma after Bonferroni correction for multiple testing (p = 0.0003 and 0.00035, respectively). DCLRE1B showed suggestive association (p = 0.0006). 28 ∼ 56% of genotyped SNPs in these genes had single SNP p < 0.05. The most significant SNPs in POLN and PRKDC had similar effects in CDKN2A (+) and CDKN2A (-) families. Our finding suggests that polymorphisms in DNA repair genes, POLN and PRKDC, were associated with increased melanoma risk in melanoma families with and without CDKN2A mutations.

摘要

皮肤恶性黑色素瘤(CMM)是一种病因学上异质的疾病,其遗传、环境(阳光暴露)和宿主(色素/痣)因素及其相互作用导致风险增加。DNA 修复基因中的遗传变异可能尤为重要,因为它们对阳光相关 DNA 损伤的反应功能改变可能与 CMM 的风险有关。然而,DNA 修复基因遗传变异的系统评估是有限的,特别是在高风险家族中。我们综合分析了具有/不具有 CDKN2A 突变的黑色素瘤易感家族中 DNA 修复基因多态性与 CMM 风险的关系。来自 53 个家族(23 个 CDKN2A(+),30 个 CDKN2A(-))的 586 名个体(183 名 CMM)对 131 个 DNA 修复基因中的 2964 个标签 SNP 进行了基因分型。采用条件逻辑回归,根据家族进行条件化,以估计每个 SNP 与 CMM 之间的趋势 p 值、比值比和 95%置信区间,调整年龄和性别。同一基因中的 SNP 的 p 值合并以产生基因特异性 p 值。经过多重检验校正(分别为 0.0003 和 0.00035),POLN 和 PRKDC 两个基因与黑色素瘤显著相关。DCLRE1B 显示出暗示性关联(p = 0.0006)。这些基因中 28%~56%的基因分型 SNP 的单 SNP p < 0.05。在 CDKN2A(+)和 CDKN2A(-)家族中,POLN 和 PRKDC 中最显著的 SNP 具有相似的作用。我们的发现表明,DNA 修复基因 POLN 和 PRKDC 中的多态性与 CDKN2A 突变阳性和阴性黑色素瘤家族中黑色素瘤风险的增加相关。

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