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DNA修复基因多态性与皮肤黑色素瘤的遗传易感性

DNA repair gene polymorphisms and genetic predisposition to cutaneous melanoma.

作者信息

Povey Joanne E, Darakhshan Fatemeh, Robertson Karen, Bisset Yvonne, Mekky Magda, Rees Jonathan, Doherty Val, Kavanagh Gina, Anderson Niall, Campbell Harry, MacKie Rona M, Melton David W

机构信息

Sir Alastair Currie Cancer Research UK Laboratories, Molecular Medicine Centre, University of Edinburgh, Western General Hospital, Crewe Road, Edinburgh, EH4 2XU, UK.

出版信息

Carcinogenesis. 2007 May;28(5):1087-93. doi: 10.1093/carcin/bgl257. Epub 2007 Jan 8.

Abstract

The incidence of cutaneous melanoma is rising rapidly in a number of countries. The key environmental risk factor is exposure to the ultraviolet (UV) component in sunlight. The nucleotide excision repair (NER) pathway deals with the main forms of UV-induced DNA damage. We have investigated the hypothesis that polymorphisms in NER genes constitute genetic susceptibility factors for melanoma. However, not all melanomas arise on sun-exposed sites and so we investigated the hypothesis that genes involved in other pathways for the repair of oxidative DNA damage may also be involved in susceptibility to melanoma. Scotland, with its high incidence of melanoma and stable homogeneous population, was ideal for this case-control study, involving 596 Scottish melanoma patients and 441 population-based controls. Significant associations were found for the NER genes ERCC1 and XPF, with the strongest associations for melanoma cases aged 50 and under [ERCC1 odds ratio (OR) 1.59, P = 0.008; XPF OR 1.69, P = 0.003]. Although an XPD haplotype was associated with melanoma, it did not contain the variant 751 Gln allele, which has been associated with melanoma in some previous studies. No associations were found for the base excision repair and DNA damage response genes investigated. An association was also found for a polymorphism in the promoter of the vitamin D receptor gene, VDR (OR 1.88, P = 0.005). The products of the two NER genes, ERCC1 and XPF, where associations with melanoma were found, act together in a rate-limiting step in the repair pathway.

摘要

在许多国家,皮肤黑色素瘤的发病率正在迅速上升。关键的环境风险因素是暴露于阳光中的紫外线(UV)成分。核苷酸切除修复(NER)途径可处理紫外线诱导的DNA损伤的主要形式。我们研究了NER基因中的多态性构成黑色素瘤遗传易感性因素的假说。然而,并非所有黑色素瘤都发生在阳光暴露部位,因此我们研究了参与氧化DNA损伤修复其他途径的基因也可能与黑色素瘤易感性有关的假说。苏格兰黑色素瘤发病率高且人口稳定同质,是这项病例对照研究的理想之地,该研究涉及596名苏格兰黑色素瘤患者和441名基于人群的对照。发现NER基因ERCC1和XPF存在显著关联,50岁及以下黑色素瘤病例的关联最强[ERCC1优势比(OR)1.59,P = 0.008;XPF OR 1.69,P = 0.003]。虽然一种XPD单倍型与黑色素瘤有关,但它不包含751 Gln变体等位基因,而在一些先前的研究中该等位基因与黑色素瘤有关。在所研究的碱基切除修复和DNA损伤反应基因中未发现关联。还发现维生素D受体基因VDR启动子中的多态性存在关联(OR 1.88,P = 0.005)。发现与黑色素瘤有关联的两个NER基因ERCC1和XPF的产物在修复途径的限速步骤中共同起作用。

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