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首页> 外文期刊>Journal of dermatological science >POMC and TP53 genetic variability and risk of basal cell carcinoma of skin: Interaction between host and genetic factors.
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POMC and TP53 genetic variability and risk of basal cell carcinoma of skin: Interaction between host and genetic factors.

机译：POMC和TP53遗传变异和皮肤基底细胞癌的风险：宿主与遗传因素之间的相互作用。

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BACKGROUND: Basal cell carcinoma (BCC) of the skin is the most common neoplasm among the Caucasian population of the western world. Ultraviolet (UV) radiation-induced p53 activation promotes cutaneous pigmentation by increasing transcriptional activity of pro-opiomelanocortin (POMC) in the skin. Induction of POMC/alpha-melanocyte-stimulating hormone (alpha-MSH) activates the melanocortin 1 receptor (MC1R), resulting in skin pigmentation. The tumor suppressor p53 is a key player in stress responses that preserve genomic stability, responding to a variety of insults including DNA damage, hypoxia, metabolic stress and oncogene activation. Malfunction of the p53 pathway is an almost universal hallmark of human tumors. Polymorphisms in the gene encoding p53 (TP53) alter its transcriptional activity, which in turn may influence the UV radiation-induced tanning response. OBJECTIVE: The aim of the present work is to test association between POMC and TP53 genetic variability, the possible interplay with host factors and the risk of basal cell carcinoma of skin. METHODS: We covered the variability of the two genes we used 17 tagging polymorphisms in 529 BCC cases and 532 healthy controls. We have also tested the possible interactions between the genetic variants and three known risk factors for BCC: skin complexion, sun effect and skin response to sun exposure. RESULTS: We did not observe any statistically significant association between SNPs in these two genes and BCC risk overall, nor interactions of SNPs with known BCC risk factors. However we found that, in the group of subjects with lower sun exposure, carriers of one copy of the C allele of the TP53 SNP rs12951053 had a decreased risk of BCC (OR=0.28, 95% CI 0.12-0.62, P=0.002). CONCLUSIONS: We have observed that the interplay of an environmental risk factor and one polymorphism in TP53 gene could modulate the risk of BCC.
机译：背景：皮肤的基底细胞癌（BCC）是西方世界白种人中最常见的肿瘤。紫外线（UV）辐射诱导的p53激活通过增加皮肤中原黑皮皮质激素（POMC）的转录活性来促进皮肤色素沉着。诱导POMC /α黑素细胞刺激激素（α-MSH）激活黑皮质素1受体（MC1R），导致皮肤色素沉着。肿瘤抑制因子p53在维持基因组稳定性的应激反应中起关键作用，对包括DNA损伤，缺氧，代谢应激和癌基因激活在内的多种损伤做出反应。 p53途径的功能异常是人类肿瘤的普遍特征。编码p53（TP53）的基因中的多态性会改变其转录活性，进而可能影响UV辐射诱导的晒黑反应。目的：本研究的目的是测试POMC和TP53基因变异之间的关联，与宿主因素的可能相互作用以及皮肤基底细胞癌的风险。方法：我们报道了529个BCC病例和532个健康对照者使用17个标签多态性的两个基因的变异性。我们还测试了遗传变异与BCC的三个已知危险因素之间可能的相互作用：皮肤肤色，日晒作用和皮肤对日晒的反应。结果：我们没有观察到这两个基因中的SNP与总体BCC风险之间有任何统计学上的显着关联，也没有观察到SNP与已知BCC危险因素的相互作用。但是，我们发现，在较低阳光照射的受试者组中，TP53 SNP rs12951053的一个C等位基因拷贝的携带者降低了BCC的风险（OR = 0.28，95％CI 0.12-0.62，P = 0.002） 。结论：我们已经观察到，环境危险因素和TP53基因的一个多态性之间的相互作用可以调节BCC的风险。

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