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家族性黑色素瘤中已知黑色素瘤易感性基因的罕见种系变异。

Rare germline variants in known melanoma susceptibility genes in familial melanoma.

机构信息

Division of Cancer Epidemiology and Genetics, National Cancer Institute, NIH, DHHS, Bethesda, MD, USA.

Cancer Genomics Research Laboratory, Leidos Biomedical Research, Frederick National Laboratory for Cancer Research, Frederick, MD, USA.

出版信息

Hum Mol Genet. 2017 Dec 15;26(24):4886-4895. doi: 10.1093/hmg/ddx368.

Abstract

Known high-risk cutaneous malignant melanoma (CMM) genes account for melanoma risk in <40% of melanoma-prone families, suggesting the existence of additional high-risk genes or perhaps a polygenic mechanism involving multiple genetic modifiers. The goal of this study was to systematically characterize rare germline variants in 42 established melanoma genes among 144 CMM patients in 76 American CMM families without known mutations using data from whole-exome sequencing. We identified 68 rare (<0.1% in public and in-house control datasets) nonsynonymous variants in 25 genes. We technically validated all loss-of-function, inframe insertion/deletion, and missense variants predicted as deleterious, and followed them up in 1, 559 population-based CMM cases and 1, 633 controls. Several of these variants showed disease co-segregation within families. Of particular interest, a stopgain variant in TYR was present in five of six CMM cases/obligate gene carriers in one family and a single population-based CMM case. A start gain variant in the 5'UTR region of PLA2G6 and a missense variant in ATM were each seen in all three affected people in a single family, respectively. Results from rare variant burden tests showed that familial and population-based CMM patients tended to have higher frequencies of rare germline variants in albinism genes such as TYR, TYRP1, and OCA2 (P < 0.05). Our results suggest that rare nonsynonymous variants in low- or intermediate-risk CMM genes may influence familial CMM predisposition, warranting further investigation of both common and rare variants in genes affecting functionally important pathways (such as melanogenesis) in melanoma risk assessment.

摘要

已知的高风险皮肤恶性黑色素瘤(CMM)基因仅占易患黑色素瘤家族中<40%的黑色素瘤风险,这表明存在其他高风险基因,或者涉及多个遗传修饰物的多基因机制。本研究的目的是通过全外显子组测序,在 76 个无已知突变的美国 CMM 家族的 144 名 CMM 患者中,系统地描述 42 个既定的黑色素瘤基因中的罕见种系变体。我们在 25 个基因中发现了 68 个罕见的(在公共和内部对照数据集中<0.1%)非同义变体。我们技术上验证了所有预测为有害的无功能、框内插入/缺失和错义变体,并在 1,559 名基于人群的 CMM 病例和 1,633 名对照中进行了随访。这些变体中的一些在家族内显示出疾病共分离。特别有趣的是,一个家族中的六个 CMM 病例/强制性基因携带者中的五个存在 TYR 中的获得性终止突变,而一个基于人群的 CMM 病例中存在一个。PLA2G6 的 5'UTR 区域中的起始获得突变和 ATM 中的错义变体分别在一个家族中的所有三个受影响的人中存在。罕见变体负担测试的结果表明,家族性和基于人群的 CMM 患者在 TYR、TYRP1 和 OCA2 等白化病基因中具有更高频率的罕见种系变体(P<0.05)。我们的结果表明,低风险或中风险 CMM 基因中的罕见非同义变体可能会影响家族性 CMM 易感性,有必要进一步研究影响黑色素瘤风险评估中功能重要途径(如黑色素生成)的基因中的常见和罕见变体。

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