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黑色素瘤及相关遗传性癌症综合征中的种系非CDKN2A变异体

Germline Non-CDKN2A Variants in Melanoma and Associated Hereditary Cancer Syndromes.

作者信息

Fiasconaro Chiara Anna, Carbone Alice, Giordano Silvia, Cavallo Francesco, Fava Paolo, Pasini Barbara, Yakymiv Yuliya, Marchisio Sara, Quaglino Pietro, Ribero Simone, Roccuzzo Gabriele

机构信息

Department of Medical Sciences, Section of Dermatology, University of Turin, 10126 Turin, Italy.

Medical Genetics Unit, AOU 'Città Della Salute e Della Scienza', 'Molinette' Hospital, 10126 Turin, Italy.

出版信息

Diseases. 2025 Jun 9;13(6):180. doi: 10.3390/diseases13060180.

Abstract

The etiology of melanoma is multifactorial and arises from the interplay of genetic, phenotypic, and environmental factors. The genetic predisposition to melanoma is influenced by a complex interaction among genes exhibiting varying levels of penetrance (high, moderate, and low), each contributing differently to the susceptibility of the disease. Furthermore, penetrance may vary based on the incidence of melanoma across diverse populations and geographical regions. Advances in genetic sequencing technologies have facilitated the identification of novel genes potentially associated with melanoma, as well as the characterization of relevant germline variants. While the most extensively researched variant is CDKN2A, recent studies have highlighted other variants unrelated to CDKN2A as significant areas of investigation. Among them, high-penetrance genes encompass CDK4, BAP1, POT1, TERT, ACD, and TERF2IP. In contrast, moderate-penetrance genes include MC1R, MITF, and SLC45A2, while low-penetrance genes consist of OCA2, TYRP1, and TYR. In addition to elevating the risk of melanoma, these genetic alterations may also predispose individuals to internal neoplasms. This review aims to provide a comprehensive overview of the definitions of sporadic, multiple primary, familial, and hereditary melanoma, with a particular emphasis on non-CDKN2A germline variants and their dermoscopic and phenotypic features.

摘要

黑色素瘤的病因是多因素的,源于遗传、表型和环境因素的相互作用。黑色素瘤的遗传易感性受到不同外显率(高、中、低)基因之间复杂相互作用的影响,每种基因对疾病易感性的贡献各不相同。此外,外显率可能因不同人群和地理区域的黑色素瘤发病率而异。基因测序技术的进步有助于鉴定可能与黑色素瘤相关的新基因,以及对相关种系变异进行特征描述。虽然研究最广泛的变异是CDKN2A,但最近的研究强调了其他与CDKN2A无关的变异是重要的研究领域。其中,高外显率基因包括CDK4、BAP1、POT1、TERT、ACD和TERF2IP。相比之下,中等外显率基因包括MC1R、MITF和SLC45A2,而低外显率基因包括OCA2、TYRP1和TYR。除了增加黑色素瘤的风险外,这些基因改变还可能使个体易患内部肿瘤。本综述旨在全面概述散发性、多发性原发性、家族性和遗传性黑色素瘤的定义,特别强调非CDKN2A种系变异及其皮肤镜和表型特征。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e416/12191738/866843bd1180/diseases-13-00180-g001.jpg

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