Genetics of melanoma progression: the rise and fall of cell senescence

被引：58

作者：

Bennett, Dorothy C. ^{[1
]}

机构：

[1] Univ London, Mol Cell Sci Res Ctr, Cranmer Terrace, London, England

来源：

PIGMENT CELL & MELANOMA RESEARCH | 2016年 / 29卷 / 02期

基金：

英国惠康基金;

关键词：

melanoma; nevus; senescence; p16; TERT; immortalization; metamortal; CUTANEOUS MALIGNANT-MELANOMA; ONCOGENE-INDUCED SENESCENCE; TERT PROMOTER MUTATIONS; DNA-DAMAGE RESPONSE; TUMOR-SUPPRESSOR; MELANOCYTIC NEVI; TRANSCRIPTION FACTOR; RECURRENT MUTATIONS; TELOMERASE ACTIVITY; GERMLINE MUTATION;

D O I：

10.1111/pcmr.12422

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

There are many links between cell senescence and the genetics of melanoma, meaning both familial susceptibility and somatic-genetic changes in sporadic melanoma. For example, CDKN2A, the best-known melanoma susceptibility gene, encodes two effectors of cell senescence, while other familial melanoma genes are related to telomeres and their maintenance. This article aimed to analyze our current knowledge of the genetic or epigenetic driver changes necessary to generate a cutaneous metastatic melanoma, the commonest order in which these occur, and the relation of these changes to the biology and pathology of melanoma progression. Emphasis is laid on the role of cell senescence and the escape from senescence leading to cellular immortality, the ability to divide indefinitely.

引用

页码：122 / 140

页数：19

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