Models and mechanisms in malignant melanoma

被引：19
作者：
Benjamin, Cara L.
Melnikova, Vladislava O.
Ananthaswamy, Honnavara N.
机构：
[1] Univ Texas, MD Anderson Canc Ctr, Dept Immunol, Houston, TX 77030 USA
[2] Univ Texas, MD Anderson Canc Ctr, Dept Canc Biol, Houston, TX 77030 USA
来源：
MOLECULAR CARCINOGENESIS | 2007年 / 46卷 / 08期
关键词：
PTEN; RAS; BRAF; melanoma; UV radiation;
D O I：
10.1002/mc.20353
中图分类号：
Q5 [生物化学]; Q7 [分子生物学];
学科分类号：
071010 ; 081704 ;
摘要：
Human melanoma represents the fastest growing malignancy in the US. The etiology of melanoma is highly debated as is the role of ultraviolet (UV) radiation in the initiation and progression of melanoma. This article discusses data from UV exposure and its relationship to the development of melanoma from various models of melanoma as well as various genetic alterations seen In oncogenic transformation of melanocytes. Genetic alterations such as the p16(INK4a) deletion, melanocortin 1 receptor (MC1R), RAS, and v-raf murine sarcoma viral oncogene homolog B1 (BRAF) may be indicative of a predisposition to melanoma development. Historical research as well as current data on the significance of the hot spot mutation in BRAF is discussed in its relative potential to the activating mutation in RAS. (c) 2007 Wiley-Liss, Inc.
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收藏
页码：671 / 678
页数：8
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