Chronic low dose UV exposure and p53 mutation: tilting the odds in early epidermal preneoplasia?
Chronic low dose UV exposure and p53 mutation: tilting the odds in early epidermal preneoplasia?
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DOI：
10.3109/09553002.2012.699697
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发表时间：
2012-10
影响因子：
2.6
通讯作者：
Jones PH
中科院分区：
文献类型：
--
作者：
Roshan A;Jones PH
本文综述了TP53基因突变和紫外光如何改变早期表皮瘤前病变中正常祖细胞的行为。癌症被认为是从单个突变细胞进化而来，这些突变细胞扩展成克隆并最终形成肿瘤。虽然恶性病变中的突变已被深入研究，但对瘤前病变的早期阶段以及环境因素如何促进突变细胞克隆的扩展知之甚少。在这里，我们回顾了紫外线辐射不仅产生新的突变，而且驱动在长期暴露的表皮中发现的众多p53突变克隆的指数增长的证据。已发表的数据与表皮稳态的新范式相一致，该范式为突变细胞的行为提供了见解。我们还考虑了为什么如此少的突变细胞进展为肿瘤的原因，并讨论了这些发现对癌症预防的意义。
This review addresses how mutation of the TP53 gene (p53) and ultraviolet light alter the behavior of normal progenitor cells in early epidermal preneoplasia. Cancer is thought to evolve from single mutant cells, which expand into clones and ultimately into tumors. While the mutations in malignant lesions have been studied intensively, less is known about the earliest stages of preneoplasia, and how environmental factors may contribute to drive expansion of mutant cell clones. Here we review the evidence that ultraviolet radiation not only creates new mutations but drives the exponential growth of the numerous p53 mutant clones found in chronically exposed epidermis. Published data is reconciled with a new paradigm of epidermal homeostasis which gives insights into the behavior of mutant cells. We also consider the reasons why so few mutant cells progress into tumors and discuss the implications of these findings for cancer prevention.
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