Photocarcinogenesis: UVA vs. UVB radiation
Photocarcinogenesis: UVA vs. UVB radiation
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DOI：
10.1159/000064535
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发表时间：
2002-09-01
期刊：
影响因子：
--
通讯作者：
de Gruijl, FR
中科院分区：
文献类型：
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作者：
de Gruijl, FR
最近的研究揭示了皮肤癌中基因改变或缺失导致致癌和肿瘤抑制信号通路受到干扰的组合：突变的 PTCH（在促有丝分裂 Sonic Hedgehog 通路中）和基底细胞癌 (BCC) 中的突变 p53 肿瘤抑制基因，可能是激活的促有丝分裂 RAS 通路和鳞状细胞癌中的突变 p53 (SCC)，并且可能是皮肤黑色素瘤中激活的 MET/RAS 通路和失活的 p16(INK4a) 肿瘤抑制因子。紫外线辐射会损伤 DNA，并可能引起基因组改变，从点突变到粗染色体错位。在 SCC 诱导实验中，UVB 辐射（波段 280-315 nm）比 UVA 辐射（315-400 nm）的致癌性更强。从人类鳞状细胞癌和基底细胞癌中发现的 p53 特征点突变可以清楚地推断出 UVB 辐射的影响。与 UVB 辐射相反，UVA 辐射的大部分诱变和致癌作用似乎是通过活性氧 (ROS) 介导的。实验表明，UVA1（340-400 nm）暴露在很大程度上没有 p53 特征点突变的情况下诱发 SCC。 UVB 和 UVA 辐射都会引起 ROS 相关的点突变（例如 G 到 T）和粗略的基因组改变（例如缺失），这些改变可能不会被认为是由 UV 辐射引起的。版权所有 (C) 2002 S. Karger AG，巴塞尔。
Recent research is revealing combinations of disturbed oncogenic and tumor-suppressive signaling pathways by altered or missing genes in skin cancers: mutated PTCH (in the mitogenic Sonic Hedgehog pathway) and mutated p53 tumor suppressor gene in basal cell carcinomas (BCC), possibly an activated mitogenic RAS pathway and mutated p53 in squamous cell carcinomas (SCC), and possibly an activated MET/RAS pathway and inactive p16(INK4a) tumor suppressor in cutaneous melanomas. UV radiation damages DNA and can give rise to genomic alterations, varying from point mutations to crude chromosomal dislocations. UVB radiation (wavelength band 280-315 nm) is more carcinogenic than UVA radiation (315-400 nm) in experimental induction of SCC. The impact of UVB radiation can be clearly inferred from the characteristic point mutations in p53 found in human SCC and BCC. In contrast to UVB radiation, much of the mutagenic and carcinogenic action of UVA radiation appears to be mediated through reactive oxygen species (ROS). Experiments have shown that UVA1 (340-400 nm) exposure induces SCC largely without the characteristic point mutations in p53. Both UVB and UVA radiation can give rise to ROS-related point mutations (e.g. G to T) and crude genomic alterations (e.g. deletions) which may not be recognized as caused by UV radiation. Copyright (C) 2002 S. Karger AG, Basel.