作者: Norbert M. Wikonkal , Douglas E. Brash
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摘要: The photons of sunlight begin a series genetic events in skin leading to cancer. UV signature mutations provide an alternative inherited as way identifying genes that are involved cancer development. They augment epidemiologic and clinical data by serving molecular evidence for the role radiation carcinogenesis. Signature present TP53 PTCH, two tumor suppressor responsible non-melanoma We review clones TP53-mutated cells normal human murine epidermis exposed UVB conclude that, addition being tumorigenic mutagen, acts promoter favoring clonal expansion mutated cells. These combined actions result individuals' carrying substantial burden keratinocytes predisposed Thus involves both single-cell problem multi-cell problem; cancer, appears drive both.