Department of Carcinogenesis, University of Texas MD Anderson Cancer Center, Smithville, TX 78957, USA.
Proc Natl Acad Sci U S A. 2010 May 18;107(20):9329-34. doi: 10.1073/pnas.1000324107. Epub 2010 May 3.
We examined the wavelength dependence of ultraviolet (UV) ra-diation (UVR)-induced melanoma in a Xiphophorus backcross hybrid model previously reported to be susceptible to melanoma induction by ultraviolet A (UVA) and visible light. Whereas ultraviolet B (UVB) irradiation of neonates yielded high frequencies of melanomas in pigmented fish, UVA irradiation resulted in melanoma frequencies that were not significantly different from unirradiated fish. Spontaneous and UV-induced melanoma frequencies correlated with the degree of pigmentation as expected from previous studies, and the histopathology phenotypes of the melanomas were not found in significantly different proportions in UV-treated and -untreated tumor-bearing fish. Our results support the conclusion that a brief early-life exposure to UVB radiation causes melanoma formation in this animal model. These data are consistent with an essential role for direct DNA damage, including cyclobutane dimers and (6-4) photoproducts, in the etiology of melanoma.
我们研究了先前报道的易患黑色素瘤的 Xiphophorus 回交杂种模型中紫外线(UV)辐射(UVR)诱导的黑色素瘤的波长依赖性,该模型易受紫外线 A(UVA)和可见光诱导黑色素瘤。虽然对新生儿进行紫外线 B(UVB)照射会导致色素鱼中黑色素瘤的高发频率,但 UVA 照射导致的黑色素瘤频率与未照射鱼没有显著差异。正如先前研究预期的那样,自发和 UV 诱导的黑色素瘤频率与色素沉着程度相关,并且在接受和未接受 UV 处理的肿瘤携带鱼中,黑色素瘤的组织病理学表型没有以显著不同的比例存在。我们的结果支持这样的结论,即短暂的早期生命暴露于 UVB 辐射会导致这种动物模型中黑色素瘤的形成。这些数据与直接 DNA 损伤(包括环丁烷二聚体和(6-4)光产物)在黑色素瘤病因学中的重要作用一致。