在众多癌症类型中，皮肤癌是最常见的类型之一。美国人一生中患皮肤癌的风险几率高达20%。大多数皮肤癌是由太阳光紫外线直接损伤DNA，引起C→T和CC→TT突变，形成环丁烷嘧啶二聚体所造成。 

传统认为，环丁烷嘧啶二聚体中胞嘧啶或5’甲基胞嘧啶迅速脱氨基形成尿嘧啶或胸腺嘧啶是皮肤癌基因突变的机制；而且普遍认为一旦离开太阳光，紫外线的损伤就会停止。

但是，华盛顿大学的学者在《科学》杂志3月份刊出的最新研究结果证明，事实并非如此。即使避开阳光，紫外线通过其他途径，仍然持续损伤皮肤细胞的DNA。这一重大研究结果揭示了黑色素瘤的形成机制。

美捷登：Mike

原文信息

Chemiexcitation of melanin derivativesinduces DNA photoproducts long after UV exposure

Science20 February 2015: Vol. 347 no. 6224 pp. 842-847

Mutations in sunlight-induced melanomaarise from cyclobutane pyrimidine dimers (CPDs), DNA photoproducts that aretypically created picoseconds after an ultraviolet (UV) photon is absorbed atthymine or cytosine. We found that in melanocytes, CPDs are generated for >3hours after exposure to UVA, a major component of the radiation in sunlight andin tanning beds. These “dark CPDs” constitute the majority of CPDsand include the cytosine-containing CPDs that initiate UV-signature C→T mutations. Dark CPDs arise when UV-induced reactive oxygen andnitrogen species combine to excite an electron in fragments of the pigmentmelanin. This creates a quantum triplet state that has the energy of a UVphoton but induces CPDs by energy transfer to DNA in a radiation-independentmanner. Melanin may thus be carcinogenic as well as protective against cancer.These findings also validate the long-standing suggestion that chemicallygenerated excited electronic states are relevant to mammalian biology.

原文链接：

http://www.sciencemag.org/content/347/6224/842.abstract 

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