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紫外线辐射在恶性黑色素瘤发生发展中的机制。

The mechanisms of UV radiation in the development of malignant melanoma.

作者信息

Situm Mirna, Buljan Marija, Bulić Suzana Otanić, Simić Dubravka

机构信息

Department of Dermatology and Venereology, University Hospital "Sestre Milosrdnice", Zagreb, Croatia.

出版信息

Coll Antropol. 2007 Jan;31 Suppl 1:13-6.

Abstract

The sunlight was one of the first agents recognized to be carcinogenic for humans. There is convincing evidence from epidemiologic studies that exposure to solar radiation is the major cause of cutaneous melanoma in light-pigmented populations and plays a role in the increasing incidence of this malignancy. The molecular mechanisms by which UV radiation exerts its varied effects are not completely understood, however, it is considered that UVA and UVB are equally critical players in melanoma formation. Whereas UVA can indirectly damage DNA through the formation of reactive oxygen radicals, UVB can directly damage DNA causing the apoptosis of keratinocytes by forming the sunburn cells. Besides action through mutations in critical regulatory genes, UV radiation may promote cancer through indirect mechanisms, e.g. immunosuppression and dysregulation of growth factors. The carcinogenic process probably involves multiple sequential steps, some, but not all of which involve alterations in DNA structure.

摘要

阳光是最早被认定对人类具有致癌性的因素之一。流行病学研究提供了令人信服的证据,表明暴露于太阳辐射是浅肤色人群皮肤黑色素瘤的主要病因,且在这种恶性肿瘤发病率上升中起作用。然而,紫外线辐射产生多种效应的分子机制尚未完全明确,不过,人们认为UVA和UVB在黑色素瘤形成过程中同样起着关键作用。UVA可通过形成活性氧自由基间接损伤DNA,而UVB则可直接损伤DNA,通过形成晒伤细胞导致角质形成细胞凋亡。除了通过关键调控基因突变起作用外,紫外线辐射还可能通过间接机制促进癌症发生,例如免疫抑制和生长因子失调。致癌过程可能涉及多个连续步骤,其中一些(但并非全部)涉及DNA结构改变。

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