Walker Graeme J, Khosrotehrani Kiarash
Experimental Dermatology Group, The University of Queensland Frazer Institute, Woolloongabba, Queensland, Australia.
Photodermatol Photoimmunol Photomed. 2025 May;41(3):e70024. doi: 10.1111/phpp.70024.
Although a role for ultraviolet radiation (UVR) in cutaneous malignant melanoma (CMM) development is accepted, there is debate over the magnitude and mechanisms given its association with intermittent but not chronic exposure.
To assess new ideas and data on the subject, review some debated topics, bringing a molecular view to epidemiological observations.
We reviewed some recent advances in the field of epidemiology and genetics, including phenome-wide association studies, evolutionary genetics related to skin cancer, and mechanisms of UVR-induced DNA adduct formation.
High rates of CMM are strongly correlated with light colored skin across the globe. CMM shares risk factors associated with UVR sensitivity with keratinocyte cancer (KC). CMM risk is dominated by MC1R, a gene regulating the proportions of black and red melanin produced. An emerging mutagenic mechanism involves reactive melanin, particularly red pheomelanin, that can itself induce DNA adducts.
Demographically, epidemiologically, and mechanistically, pigmentation status is central to CMM risk and a shared genetic susceptibility, comprising several pigmentation genes, between CMM and KCs. In the general population, CMM risk is associated with pale skin and poor tanning ability, mechanistically due to a relative lack of protection against UVR adduct formation, or perhaps via an alternate manner in individuals with abundant pheomelanin. Overall, evidence suggests that UVR exposure impacts CMM risk.
尽管紫外线辐射(UVR)在皮肤恶性黑色素瘤(CMM)发生中的作用已被认可,但鉴于其与间歇性而非慢性暴露的关联,关于其影响程度和机制仍存在争议。
评估该主题的新观点和数据,回顾一些有争议的话题,从分子角度审视流行病学观察结果。
我们回顾了流行病学和遗传学领域的一些最新进展,包括全表型关联研究、与皮肤癌相关的进化遗传学以及UVR诱导DNA加合物形成的机制。
全球范围内,CMM的高发病率与浅色皮肤密切相关。CMM与角质形成细胞癌(KC)具有与UVR敏感性相关的共同风险因素。CMM风险主要由MC1R基因决定,该基因调节黑色和红色黑色素的生成比例。一种新出现的诱变机制涉及反应性黑色素,尤其是红色褐黑素,其本身可诱导DNA加合物形成。
从人口统计学、流行病学和机制学角度来看,色素沉着状态对于CMM风险以及CMM和KCs之间共同的遗传易感性(包括多个色素沉着基因)至关重要。在一般人群中,CMM风险与皮肤白皙和晒黑能力差有关,其机制是相对缺乏对UVR加合物形成的保护,或者可能是通过褐黑素丰富个体的另一种方式。总体而言,有证据表明UVR暴露会影响CMM风险。