Department of Dermatology and Cutaneous Surgery, University of Miami Miller School of Medicine, Miami, Florida, USA.
J Am Acad Dermatol. 2013 Jan;68(1 Suppl 1):S10-9. doi: 10.1016/j.jaad.2012.09.053.
Actinic keratoses are proliferations of transformed neoplastic keratinocytes in the epidermis that are the result of cumulative ultraviolet (UV) radiation from sun exposure. They are commonly found on sites of sun-exposed skin such as the face, balding scalp, and back of the hand. Although UV exposure does exert certain beneficial effects on the skin, excessive exposure to UV radiation induces multiple cascades of molecular signaling events at the cellular level that produce inflammation, immunosuppression, failure of apoptosis, and aberrant differentiation. Cumulatively, these actions result in mutagenesis and, ultimately, carcinogenesis. This article provides a brief overview of the key mediators that are implicated in the pathobiology of actinic keratosis. Three evolutionary possibilities exist for these keratoses in the absence of treatment: (1) spontaneous remission, which can be common; (2) remaining stable, without further progression; or (3) transformation to invasive squamous cell carcinoma, which may metastasize. Because the effects of UV radiation on the skin are complex, it is not yet fully clear how all of the mediators of actinic keratosis progression are interrelated. Nonetheless, some represent potential therapeutic targets, because it is clear that directing therapy to the effects of UV radiation at a number of different levels could interrupt and possibly reverse the mechanisms leading to malignant transformation.
光化性角化病是表皮中转化性肿瘤角质形成细胞的增殖，是由于暴露于阳光的紫外线（UV）辐射的累积所致。它们通常出现在暴露于阳光的皮肤部位，如面部、脱发的头皮和手背。虽然紫外线暴露对皮肤有一定的有益作用，但过度暴露于紫外线辐射会在细胞水平上产生多种级联的分子信号事件，导致炎症、免疫抑制、细胞凋亡失败和异常分化。这些作用累积起来会导致突变，并最终导致癌变。本文简要概述了光化性角化病发病机制中涉及的关键介质。如果不治疗，这些角化病有三种进化的可能性：（1）自发缓解，这是常见的；（2）保持稳定，没有进一步进展；或（3）转化为侵袭性鳞状细胞癌，可能转移。由于紫外线对皮肤的影响很复杂，目前还不完全清楚光化性角化病进展的所有介质是如何相互关联的。尽管如此，一些代表潜在的治疗靶点，因为很明显，针对紫外线在多个不同水平的影响进行治疗可以中断并可能逆转导致恶性转化的机制。
