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Review
. 2025 Apr;41(4):e12946.
doi: 10.1002/kjm2.12946. Epub 2025 Feb 5.

Photocarcinogenesis of the skin: Current status and future trends

Ting-Ting Yang  1 , Cheng-Che E Lan  2
Affiliations
Review

Photocarcinogenesis of the skin: Current status and future trends

Ting-Ting Yang et al. Kaohsiung J Med Sci. 2025 Apr.

Abstract

Solar radiation is essential for life on Earth but is also a major contributor to skin carcinogenesis. Solar radiation, particularly ultraviolet (UV) B (280-320 nm) and UVA (320-400 nm), induces photocarcinogenesis via various pathways. UV light can directly cause DNA damage, resulting in genetic mutations if not repaired correctly. UV light can also induce photocarcinogenesis by generating reactive oxygen species, inducing immunosuppression and inflammation. Recently, visible light (400-760 nm) has been shown to contribute to photocarcinogenesis by activating oxidative pathways. In addition to the irradiation dose (fluence, J/m2), UVB irradiance (W/m2) is also considered a factor influencing photocarcinogenesis. In this review, we summarize the mechanisms of photocarcinogenesis and provide strategies to prevent skin cancer.

Keywords: skin cancer; ultraviolet radiation; visible light.

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Conflict of interest statement

The authors declare no conflicts of interest.

Figures

FIGURE 1
FIGURE 1
Summary of cutaneous photocarcinogenesis mechanisms. Ultraviolet A (UVA) and ultraviolet B (UVB) induce photocarcinogenesis by triggering DNA damage, oxidative stress, immunosuppression, and inflammatory pathway activation. Visible light (VL) also contributes to photocarcinogenesis by inducing oxidative stress. CPD, cyclobutane‐pyrimidine dimer; MIF, macrophage inhibitory factor; NOS, nitric oxide synthase; NOX, nicotinamide adenine dinucleotide phosphate oxidase; PAF, platelet‐activating factor; 6‐4PP, 6–4 photoproducts.
FIGURE 2
FIGURE 2
Fluence (J/m2) is the product of irradiance (W/m2) and total irradiation time (s). Prolonged exposure time is required to achieve equivalent fluence for low irradiance ultraviolet B (LIUVB) irradiation (blue area) compared to high irradiance ultraviolet B (HIUVB) irradiation (red area).
FIGURE 3
FIGURE 3
Low irradiance ultraviolet B (LIUVB) induces more aberrant epidermal cell proliferation and tumor burden than high irradiance ultraviolet B (HIUVB) by inducing more reactive oxygen species (ROS) and cyclobutane pyrimidine dimer (CPD) formation.
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