Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
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.

PubMed Disclaimer

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.
See this image and copyright information in PMC

References

    1. Hansen V. Spectral distribution of solar radiation on clear days: a comparison between measurements and model estimates. J Climate Appl Meteor. 1984;23(5):772–780.
    1. Diffey BL. Ultraviolet radiation and human health. Clin Dermatol. 1998;16(1):83–89. - PubMed
    1. Jussila A, Huotari‐Orava R, Ylianttila L, Partonen T, Snellman E. Narrow‐band ultraviolet B radiation induces the expression of β‐endorphin in human skin in vivo. J Photochem Photobiol B Biol. 2016;155:104–108. - PubMed
    1. Kalajian TA, Aldoukhi A, Veronikis AJ, Persons K, Holick MF. Ultraviolet B light emitting diodes (LEDs) are more efficient and effective in producing vitamin D3 in human skin compared to natural sunlight. Sci Rep. 2017;7(1):11489. - PMC - PubMed
    1. Valejo Coelho MM, Matos TR, Apetato M. The dark side of the light: mechanisms of photocarcinogenesis. Clin Dermatol. 2016;34(5):563–570. - PubMed

Substances