Circadian Rhythm Disruption and Cutaneous Carcinogenesis

Circadian rhythms regulate DNA repair, cell-cycle control, apoptosis, pigmentation, barrier function, and immune surveillance in skin, and their disruption may increase susceptibility to ultraviolet-induced carcinogenesis.

This narrative review synthesizes mechanistic, experimental, epidemiologic, and translational studies on circadian rhythm disruption and skin neoplasms, with emphasis on melanoma and nonmelanoma skin cancer.

Core clock genes such as CLOCK, BMAL1, PER, and CRY orchestrate daily oscillations in cutaneous physiology, including nucleotide excision repair and inflammatory signaling. Experimental studies show that ultraviolet (UV) exposure during circadian phases with low DNA repair capacity produces more persistent lesions and more tumors, while human meta-analytic evidence suggests a modest increase in melanoma risk among shift workers. Evidence for basal cell carcinoma and squamous cell carcinoma is less consistent, likely because of differences in UV exposure, occupation, and confounding by behavior.

Circadian disruption is a plausible modifier of skin cancer risk, particularly for melanoma, through effects on UV DNA repair, immune surveillance, melatonin signaling, and tumor biology. Further prospective studies using objective circadian biomarkers and dermatology-specific endpoints are needed.