# Photoprotection for Skin Cancer: What’s New

**Authors:** Yolanda Gilaberte, Andrés Ederra-Galé, Juan J. García-Alfonso, Tamara Gracia-Cazaña

PMC · DOI: 10.3390/cancers18040634 · 2026-02-15

## TL;DR

This paper reviews new strategies for skin cancer prevention, including sunscreens, antioxidants, and DNA-repair enzymes, emphasizing the need for comprehensive photoprotection.

## Contribution

The paper provides an updated review of emerging photoprotective strategies and their effectiveness in preventing skin cancer.

## Key findings

- Daily sunscreen use reduces actinic keratoses and squamous cell carcinoma in high-risk individuals.
- DNA-repair enzymes and antioxidants like Polypodium leucotomos extract show preventive effects on skin damage and carcinogenesis.
- Visible light and broad-spectrum protection are increasingly recognized as important in skin cancer prevention.

## Abstract

Skin cancer is the most common cancer worldwide, and excessive exposure to sunlight is its main preventable cause. This review summarizes current evidence on sunscreens, oral supplements, antioxidants, and DNA-repair enzymes for preventing actinic keratoses and skin cancer. Regular daily sunscreen use reduces actinic keratoses and squamous cell carcinoma, particularly in individuals at high risk, while additional strategies may provide further benefit. Emerging evidence also suggests that visible light and other environmental factors contribute to skin damage and may play a role in skin carcinogenesis. The findings discussed here highlight the importance of comprehensive and individualized photoprotection strategies to improve skin cancer prevention and guide future research and clinical practice.

Background: Skin cancer is the most common malignancy worldwide. Although photoprotection is the cornerstone of skin cancer prevention, evidence regarding the role of other radiations different from the ultraviolet radiation and the efficacy of sunscreens, oral supplements, DNA-repair enzymes, and antioxidants continues to evolve. Objectives: To review the current evidence on photoprotective strategies and assess their role in preventing actinic keratoses (AK), keratinocyte carcinomas and melanoma. Methods: A narrative review of the literature was conducted using PubMed (2010–2025), including studies in English and Spanish. Search terms comprised “photoprotection,” “sunscreen,” “oral photoprotection,” “skin cancer,” “melanoma,” “keratinocyte cancer,” “UV radiation,” “non-melanoma skin cancer” and related concepts. Articles were selected for clinical relevance. Results: Daily sunscreen use significantly reduces AK and cutaneous squamous cell carcinoma in high-risk individuals, although evidence for basal cell carcinoma and melanoma prevention remains heterogeneous. Balanced broad-spectrum protection, including UVA and visible light filtering, seems to be important, whereas high-energy visible light needs further investigation. DNA-repair enzymes have shown reductions in cyclobutane pyrimidine dimers and clinical improvement of AK. Antioxidants such as Polypodium leucotomos extract, topical and oral, exhibit preventive effects on actinic damage and carcinogenesis. Topical and especially oral nicotinamide demonstrate chemopreventive potential in immunocompetent patients. Vulnerable populations—including transplant recipients, XP patients, individuals with albinism, and outdoor workers—require tailored photoprotection strategies with demonstrated benefit. Conclusions: Photoprotection extends far beyond UV filters, encompassing biological ingredients, antioxidants, oral supplements, and broad-spectrum strategies that target the full exposome. Comprehensive, behaviour-based photoprotection programmes are essential for high-risk groups.

## Linked entities

- **Diseases:** skin cancer (MONDO:0002898), squamous cell carcinoma (MONDO:0005096), basal cell carcinoma (MONDO:0005341), melanoma (MONDO:0005105)

## Full-text entities

- **Genes:** Il6 (interleukin 6) [NCBI Gene 16193] {aka Il-6}, CEBPB (CCAAT enhancer binding protein beta) [NCBI Gene 1051] {aka C/EBP-beta, IL6DBP, NF-IL6, TCF5}, FOSL1 (FOS like 1, AP-1 transcription factor subunit) [NCBI Gene 8061] {aka FRA, FRA1, fra-1}, Cxcr1 (C-X-C motif chemokine receptor 1) [NCBI Gene 227288] {aka Il8ra}, TP53 (tumor protein p53) [NCBI Gene 7157] {aka BCC7, BMFS5, LFS1, P53, TRP53}, SRF (serum response factor) [NCBI Gene 6722] {aka MCM1}, ELF3 (E74 like ETS transcription factor 3) [NCBI Gene 1999] {aka EPR-1, ERT, ESE-1, ESX}, ENDOV (endonuclease V) [NCBI Gene 284131], IRF1 (interferon regulatory factor 1) [NCBI Gene 3659] {aka IMD117, IRF-1, MAR}, MMP1 (matrix metallopeptidase 1) [NCBI Gene 4312] {aka CLG}, OGG1 (8-oxoguanine DNA glycosylase) [NCBI Gene 4968] {aka HMMH, HOGG1, MUTM, OGH1}, NFKB1 (nuclear factor kappa B subunit 1) [NCBI Gene 4790] {aka CVID12, EBP-1, KBF1, NF-kB, NF-kB1, NF-kappa-B1}, Ccnd1 (cyclin D1) [NCBI Gene 12443] {aka CycD1, Cyl-1, PRAD1, bcl-1, cD1}, KLF4 (KLF transcription factor 4) [NCBI Gene 9314] {aka EZF, GKLF}, COX2 (cytochrome c oxidase subunit II) [NCBI Gene 4513] {aka COII, MTCO2}, EGR1 (early growth response 1) [NCBI Gene 1958] {aka AT225, G0S30, KROX-24, NGFI-A, TIS8, ZIF-268}, TNF (tumor necrosis factor) [NCBI Gene 7124] {aka DIF, IMD127, TNF-alpha, TNFA, TNFSF2, TNLG1F}, PTGS2 (prostaglandin-endoperoxide synthase 2) [NCBI Gene 5743] {aka COX-2, COX2, GRIPGHS, PGG/HS, PGHS-2, PHS-2}, IL1A (interleukin 1 alpha) [NCBI Gene 3552] {aka IL-1 alpha, IL-1A, IL1, IL1-ALPHA, IL1F1}, PARP1 (poly(ADP-ribose) polymerase 1) [NCBI Gene 142] {aka ADPRT, ADPRT 1, ADPRT1, ARTD1, PARP, PARP-1}, NFE2L2 (NFE2 like bZIP transcription factor 2) [NCBI Gene 4780] {aka IMDDHH, NRF2, Nrf-2}, CENPX (centromere protein X) [NCBI Gene 201254] {aka CENP-X, D9, FAAP10, MHF2, STRA13}, FAS (Fas cell surface death receptor) [NCBI Gene 355] {aka ALPS1A, APO-1, APT1, CD95, FAS1, FASTM}, MTOR (mechanistic target of rapamycin kinase) [NCBI Gene 2475] {aka FRAP, FRAP1, FRAP2, RAFT1, RAPT1, SKS}, Padis4 (MMTV LTR integration site 4) [NCBI Gene 110072] {aka Pad4}, Mki67 (antigen identified by monoclonal antibody Ki 67) [NCBI Gene 17345] {aka D630048A14Rik, Ki-67, Ki67}, Il23a (interleukin 23, alpha subunit p19) [NCBI Gene 83430] {aka IL-23, p19}
- **Diseases:** SCC (MESH:D002294), pruritus (MESH:D011537), INCREASE (MESH:D000067251), SAD (MESH:D003865), carcinogenesis (MESH:D063646), Skin Cancer (MESH:D012878), cutaneous (MESH:D018366), AK (MESH:D055623), pigmentation (MESH:D010859), KC (MESH:D009369), hyperpigmentation (MESH:D017495), hypopigmentation (MESH:D017496), skin damage (MESH:D012871), pain (MESH:D010146), Melanoma (MESH:D008545), injury to (MESH:D014947), Disease (MESH:D004194), melanocytic nevi (MESH:D009508), chronic inflammation (MESH:D007249), keratinocyte carcinomas (MESH:C580062), albinism (MESH:D000417), XP (MESH:D014983), BCC (MESH:D002280), cutaneous melanoma (MESH:C562393), skin erosion (MESH:D014077), sunburn (MESH:D013471), actinic damage (MESH:D010787), nevi (MESH:D009506), cardiovascular (MESH:D002318), carcinogenic (MESH:D011230), DECREASE (MESH:D009123)
- **Chemicals:** 8-OH-dG (MESH:D000080242), Vitamin C (MESH:D001205), Resveratrol (MESH:D000077185), piroxicam (MESH:D010894), catechins (MESH:D002392), isoprenoid (MESH:D013729), CPD (MESH:D011740), ferulic acid (MESH:C004999), free radicals (MESH:D005609), Nicotinamide (MESH:D009536), linolenic acid (MESH:D017962), water (MESH:D014867), fluorouracil (MESH:D005472), eicosapentaenoic acid (MESH:D015118), lipid peroxides (MESH:D008054), azathioprine (MESH:D001379), Vitamin E (MESH:D014810), bromodeoxyuridine (MESH:D001973), lactic acid (MESH:D019344), Omega-3 fatty acids (MESH:D015525), panthenol (MESH:C007288), octatrienoic acid (MESH:C062198), Vitamin D (MESH:D014807), mycophenolate (MESH:D009173), 1,25(OH)2D (MESH:C097949), DHA (MESH:C027493), ROS (MESH:D017382), flavonoids (MESH:D005419), DMSO (MESH:D004121), imiquimod (MESH:D000077271), NAD+ (MESH:D009243), Calcitriol (MESH:D002117), melanin (MESH:D008543), alpha-tocopherol (MESH:D024502), lipid (MESH:D008055), glutathione (MESH:D005978), ATP (MESH:D000255), polyphenol (MESH:D059808), tocopherol (MESH:D024505), ergocalciferol (MESH:D004872), 8-oxo-7,8-dihydroguanine (MESH:C024829), urea (MESH:D014508), D3 (MESH:D002762), Caffeine (MESH:D002110), cyclosporine (MESH:D016572), tacrolimus (MESH:D016559), PUFA (MESH:D005231), gamma-tocopherol (MESH:D024504), SPF 100 (-), eicosanoid (MESH:D015777)
- **Species:** Mus musculus (house mouse, species) [taxon 10090], Escherichia coli (E. coli, species) [taxon 562], Micrococcus luteus (species) [taxon 1270], Homo sapiens (human, species) [taxon 9606], Tequatrovirus T4 (species) [taxon 10665]
- **Cell lines:** HaCaT — Homo sapiens (Human), Spontaneously immortalized cell line (CVCL_0038)

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Source: https://tomesphere.com/paper/PMC12939393