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Actinic Keratosis: Current Concepts in Pathogenesis, Risk Stratification, Management, and Prevention.

Created on 13 Nov 2026

Authors

Amrita Sandhu, Chiamaka C Ogbuefi, Devendra K Agrawal

Published in

Journal of cancer science and clinical therapeutics. Volume 10. Issue 3. Pages 98-116. Epub Sep 02, 2026.

Abstract

Actinic keratosis (AK) is among the most frequently encountered premalignant skin lesions in clinical practice and is now widely regarded as part of the biologic spectrum that can progress to cutaneous squamous cell carcinoma (cSCC). The global prevalence of AK continues to increase because of aging populations, cumulative ultraviolet (UV) radiation exposure, and increasing survival of high-risk populations, highlighting its growing public health impact. Advances in molecular and cellular research have expanded the understanding of AK pathogenesis, demonstrating that chronic UV-induced DNA damage, oxidative stress, immune dysregulation, and field cancerization interact to drive the development and progression of dysplastic keratinocytes. Despite the availability of multiple lesion-directed and field-directed treatment options, management remains challenging because of disease recurrence, patient adherence, variability in treatment response, and the inability to reliably identify which lesions are most likely to progress to invasive cSCC. Emerging molecular biomarkers, genomic profiling, noninvasive imaging technologies, and novel therapeutic strategies have the potential to improve individualized risk assessment and treatment selection but require further clinical validation before widespread implementation. This critical review provides a comprehensive overview of the current understanding of AK, including its epidemiology, risk factors, pathogenesis, progression to cSCC, risk stratification, contemporary treatment approaches, barriers to effective management, preventive strategies, and future directions. Continued integration of molecular insights with patient-centered care may improve early detection, personalize therapeutic decision-making, and reduce the burden of keratinocyte carcinogenesis.

PMID:
43022671
Bibliographic data and abstract were imported from PubMed on 13 Nov 2026.

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