Advancements in elucidating the pathogenesis of actinic keratosis: present state and future prospects

Abstract

Solar keratosis, also known as actinic keratosis (AK), is becoming increasingly prevalent. It is a benign tumor that develops in the epidermis. Individuals with AK typically exhibit irregular, red, scaly bumps or patches as a result of prolonged exposure to UV rays. These growths primarily appear on sun-exposed areas of the skin such as the face, scalp, and hands. Presently, dermatologists are actively studying AK due to its rising incidence rate in the United States. However, the underlying causes of AK remain poorly understood. Previous research has indicated that the onset of AK involves various mechanisms including UV ray-induced inflammation, oxidative stress, complex mutagenesis, resulting immunosuppression, inhibited apoptosis, dysregulated cell cycle, altered cell proliferation, tissue remodeling, and human papillomavirus (HPV) infection. AK can develop in three ways: spontaneous regression, persistence, or progression into invasive cutaneous squamous cell carcinoma (cSCC). Multiple risk factors and diverse signaling pathways collectively contribute to its complex pathogenesis. To mitigate the risk of cancerous changes associated with long-term UV radiation exposure, prompt identification, management, and prevention of AK are crucial. The objective of this review is to elucidate the primary mechanisms underlying AK malignancy and identify potential treatment targets for dermatologists in clinical settings.

An Update on Non-Invasive Skin Imaging Techniques in Actinic Keratosis—A Narrative Review

“…The main factor for developing actinic keratoses is UV radiation. After the intermittent exposure to sunlight and the constant oxidative stress that occurs in the cells, the dysplastic intraepidermal keratinocytes proliferate, and this process is enhanced by factors such as DNA damage, inflammation, immunosuppression, and mutagenesis [12]. This phenomenon also occurs on the molecular level since UVB can affect the tumor suppressor proteins such as p53, p16INK4a, and PTEN, which also contribute to the progression to a malignant entity [13].…”