Article first published online: 11 Sep 2019
Actinic keratoses ( AK s) are common premalignant skin lesions triggered by excessive ultraviolet exposure. The majority of AK s regress or persist, but some progress to squamous cell carcinomas. Biomarkers associated with their persistence, progression and regression have not been characterized.
We performed skin biopsies in patients with extensive actinic damage to identify biomarkers that correlate with clinical progression and regression of AK s.
This was an observational study of a cohort of patients with extensive actinic damage. AK s were mapped on a clear plastic template in 26 patients at months 3, 6, 9 and 11. Biopsies were taken from randomly selected, predetermined AK s and were evaluated for p53, E‐cadherin, Snail, Slug and Twist. The study is registered at Clinicaltrials.gov: NCT 00027976.
p53 exhibited greater expression in clinically apparent AK s (histological score 2·89 ± 1·45) than in regressed AK s (0·75 ± 0·96); P < 0·01. There was also significantly less membrane E‐cadherin, the lack of which is a marker of epithelial–mesenchymal transition, in clinically apparent AK s (1·89 ± 1·81) than in sun‐exposed skin (3·07 ± 1·75); P < 0·005. The E‐cadherin transcription repressors Snail, Slug and Twist were increased in AK s compared with sun‐exposed skin. A limitation of the study is that measurement of histological biomarkers was not a primary end point. In addition, patients were allowed to apply sunscreens.
At the molecular level, loss of E‐cadherin and an increase in p53 are linked to the dynamic interplay between the persistence, progression and regression of AK s.
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