Finally, the absence of differences in p53 and p16 expressions is at variance with other epithelia where the classical pathway is associated with human papillomavirus infection and can be explained by the fact that both AK pathways share identical mechanisms of actinic oncogenesis.
The aims of this study were to assess (1) the relation between risk factors for carcinogenesis, sun exposure and immune status, and p16 or p53 expression, and (2) to assess differences in p16 and p53 expression between KINs and SCCs.
Six different mutations (12%) were detected in exon 2 of p16 (common to p16alpha and p16beta), in five out of 21 squamous lesions (24%) (one AK and four SCCs) and one out of 28 BCCs (3.5%).