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 AKs.What's already known about this topic?
Solar elastosis and p53 expression were higher and VDR expression was lower in patients than in HCs; however, there was no statistical difference between them in relation to the pathological grade of AK.
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 purpose of this study was to investigate whether the expression of apoptosis-associated molecules such as Erdr1, p53 and bcl-2 was affected by the treatment of ingenol mebutate in AK.
To investigate the potential roles of PTTG1 in epidermal carcinogenesis and malignant progression, the expression of PTTG1 was analysed by immunohistochemistry along with Ki67, keratin 10 (K10) and p53 in tissue samples of cutaneous squamous cell carcinomas (SCC), actinic keratoses (AK) and Bowen's disease (BD).
Furthermore, with regard to p53 expression, two groups of lesions exist: one showing a low level of expression of p53 that includes normal skin, skin with various degrees of SE and SCC from sun-protected areas, and a second group showing a high level of expression that includes SK and SCC occurring on sun-damaged skin.
The evaluation of a large number of AK specimens in this study have found a low gene mutation rate in low-graded AK lesions. p53 mutations rather than p16(INK4a) and/or Ha-ras mutations may be an early event in the development of AK to cutaneous SCC.
Molecular analyses of melanoma in situ and of solar keratosis, a prototype of early SCC in situ, show that loss of p16(INK4a)/p14(ARF) and dysfunction of p53 play a critical role, respectively.
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.
We conclude that inhibition of the premalignant AK lesions as well as a reduction in the expression of p53 and in spermidine concentrations may serve as surrogate endpoint biomarkers of DFMO and possibly other topically administered skin cancer chemopreventive agents.
The specific effect of UVR on the p53 tumor suppressor gene, including its impact on apoptosis, in humans, and in animals, suggests a cause-effect relationship between UVR and the earliest mutations seen in AKs.
We searched for p16, Cdk4 and p53 gene mutations in 20 squamous cell carcinomas (SSCs), 1 actinic keratosis (AK), and 28 basal cell carcinomas (BCCs), using PCR-SSCP.
Surprisingly, skin found to harbor p53 clones showed no clusters of Ki67 positive cells, unlike the situation for actinic keratoses or basal cell carcinomas.
It is concluded that aberrations of the p53 gene and ras genes are induced through independent processes of ultraviolet irradiation in the course of carcinogenic change from solar keratosis to squamous cell carcinoma.