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PubMed2004

The expression of p63 in actinic keratoses, seborrheic keratosis, and cutaneous squamous cell carcinomas.

BACKGROUND: p63 is a tumor suppressor that likely plays a role in the development of squamous cell carcinomas (SCCs) and possibly premalignant and benign skin tumors. Little data is available on its expression in these tumors. OBJECTIVE: To study the keratinocyte expression profile of p63 in 17 SCCs, 7 actinic keratoses, 2 Bowens tumors, and 7 seborrheic keratoses. METHODS: Skin tumors specimens were stained with an antibody to p63. Quantitative and qualitative data was collected on the staining. RESULTS: There was a statistically significant increase in p63 staining of SCCs when compared with normal. Seborrheic keratoses and actinic keratoses showed a trend towards increased expression in the basal layer compared with normal skin. The pattern of expression showed diffuse staining in SCCs. In actinic keratoses and seborrheic keratoses the pattern was most prominent in the basal layer. CONCLUSIONS: p63 expression is greater and different in SCCs when compared with normal skin, actinic keratoses, and seborrheic keratoses. Interestingly seborrheic keratoses and Bowens lesions showed expression that was mostly restricted to the basal layer, however significant diffuse staining was also noted. Our results support the notion that p63 plays a role in cell differentiation and tumorigenesis of skin tumors.

Biomarkers, Tumor↗

PubMed1995

Cyclin D and retinoblastoma gene product expression in actinic keratosis and cutaneous squamous cell carcinoma in relation to p53 expression.

Abnormality of the molecules regulating the cell cycle has been shown to lead cells to transformation. Recently, overexpression of cyclin D protein, one of the G1 cyclins, and the abnormality of the retinoblastoma gene have been found in various human cancers. We analyzed the expression of cyclin D, retinoblastoma gene product (pRB) and p53 in actinic keratoses (AKs) and cutaneous squamous cell carcinomas (SCCs) by immunohistochemistry to elucidate the role of these molecules in keratinocyte carcinogenesis. In the normal epidermis, a few cyclin D positive cells were seen mainly at the basal layer. In 11 seborrheic keratoses, no overexpression of cyclin D was observed. Twelve of 26 AKs (46%) and 27 of 45 SCCs (60%) showed cyclin D overexpression. A few pRB positive cells were seen in the basal layer and in the suprabasal spinous layer of the normal epidermis. An abnormality of pRB, loss of expression, was seen in 2 of 26 AKs (8%) and 7 of 45 SCCs (16%). p53 protein was positive in 12 of 26 AKs (46%) and 24 of 45 SCCs (53%). Forty-five SCCs examined were divided into 22 ultraviolet (UV)-related SCCs and 23 UV-unrelated SCCs. Though UV-related SCCs showed a significantly higher incidence of p53 positivity, as previously reported by us, no significant difference in cyclin D overexpression and loss of the pRB expression was observed between UV-related and UV-unrelated SCCs. These results suggest that cyclin D overexpression is frequently involved in keratinocyte carcinogenesis and that this is an early event, as well as p53 abnormality. In addition, abnormality of the retinoblastoma gene is also related to epidermal cell carcinogenesis, though the frequency is relatively low.

Carcinoma, Squamous Cell↗

PubMed1958