An overview of Bcl-2 expression in histopathological variants of basal cell carcinoma, squamous cell carcinoma, actinic keratosis and seborrheic keratosis.
The Bcl-2 protein has been shown to suppress cell death and protects cell against apoptosis induced by different death-inducing signals. In this study the authors have analyzed imunohistochemically the expression of Bcl-2 protein in the histopathological variants of the most common malignant tumors of the skin--basal cell carcinoma (BCC) and squamous cell tumor (SCC), as well as in the precancerous lesion actinic keratosis (AK) and in benign tumor seborrheic keratosis (SK). Bcl-2 expression in solid, adenoid and cystic variants of BCC exhibited immunoreactivity of tumor stroma with more intense staining among peripheral palisading cells. Morphoeic variant demonstrated reduced amount of Bcl-2 expression. Among SCC in all samples, tumor tissue lack to express Bcl-2 positivity. In cases of hypertrophic and atrophic variants of AK, Bcl-2 expression was confined to basal cell layer, as well as in one case of hypertrophic variant in suprabasal cells. In three histological variants of SK expresseion of Bcl-2 protein was in areas of basaloid proliferation, while in areas of squamous differentiation was negative. In clonal variant immunostaining was positive among cells in characteristic "nests" Distribution of Bcl-2 protein expression in solid, adenoid and cystic variant of BCC showed that peripheral proliferating cells are protected against apoptosis what permits tumor growth. In morpheaform variant reduced amount of Bcl-2 expression indicated that this variant of BCC has increased cell proliferation, and in practice shows tendency for recurrence and difficulties to eradicate. Bcl-2 expression supports the observation that tumor cells are derived from basal keratinocytes. In SCC, lack of Bcl-2 expression indicates that origin of tumor cells is from more differentiated suprabasal keratinocytes. In AK results suggest that immunoreactivity is regulated with respect of the keratinocyte's differentiation status, but not closely correlate with proliferative rate.
Puizina-Ivić
Neira
N
Clinic of Dermatovenerology, School of Medicine, University of Split, Split, Croatia. neira.puizina@kbsplit.hr
Sapunar
Damir
D
Marasović
Dujomir
D
Mirić
Lina
L
D017209:Apoptosis; D002280:Basal Cell Carcinoma / Q000378:metabolism* / Q000473:pathology; D002294:Carcinoma, Squamous Cell / Q000378:metabolism* / Q000473:pathology; D016022:Case-Control Studies; D006801:Humans; D007150:Immunohistochemistry; D055623:Keratosis, Actinic / Q000378:metabolism* / Q000473:pathology; D017492:Keratosis, Seborrheic / Q000378:metabolism* / Q000473:pathology; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000378:metabolism*; D012878:Skin Neoplasms / Q000378:metabolism* / Q000473:pathology
D019253:Proto-Oncogene Proteins c-bcl-2