Literature DB >> 8082073

bcl-2 expression in epidermal keratinocytic diseases.

K Nakagawa1, K Yamamura, S Maeda, M Ichihashi.   

Abstract

BACKGROUND: The bcl-2 protein has been shown to suppress apoptosis, and overexpression of the bcl-2 protein has been reported in several malignant tumors. Skin is one of the largest organs in the body, and the most common human malignancies arise from keratinocytes in the epidermis. In this paper, the authors analyzed immunohistochemically the expression of the bcl-2 protein in several keratinocytic (KC) tumors and inflammatory skin disorders to investigate the role of bcl-2 in the development of benign and malignant skin tumors.
METHODS: Seventy-two frozen tissues from patients with inflammatory KC proliferation (chronic dermatitis [CD] and psoriasis vulgaris [PV]), seborrheic keratosis (SK), carcinoma in situ of KC tumors (actinic keratosis [AK] and Bowen's disease [BD]), basal cell carcinoma (BCC), and squamous cell carcinoma (SCC), 2 SCC cell lines, and 20 normal skin were immunostained with an anti-bcl-2 monoclonal antibody.
RESULTS: Tissue with normal KC, CD, PV, and SK scarcely expressed the bcl-2 protein. Seventy-three percent of tissue with BD, 25% with AK, 67% with BCC, and 100% with SCC showed obvious bcl-2 protein expression. bcl-2 expression of BCC, BD, and SCC was restricted to the involved lesions, and surrounding normal tissue with KCs were bcl-2 negative. Interestingly, tissue with atrophic AK expressed no bcl-2 protein (none of five cases), whereas tissue with hypertrophic AK reacted weakly with the anti-bcl-2 antibody (two of three cases).
CONCLUSIONS: bcl-2 protein expression in patients with KC may be related to tumorigenic proliferation possibly due to enhanced cell survival, but not when inflammatory proliferation of keratinocytes is present.

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Year:  1994        PMID: 8082073     DOI: 10.1002/1097-0142(19940915)74:6<1720::aid-cncr2820740613>3.0.co;2-t

Source DB:  PubMed          Journal:  Cancer        ISSN: 0008-543X            Impact factor:   6.860


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