Oral squamous cell carcinoma is associated with decreased bcl-2/bax expression ratio and increased apoptosis

Expression of bcl-2 and bax and apoptosis were studied in fresh frozen samples of normal oral epithelium (OE, n = 7) and oral squamous cell carcinomas (OSCC, n = 16) by immunohistochemistry and the TUNEL method. In OE, bcl-2 was expressed in both basal (96.6% ± 2.3% [mean ± SD]) and suprabasal (91.8...

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Published inHuman pathology Vol. 30; no. 9; pp. 1097 - 1105
Main Authors Loro, Lado Lako, Vintermyr, Olav Karsten, Liavaag, Per Gunnar, Jonsson, Roland, Johannessen, Anne Christine
Format Journal Article
LanguageEnglish
Published New York, NY Elsevier Inc 01.09.1999
Elsevier
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ISSN0046-8177
1532-8392
DOI10.1016/S0046-8177(99)90229-0

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Summary:Expression of bcl-2 and bax and apoptosis were studied in fresh frozen samples of normal oral epithelium (OE, n = 7) and oral squamous cell carcinomas (OSCC, n = 16) by immunohistochemistry and the TUNEL method. In OE, bcl-2 was expressed in both basal (96.6% ± 2.3% [mean ± SD]) and suprabasal (91.8% ± 6.2%) compartments. In OSCC, compared with OE, there was a marked reduction of bcl-2-positive cells in the basal part, and in the central parts of well-differentiated (33.0% ± 19.7%, P < .001) and moderately differentiated (6.1% ± 4.6%, P < .001) and also in poorly differentiated (1.9% ± 0.2%, P < .001) tumors. More cells expressed bax in the suprabasal layer of OE (65.6% ± 9.9%) and central parts of OSCC than in the basal layer of OE (19.1% ± 4.1%) and basal parts of OSCC. A higher proportion of cells expressed bax in the central part of well-differentiated OSCC (74.3% ± 8.2%) than in poorly differentiated OSCC (24.9% ± 9.7%, P < .001). Apoptotic cell death was more pronounced in OSCC (1.5% ± 0.9%) than in OE (0.4% ± 0.1%, P < .05). We conclude that, in OSCC, compared with OE, there is a decreased bcl-2 expression, a lowered bcl-2/bax ratio and increased apoptosis. The expression of bax correlates with histological tumor grading in oral squamous cell carcinoma.
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ISSN:0046-8177
1532-8392
DOI:10.1016/S0046-8177(99)90229-0