Prognostic significance of the bcl-2 apoptotic family of proteins in primary and recurrent cervical cancer
Crawford, R. A. and Caldwell, C. J. and Iles, Ray K. and Lowe, D. and Shepherd, John H. and Chard, Tim (1998) Prognostic significance of the bcl-2 apoptotic family of proteins in primary and recurrent cervical cancer. British Journal of Cancer, 78 (2). pp. 210-214. ISSN 0007-0920
Official URL: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC206289...
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bcl-2 is one of a family of genes that control the apoptotic threshold of a cell. bcl-2 protein and its anti-apoptotic homologue, mcl-1, with the pro-apoptotic protein, bax, are thought to function by forming homo- and heterotypic dimers that then control the progression to apoptosis. p53 is also involved as a down-regulator of bcl-2 and a promoter of bax. To determine the effect of these apoptotic mechanisms, we used immunohistochemistry to determine the prognostic significance of the expression of bcl-2, mcl-1, bax and p53 in primary and recurrent cervical cancer. Tissues from 46 patients with primary cervical cancer and 28 women with recurrent carcinoma were stained for bcl-2, mcl-1, bax and p53. Kaplan-Meier survival analysis was performed using the log-rank test for differences between groups. In the primary disease group, positive staining for bcl-2 was associated with a better 5-year survival (bcl-2 +ve, 84% vs bcl-2 -ve, 53%, P = 0.03). Positive staining for p53 was associated with a survival disadvantage (p53 +ve, 4-year survival 38% vs p53 -ve, 4-year survival 78%, P = 0.02). mcl-1 and bax staining were not useful as prognostic indicators in primary disease. No marker was prognostic in recurrent disease. Positive bcl-2 staining defines a group of patients with primary disease with a good prognosis. p53, an activator of the bax promoter, identifies a group with a worse outcome. In recurrent disease, none of the markers reflected prognosis.
|Research Areas:||School of Science and Technology > Natural Sciences|
|Citations on ISI Web of Science:||47|
|Deposited On:||02 Nov 2009 13:29|
|Last Modified:||26 Jul 2014 17:51|
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