Background: We investigated the role of apoptosis and its potential alterations in laryngeal squamous cell carcinomas (LSCCs) by evaluating bax, bcl-2 and p53 protein expression in 50 cases and by characterising the molecular status of the bax and p53 genes. Material and Methods: p53 and bax gene mutations were investigated by means of PCR/SSCP and direct DNA sequencing, and bax, bcl-2 and p53 protein expression by means of immunohistochemistry. Results: We identified p53 gene mutations in 17/50 cases (34%); p53 expression in 26 of the 50 cases (52%); bcl-2 expression in 5/50 cases (10%); bax expression in 32/47 cases (68%). 18/33 cases with a wild type p53 gene overexpressed p53 protein: 12 cases (≃ 66%) were bax+/bcl-2-. Of the remaining cases without p53 protein expression, seven cases (≃ 47%) were bax+/bcl-2-. Conclusions: Our observations suggest that the overexpression of p53 may contribute to the repression of bcl-2 and the induction of bax expression in LSCCs. However, the fact that a number of cases not expressing p53 did not present any clear up-regulation of bax or down-regulation of bcl-2 suggests that bcl-2 and bax may be regulated by various mechanisms other than p53.
Immunohistochemical and molecular analysis of bax, bcl-2 and p53 genes in laryngeal squamous cell carcinomas / N.S. Fracchiolla, P. Capaccio, N. Carboni, A.V. Pagliari, A. Neri, D. Ronchett, G. Pruneri, M.G. Silvotti, L. Pignataro, R. Buffa, G. Broich. - In: ANTICANCER RESEARCH. - ISSN 0250-7005. - 19:2 A(1999 Mar), pp. 1043-1051.
Immunohistochemical and molecular analysis of bax, bcl-2 and p53 genes in laryngeal squamous cell carcinomas
P. Capaccio;A. Neri;G. Pruneri;L. Pignataro;
1999
Abstract
Background: We investigated the role of apoptosis and its potential alterations in laryngeal squamous cell carcinomas (LSCCs) by evaluating bax, bcl-2 and p53 protein expression in 50 cases and by characterising the molecular status of the bax and p53 genes. Material and Methods: p53 and bax gene mutations were investigated by means of PCR/SSCP and direct DNA sequencing, and bax, bcl-2 and p53 protein expression by means of immunohistochemistry. Results: We identified p53 gene mutations in 17/50 cases (34%); p53 expression in 26 of the 50 cases (52%); bcl-2 expression in 5/50 cases (10%); bax expression in 32/47 cases (68%). 18/33 cases with a wild type p53 gene overexpressed p53 protein: 12 cases (≃ 66%) were bax+/bcl-2-. Of the remaining cases without p53 protein expression, seven cases (≃ 47%) were bax+/bcl-2-. Conclusions: Our observations suggest that the overexpression of p53 may contribute to the repression of bcl-2 and the induction of bax expression in LSCCs. However, the fact that a number of cases not expressing p53 did not present any clear up-regulation of bax or down-regulation of bcl-2 suggests that bcl-2 and bax may be regulated by various mechanisms other than p53.Pubblicazioni consigliate
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