Polymorphisms of p53, GSTM1 and GSTT1, and HPV in uterine cervix adenocarcinoma

Objective: To analyze the participation of glutathione-S-transferase (GST) M I and T I polymorphisms associated protein p53 polymorphism at codon 72 and in the presence of HPV in the carcinogenesis of uterine cervix adenocarcinoma. Methods: Forty-three samples of uterine cervix adenocarcinoma were s...

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Detalles Bibliográficos
Autores: Carvalho, Carmen Regina Nogueira de [UNIFESP], Silva, Ismael Dale Cotrim Guerreiro da [UNIFESP], Pereira, J. S. [UNIFESP], Nogueira-de-Souza, Naiara Corrêa [UNIFESP], Focchi, Gustavo Rubino de Azevedo [UNIFESP], Ribalta, Julisa Chamorro Lascasas [UNIFESP]
Tipo de recurso: artículo
Estado:Versión publicada
Fecha de publicación:2008
País:Brasil
Institución:Universidade Federal de São Paulo (UNIFESP)
Repositorio:Repositório Institucional da UNIFESP
Idioma:inglés
OAI Identifier:oai:repositorio.unifesp.br:11600/43600
Acceso en línea:http://www.irog.net/download/?magazine=102
http://repositorio.unifesp.br/handle/11600/43600
Access Level:acceso abierto
Palabra clave:p53
GSTM1
GSTT1
HPV
Adenocarcinoma
Descripción
Sumario:Objective: To analyze the participation of glutathione-S-transferase (GST) M I and T I polymorphisms associated protein p53 polymorphism at codon 72 and in the presence of HPV in the carcinogenesis of uterine cervix adenocarcinoma. Methods: Forty-three samples of uterine cervix adenocarcinoma were studied and 86 samples of endocervical cells of women without tumors formed the control group. The presence of HPV was determined in order to genotype the isoforms of p53 at codon 72, GSTM1. GSTM1*0, GSTT1 and GSTT1*0 which were evaluated by the PCR method. Results: HPV was present in 97.67% of the adenocarcinoma cases and in 31.40% of the control group. Statistical analysis showed differences (p = 0.001) and an OR of 113.3 (CI 95%: 13.67-947.14). GSTT1 and GSTT1*0 analysis showed a significant difference between the groups (p = 0.001) with an OR of 4.58 (CI 95%: 2.041-10.28) (p < 0.001) for the presence of GSTT1*0. When it was associated with HPV OR was 6.6 (CI 95%: 0.04-0.50). Analyses of p53 and GSTM1 and GSTM1*0 either alone or associated with HPV were not significant. Conclusion: The presence of GSTT1*0 increased the risk for uterine cervix adenocarcinoma development while the allele GSTT1 had it protective action. The other isoforms did not appear to participate in the carcinogenesis of uterine cervix adenocarcinoma.