Journal of Cancer Research and Clinical Oncology

, 132:521

Role of glutathione-S-transferase and codon 72 of P53 genotypes in epithelial ovarian cancer patients

Authors

  • Elaine Cristina Morari
    • Laboratory of Cancer Molecular Genetics, Department of Medicine, Medical Sciences FacultyState University of Campinas-UNICAMP
  • Andre Bacellar Costa Lima
    • Laboratory of Cancer Molecular Genetics, Department of Medicine, Medical Sciences FacultyState University of Campinas-UNICAMP
  • Natassia Elena Bufalo
    • Laboratory of Cancer Molecular Genetics, Department of Medicine, Medical Sciences FacultyState University of Campinas-UNICAMP
  • Janaina Luisa Leite
    • Laboratory of Cancer Molecular Genetics, Department of Medicine, Medical Sciences FacultyState University of Campinas-UNICAMP
  • Fabiana Granja
    • Laboratory of Cancer Molecular Genetics, Department of Medicine, Medical Sciences FacultyState University of Campinas-UNICAMP
    • Laboratory of Cancer Molecular Genetics, Department of Medicine, Medical Sciences FacultyState University of Campinas-UNICAMP
Original Paper

DOI: 10.1007/s00432-006-0099-3

Cite this article as:
Morari, E.C., Lima, A.B.C., Bufalo, N.E. et al. J Cancer Res Clin Oncol (2006) 132: 521. doi:10.1007/s00432-006-0099-3

Abstract

Purpose. A series of polymorphisms in germ-line DNA have been investigated in an effort to delineate polygenic models of cancer susceptibility and prognosis. As low-penetrance susceptibility genes may combine additively or multiplicatively and contribute to cancer incidence and to the response to chemotherapy, we studied GSTT1, GSTM1, GSTO2, GSTP1 and codon 72 of p53 genotype profiles in ovarian cancer patients. Methods. We compared 69 ovarian cancer patients with 222 control healthy women paired for ethnic and life-style characteristics. Outcome was evaluated in 29 stage III and IV patients submitted to a platinum-based chemotherapy followed-up for 6–29 months (17 ± 9 months). Results.GSTT1, GSTM1, GSTO2 and GSTP1 genes presented a similar genotype distribution, but codon 72 of p53 gene wild-type variant was less frequent in ovarian cancer patients than in controls (χ2; = 0.0004). Conclusions. We were unable to demonstrate any association between the GST genotypes studied and the risk of ovarian cancer but the inheritance of a heterozygous Arg/Pro genotype of p53 increased the risk of ovarian cancer more than 2.5 times (OR = 2.571; 95% CI = 1.453–4.550). There was no association of the studied genes to any clinical or pathological feature of the patients or to their response to chemotherapy.

Keywords

SusceptibilityResponse to treatmentGermline polymorphic inheritance

Copyright information

© Springer-Verlag 2006