Assessment of glutathione S-transferaseM1 (GSTM1) and its polymorphisms GSTM1 null in the response to treatment with chemotherapy in advanced ovarian carcinoma

Abstract

Objective: To assess if the genotype of the glutathione S-transferase M1 (GSTM1) enzyme and its GSTM1 null polymorphism can influence the response to chemotherapeutic treatment of advanced ovarian cancer. Methods: Case-control study of 112 patients with advanced ovarian cancer submitted to chemotherapy during the period from January 1995 to December 2005. The tissue to study the GSTM1 genotype and its deletion came from surgical staging to treat ovarian cancer. The PCR product generates two distinct genotypes, characterized as positive and null. The response to chemotherapy was evaluated using the World Health Organization (WHO) criteria. Patients were classified as having: a) no response, b) a response. Results: The presence of GSTM1 or its GSTM1 null polymorphism did not influence the preoperative chemotherapy response. Among the patients who did respond, 88.9% presented with positive GSTM1 and 11.1% with null GSTM1. Among the patients that did not respond, 85.71% presented with positive GSTM1 and 14.29% with null GSTM1 (p = 0.825). GSTM1 and its GSTM1 null polymorphism had no influence on the postoperative response to chemotherapy. Among the patients who did respond, 80.65% presented with positive GSTM1 and 19.35% with null GSTM1. Among the patients who did not respond, 87.50% presented with positive GSTM1 and 12.5% with the null polymorphism (p = 0.553). Conclusion: No difference was observed in the response to treatment with chemotherapy in patients with advanced ovarian cancer, as to the GSTM1 genotype compared to its GSTM1 null polymorphism.

An Overview of Registered Clinical Trials on Glucosinolates and Human Health: The Current Situation

“…The authors found that GSTM1-null and GSTM1-positive subjects have different SFN metabolites concentrations in plasma and different rates of urinary excretion of SFN metabolites after broccoli consumption that could be explained by the GSTM genotype. These results were in line with the observations reported by other authors documenting a different GST activity and metabolism of GSLs ( 86 , 87 ). Furthermore, numerous epidemiological studies associated GST polymorphisms with a different level of protection against oxidative stress other than an increased susceptibility to cancer diseases ( 88 , 89 ).…”