Simultaneous Detection of GSTM1, GSTT1 Polymorphisms and its Relationship to Resistance to Chemotherapy Drugs in Esophagus Cancer Patients

Abstract:
Background
Genetic polymorphisms in enzymes involved in carcinogen metabolism have been shown to influence susceptibility to cancer. The glutathione S-transferase (GST) genes are involved in the detoxification of a broad range of toxic substances, so polymorphic deletions of GSTM1 and GSTT1 genes may involve as a risk factor for esophagus carcinoma. The aim of this research was to investigate the association between null mutations of GSTM1 and GSTT1 genes with esophagus carcinoma susceptibility in Iranian patients were under chemo therapy with platinum drugs.
Methods
We conducted a case –control study of 50 esophagus carcinoma cases and 50 controls. Genomic DNA was extracted from blood samples, then GSTM1 and GSTT1 deletion variants were genotyped by multiplex PCR assay. Logistic regression analysis was used by SPSS 19 to estimate odds ratios and 95% confidence intervals (95% CI).
Results
Our results indicate that the frequency of esophagus cancer patients with the GSTM1 null genotype is significantly higher than that of the normal controls (48% and 13%, respectively) with an odds ratio (OR) of 2.62 and (p=0.024), In contrast, our investigation failed to demonstrate any difference in the distribution of GSTT1 null genotype between patients and controls (32 and 24% respectively) (p=0.37).In this study (26 patients) 52% of patients with esophageal cancer who were treated with chemotherapy, not turning a useful these drugs. In most cases (18%), they were persons with Null genotype in both genes.
Conclusion
the results of the current study indicate that GSTM1 may be genetic susceptibility factor involved in early events leading to the development of esophageal cancer. Polymorphisms of GSTT1 were not associated with the increased esophageal cancer risk.
Language:
Persian
Published:
Razi Journal of Medical Sciences, Volume:24 Issue: 1, 2017
Pages:
1 to 9
https://magiran.com/p1703912  
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