GENETIC POLYMORPHISMS IN GLUTATHIONE-S-TRANSFERASE-MU AND GLUTATHIONE-S-TRANSFERASE-THETA, N-ACETYLTRANSFERASE, AND CYP1A1 AND RISK OF GLIOMAS

Citation
Z. Trizna et al., GENETIC POLYMORPHISMS IN GLUTATHIONE-S-TRANSFERASE-MU AND GLUTATHIONE-S-TRANSFERASE-THETA, N-ACETYLTRANSFERASE, AND CYP1A1 AND RISK OF GLIOMAS, Cancer epidemiology, biomarkers & prevention, 7(6), 1998, pp. 553-555
Citations number
23
Categorie Soggetti
Oncology,"Public, Environmental & Occupation Heath
ISSN journal
10559965
Volume
7
Issue
6
Year of publication
1998
Pages
553 - 555
Database
ISI
SICI code
1055-9965(1998)7:6<553:GPIGAG>2.0.ZU;2-M
Abstract
The role of genetic polymorphisms in modulating susceptibility to carc inogenic exposures has been well explored for tobacco-related neoplasm s but not for other neoplasms including gliomas, It is relevant to exp lore these polymorphisms because certain carcinogenic exposures such a s nitrosamines are implicated in the risk of gliomas, We therefore con ducted a pilot case-control study to examine the role of polymorphisms in GSTM1, GSTT1, NAT2 (rapid, intermediate, and slow acetylation), an d CYP1A1 and risk of glioma, Ninety patients diagnosed with glioma wer e ascertained as part of an ongoing genetic epidemiological study and were age, gender, and race matched with 90 healthy controls. We used P CR based methodology to determine the prevalence of the above genetic polymorphisms using sequences and PCR conditions directly adapted from studies reported previously. We calculated univariate od;ls ratios an d performed multiple logistic regression to assess interactions betwee n polymorphisms, We found no statistically significant associations be tween the null genotypes of GSTM1 and GSTT1, and CYP1A1 and risk of gl iomas, However, there was an intriguing pattern with NAT2 acetylation status (odds ratios, 1.81, 1.34, and 0.61 for rapid, intermediate, and slow acetylation, respectively; P = 0.10 for trend), It is unlikely t hat any single polymorphism is sufficiently predictive of risk, and a panel of markers integrated with epidemiological data should be conduc ted on a large number of study subjects to fully understand the role o f genetic polymorphisms and brain tumor risk.