Glutathione S-transferase theta 1 gene deletion and risk of acute myeloid leukemia

Individuals with a homozygous deletion of the glutathione S-transferase the ta 1 (GSTT1) gene lack GSTT1 enzymatic detoxification of environmental carc inogens by conjugation with glutathione. The GSTT1 gene deletion has been a ssociated with carcinogen-induced chromosomal changes in lymphocytes, and s ome but not all epidemiological evidence has suggested that the GSTT1 gene deletion may increase susceptibility to myelodysplasia. We conducted a case -control study to test whether individuals with an inherited homozygous del etion of the GSTT1 gene are at increased risk of acute myeloid leukemia (AM L). The GSTT1 and GST mu 1 (GSTM1) genotypes were determined by PCR using l ymphocyte or bone marrow DNA from 297 AML patients and 152 controls. AML pa tients were selected from Southwest Oncology Group clinical studies, and co ntrols were identified by random digit dialing in Washington state. No asso ciation was observed between the GSTT1 gene deletion and AML [race-adjusted odds ratio (OR), 0.94; 95% confidence interval (CI), 0.55-1.60] or between the GSTM1 gene deletion and AML (race-adjusted OR, 1.26; 95% CI, 0.85-1.88 ). Patients with secondary AML had a slightly higher prevalence of the GSTT 1 and GSTM1 gene deletions compared with de novo AML patients or controls, but this was consistent with chance. Exploratory analyses of AML cytogeneti cs suggested a few associations, i.e., between the GSTT1 gene deletion and trisomy 8, and between the GSTM1 gene deletion and non-8 trisomies or inv(1 6). These results do not support the hypothesis that the GSTT1 gene deletio n is related to the incidence of AML.