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Blood, 1 July 2002, Vol. 100, No. 1, pp. 67-71
CLINICAL OBSERVATIONS, INTERVENTIONS, AND THERAPEUTIC TRIALS
Glutathione S-transferase genotypes, genetic
susceptibility, and outcome of therapy in childhood acute
lymphoblastic leukemia
Stella M. Davies,
Smita Bhatia,
Julie A. Ross,
William R. Kiffmeyer,
Paul S. Gaynon,
Gretchen A. Radloff,
Leslie L. Robison, and
John P. Perentesis
From the Children's Oncology Group, Arcadia, CA; the
City of Hope Medical Center, Duarte, CA; and Childrens Hospital Los
Angeles, CA; and the Department of Pediatrics, University of Minnesota,
Minneapolis.
The glutathione S-transferase (GST) genes are involved
in the metabolism of environmental carcinogens and of some classes of
chemotherapy drugs. GSTM1 and GSTT1 genotypes are polymorphic in humans, and the phenotypic absence of enzyme activity is caused by a
homozygous inherited deletion of the gene. Previous, smaller studies of
childhood acute lymphoblastic leukemia (ALL) provided contrasting data
on the role of the GST genotype in susceptibility and treatment
outcomes. We analyzed GST genotypes in 710 children with ALL treated by
the Children's Cancer Group. Frequencies were compared with
those of normal controls, and outcomes were analyzed according to
genotype. Comparisons of gene frequencies in ALL case and control
patients showed similar frequencies (54% vs 53% GSTM1 null in whites,
P = .9; 40% versus 32% in blacks,
P = .45; 16% versus 15% GSTT1 null in whites,
P = .8; 17% versus 28% in blacks,
P = .3). ALL was not associated with the GSTM1-null
genotype or the double-null genotype in blacks or whites, in contrast
to previous reports. Stratification of cases by age at diagnosis, sex, white blood cell count at diagnosis, B or T
lineage, or cytogenetics revealed no differences in genotype
frequencies. Analysis of treatment outcomes showed no differences in
outcome according to GST genotype; in particular, there were no
differences in frequencies of relapse at any site. These data,
representing a larger series than any reported previously, suggest that
GST genotype does not affect etiology or outcome of childhood ALL.
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