|
Leukemia, Myelocytic, Acute
|
0.100 |
Biomarker
|
disease |
BEFREE |
GSTM1 had the highest frequency for gene gain (45.45, 39.18, 31.01, and 34.77%, respectively) and for gene loss (18.18, 29.38, 20.89, and 26.68%, respectively) in DLBL, acute myeloid leukemia, liver hepatocellular carcinoma, and LUSC.
|
25379720 |
2015 |
|
Leukemia, Myelocytic, Acute
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
Our study suggested that GSTT1 null genotype and GSTT1/GSTM1 double-null genotype were associated with a worse treatment outcome for AML patients, especially in Asian population.
|
24994605 |
2014 |
|
Leukemia, Myelocytic, Acute
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
Association of GSTTI and GSTM1 variants with acute myeloid leukemia risk.
|
24854448 |
2014 |
|
Leukemia, Myelocytic, Acute
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
The pooled analyses revealed that the GSTM1-null genotype was associated with an increased risk of acute myeloid leukemia in East Asians (P = 0.01; odds ratio = 1.22; 95% confidence interval = 1.05-1.42), and GSTT1-null genotype in Caucasians (P < 0.0001; odds ratio = 1.48; 95% confidence interval = 1.29-1.69).
|
25145382 |
2014 |
|
Leukemia, Myelocytic, Acute
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
Finally, patients with both GSTM1 and ALOX12 methylated, demonstrated worse outcomes when all AML patients were assessed (OS; P = 0·000411) as well as within AML NOS (DFS; P = 0·0023), AML with intermediate cytogenetic risk (OS; P = 0·0104) and normal karyotype AML (OS; P = 0·00636).
|
22924777 |
2012 |
|
Leukemia, Myelocytic, Acute
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
In classification and regression tree analysis, combinations of GSTM1 present, CYP1A12C AA or GG, EPHX1 exon3 TC, and EPHX1 exon4 AA or GG genotype strongly enhanced the risk of AML (OR = 5.89; 95% CI = 1.40-26.62; P = 0.01).
|
22930568 |
2012 |
|
Leukemia, Myelocytic, Acute
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
Clinical significance of GSTM1 and GSTT1 polymorphisms in younger patients with acute myeloid leukemia of intermediate-risk cytogenetics.
|
18760837 |
2009 |
|
Leukemia, Myelocytic, Acute
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
However, fixed-effects model showed significant risk of AML in the presence of null genotypes of GSTM1 and GSTT1(p < 0.05).
|
19811334 |
2009 |
|
Leukemia, Myelocytic, Acute
|
0.100 |
GeneticVariation
|
disease |
LHGDN |
Clinical significance of GSTM1 and GSTT1 polymorphisms in younger patients with acute myeloid leukemia of intermediate-risk cytogenetics.
|
18760837 |
2009 |
|
Leukemia, Myelocytic, Acute
|
0.100 |
GeneticVariation
|
disease |
LHGDN |
Polymorphisms in transporter and phase II metabolism genes as potential modifiers of the predisposition to and treatment outcome of de novo acute myeloid leukemia in Israeli ethnic groups.
|
18207572 |
2008 |
|
Leukemia, Myelocytic, Acute
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
All these findings suggest that GSTM1-null genotype alone or in coordination with the relevant genotypes of other metabolic enzymes might be susceptibility factors in the etiology of ANLL.
|
18414197 |
2008 |
|
Leukemia, Myelocytic, Acute
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
Glutathione S-transferases (GSTT1 and GSTM1) genes polymorphisms and the treatment response and prognosis in Chinese patients with de novo acute myeloid leukemia.
|
18035413 |
2008 |
|
Leukemia, Myelocytic, Acute
|
0.100 |
Biomarker
|
disease |
BEFREE |
In the population studied, persons with glutathione-S-transferase M1 null genotype and N-acetyl transferase 2*6B allele are at increased risk of developing AML, and the risk is considerably enhanced in persons with both glutathione-S-transferase M1 and N-acetyl transferase 2 deficiency.
|
18287869 |
2008 |
|
Leukemia, Myelocytic, Acute
|
0.100 |
GeneticVariation
|
disease |
LHGDN |
In the present study, we genotyped 153 patients diagnosed with de novo acute myeloid leukemia (AML) to clarify the influence of the genetic polymorphisms CYP1A1*2A, CYP3A4*1B, CYP2E1*5B, del{GSTT1}, del{GSTM1}, and NQO1*2 on disease outcome.
|
17118447 |
2007 |
|
Leukemia, Myelocytic, Acute
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
In the present study, we genotyped 153 patients diagnosed with de novo acute myeloid leukemia (AML) to clarify the influence of the genetic polymorphisms CYP1A1*2A, CYP3A4*1B, CYP2E1*5B, del{GSTT1}, del{GSTM1}, and NQO1*2 on disease outcome.
|
17118447 |
2007 |
|
Leukemia, Myelocytic, Acute
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
The prevalence of CYP1A1*2A, *2B and *4 alleles and of GSTM1 and GSTT1 homozygous deletions was examined in 193 patients with AML and 273 normal individuals using polymerase chain reaction (PCR)-based methods.
|
15194533 |
2004 |
|
Leukemia, Myelocytic, Acute
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
If we further divide the AML group into patients in which the burden of DNA damage is increased, because of the deletion of the GSTM1 gene, the risk of development of AML is further increased (OR, 15.26; 95% CI, 1.83-127.27).
|
15102670 |
2004 |
|
Leukemia, Myelocytic, Acute
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
We investigated the prognostic significance of genetic polymorphism in glutathione-S transferase mu 1 (GSTM1), glutathione-S transferase theta 1 (GSTT1), NAD(P)H:quinone oxidoreductase (NQO1) and myeloperoxidase (MPO), the products of which are associated with drug metabolism as well as with detoxication, in 193 patients with de novo acute myeloid leukemia (AML) other than M3.
|
11840286 |
2002 |
|
Leukemia, Myelocytic, Acute
|
0.100 |
GeneticVariation
|
disease |
LHGDN |
Using polymerase chain reactions, we analyzed the GSTM1 and GSTT1 genotype in 106 patients with AML (median age, 60.5 years; range, 19-76 years).
|
12351375 |
2002 |
|
Leukemia, Myelocytic, Acute
|
0.100 |
Biomarker
|
disease |
BEFREE |
We genotyped GSTT1 and GSTM1 in 306 children with AML receiving chemotherapy on Children's Cancer Group therapeutic studies.
|
11230469 |
2001 |
|
Leukemia, Myelocytic, Acute
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
Our observation of a 4.7-fold (95% CI: 2.1-11.0) and 2.3-fold (95% CI: 1.0-5.2) increased risk associated with the GSTM1 and GSTT1 null genotypes, respectively, and a 6.6-fold (95% CI: 2.4-7.9) increased risk associated with the combined null genotype presents preliminary evidence that the inherited absence of this carcinogen detoxification pathway may be an important determinant of AML.
|
11488937 |
2001 |
|
Leukemia, Myelocytic, Acute
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
No association 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).
|
10815689 |
2000 |