Characterization of MTHFR, GSTM1, GSTT1, GSTP1, and CYP1A1 genotypes in childhood acute leukemia

Balta, Günay; Yüksek, Nazmiye; Ozyurek, Emel; Ertem, Ulya; Hiçsönmez, G; Altay, Çiğdem; Gürgey, Aytemiz

doi:10.1002/ajh.10339

Cited by 91 publications

(83 citation statements)

References 20 publications

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“…CYP 1A1*2A allele frequency has been found to be significantly increased in children with ALL as compared to normal controls in a French-Canadian population (OR ¼ 1.8; 95% CI, 1.1, 3.1) [16]. However, there is no difference in this allele frequency between Turkish children with ALL and healthy volunteers [17]. Our Thai population has a high prevalence of CYP 1A1*2A and *2B variants when compared to Caucasians or African Americans [18].…”

Section: Discussionmentioning

confidence: 91%

Polymorphisms of drug‐metabolizing enzymes and risk of childhood acute lymphoblastic leukemia

et al. 2005

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The involvement of phase I and II enzymes is well documented in the metabolism of a wide range of drugs and xenobiotics. Single-nucleotide polymorphisms (SNPs) of these enzymes are also known to alter their protein expression and function. Moreover, genetic susceptibility and environmental exposure have been proposed to be an etiology of cancer. We hypothesized that polymorphisms of these enzymes might affect the risk of childhood acute lymphoblastic leukemia (ALL). CYP 1A1, CYP 3A4*1B, CYP 3A5*3, CYP 3A5*6, GSTM1, and GSTT1 polymorphisms were genotyped by using PCR-RFLP in 107 children with ALL and 320 healthy controls. Allele and genotype frequencies of each of the SNPs were compared between two groups. It was found that the allele frequencies of CYP 1A1*1, *2A, *2B, and *4 were not different between cases and controls. CYP 3A4*1B allele frequency was only 0.8% and 0.9% in ALL and controls, respectively. CYP 3A5*1/*1, *1/*3, and *3/*3 genotype frequencies showed no statistically significant difference between patients and controls. CYP 3A5*6 was not detected in our population. The GSTM1 null genotype was significantly increased in children with ALL (OR 1.7; 95% CI, 1.0, 2.7). In contrast, the GSTT1 null genotype did not show this effect. Our data thus demonstrate that the GSTM1 null genotype might increase the risk of childhood ALL in a Thai population. Am.

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Section: Discussionmentioning

confidence: 91%

Polymorphisms of drug‐metabolizing enzymes and risk of childhood acute lymphoblastic leukemia

et al. 2005

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“…CYP1 family enzyme expressions are increased in myeloblastic and lymphoid cell lines, and CYP1 enzymes may contribute to the carcinogenesis of hematopoietic cells [5]. Several groups found that CYP1A1*2 variant allele was not related with childhood acute leukemias [36,52], whereas Sinnett et al showed CYP1A1*2A is one of the significant risk determinants of ALL [31]. Another study from Turkey found homozygous CYP1A1*2A genotype to be under-represented in ALL patients as compared to controls [36].…”

Section: Discussionmentioning

confidence: 99%

Role ofCYP2D6, CYP1A1, CYP2E1, GSTT1, andGSTM1 genes in the susceptibility to acute leukemias

Sayitoğlu¹,

Hatırnaz²,

Erensoy³

et al. 2006

Am. J. Hematol.

101

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Acute leukemias (ALs) are heterogeneous diseases. Functional polymorphisms in the genes encoding detoxification enzymes cause inter-individual differences, which contribute to leukemia susceptibility. The CYP2D6, CYP1A1, CYP2E1, GSTT1, and GSTM1 polymorphisms in ALL (n = 156) and AML (n = 94) patients and 140 healthy controls were genotyped by PCR and/or PCR-RFLP using blood or bone marrow samples. No association was observed between the GSTT1 gene deletion and patients (OR = 0.8, 95% CI = 0.4-1.7 for AMLs and OR = 0.9, 95% CI ¼ 0.5-1.6 for ALLs). Patients with ALL and AML had a higher prevalence of the GSTM1 deletions compared to controls but only the difference among adult AML patients (OR = 2.1, 95% CI = 1.0-4.2) was statistically significant. The CYP2D6*3 variant allele frequency was lower in the overall acute leukemia patients (0.6%) compared to controls (P = 0.03). CYP2D6*1/*3 genotype frequency also showed a protective association in AML patients (OR = 0.09, 95% CI = 0.01-1.7; P = 0.04). We also found a risk association for CYP2E1*5 in ALL and AML (OR = 3.6, 95% CI = 1.4-9.4 and OR = 3.9, 95% CI = 1.4-10.5, respectively). No association was found for the studied CYP2D6*4, CYP1A1*2A, and GSTT1''null'' variants and the risk of acute leukemia (ALL or AML). This case-control study suggests a contribution of CYP2E1, CYP2D6, and GSTM1 ''null'' variants to the development of acute leukemias. Am.

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“…Published data indicate that xenobiotic-metabolizing polymorphic alleles in some populations correlate with increased risk of different lymphoproliferative diseases [18][19][20][21][22]. The majority of articles were devoted to the analysis of acute leukemia and, particularly, childhood leukemia [21,[23][24][25]. Thus, it would be interesting to investigate associations between polymorphous variants of xenobiotic-metabolizing genes and risk of development of other lymphoproliferative diseases.…”

Section: Introductionmentioning

confidence: 99%

Polymorphisms in xenobiotic‐metabolizing genes and the risk of chronic lymphocytic leukemia and non‐Hodgkin's lymphoma in adult Russian patients

et al. 2007

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Polymorphisms in genes coding xenobiotic-metabolizing enzymes are considered as risk factors modifying susceptibility to cancer. We developed a biochip for the analysis of 18 mutations in 10 genes of metabolizing system: CYP1A1, CYP2D6, GSTT1, GSTM1, MTHFR, MTRR, NQO1, CYP2C9, CYP2C19, and NAT2. Using allele-specific hybridization on the biochip 76 T-cell non-Hodgkin's lymphoma (NHL) patients, 83 B-cell chronic lymphocytic leukemia (B-CLL) patients, and 177 healthy donors were tested. Polymorphic CYP1A1 alleles were more frequent in B-CLL patients relative to normal controls, for example, a combination of polymorphic variants 4887C > A, 4889A > G, and 6235T > C (OR 5 1.76, 95% CI 5 1.0-3.1). The GSTM1 null genotype was more frequent in NHL patients relative to controls (OR 5 1.82, 95% CI 5 1.1-3.1). The combination of unfavorable polymorphic CYP1A1 variants and GSTM1 null genotype was found more frequently in B-CLL patients relative to controls (OR 5 2.52, 95% CI 5 1.3-4.9). In addition, male B-CLL patients demonstrated a significantly increased occurrence of heterozygous and homozygous allele *2 of CYP2C9 gene (OR 5 2.38, 95% CI 5 1.1-5.2) as well as a combination of alleles *2 and *3 of the gene (OR 5 2.09, 95% CI 5 1.1-3.9). Thus, our findings show the association between polymorphic alleles of CYP1A1, GSTM1, and CYP2C9 genes and the risk to develop NHL or B-CLL. The developed biochip can be considered as a convenient analytical tool for research studies and predictive analysis in oncohematology. Am. J. Hematol. 83:279-287, 2008. V

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Characterization of MTHFR, GSTM1, GSTT1, GSTP1, and CYP1A1 genotypes in childhood acute leukemia

Cited by 91 publications

References 20 publications

Polymorphisms of drug‐metabolizing enzymes and risk of childhood acute lymphoblastic leukemia

Polymorphisms of drug‐metabolizing enzymes and risk of childhood acute lymphoblastic leukemia

Role ofCYP2D6, CYP1A1, CYP2E1, GSTT1, andGSTM1 genes in the susceptibility to acute leukemias

Polymorphisms in xenobiotic‐metabolizing genes and the risk of chronic lymphocytic leukemia and non‐Hodgkin's lymphoma in adult Russian patients

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