Genetic polymorphisms of metabolic enzymes CYP1A1, CYP2D6, GSTM1 and GSTT1 and leukemia susceptibility

Chen, Hanchun; Hu, Weixin; Liu, Qingxia; Li, Wenkai; Chen, Fangzhi; Rao, Zhou-Zhou; Liu, Xin-Fa; Luo, Yang; Cao, Yanyan

doi:10.1097/cej.0b013e3282b72093

Cited by 50 publications

(50 citation statements)

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“…Loureno et al, 2005 reported that in Brazil the individuals with GSTM1 (OR = 0.98; 95% CI: 0.65-1.50), GSTT1 (OR = 1.06; 95% CI: 0.62-1.80) and combined null genotypes (OR = 0.84; 95% CI: 0.36-1.96) are at similar risk of CML as compared with those without the null genotypes (Rollinson et al, 2005). Similar results were also reported by Chen et al, 2008, where no significant difference was observed in the frequencies of GSTM1, GSTT1 or combined genotypes between cases and controls (Chen et al, 2008).…”

Section: Discussionsupporting

confidence: 78%

Polymorphic Variation in Glutathione-S-transferase Genes and Risk of Chronic Myeloid Leukaemia in the Kashmiri Population

Bhat

Bhat²,

Wani³

et al. 2012

Asian Pacific Journal of Cancer Prevention

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Cancer is a complex disease and the genetic susceptibility to it could be an outcome of the inherited difference in the capacity of xenobiotic metabolizing enzymes. Glutathione-S-transferases (GSTs) are phase II metabolizing enzymes whose various genotypes have been associated with increased risk of different types of cancer. Null mutations caused by the deletion of the entire gene result in the absence of the enzymatic activity and increase in the risk of developing cancer including chronic myeloid leukaemia (CML). In the present case-control study we evaluated the effect of null mutations in GSTM1 and GSTT1 genes on the risk of developing CML. The study included 75 CML patients (43 males and 32 females; age (mean ± S.D) 42.3 ± 13.4 years) and unrelated non-malignant controls (76 male and 48 females; age (mean ± S.D) 41.5 ± 12.9). The distribution of GSTM1 and GSTT1 genotypes in CML patients and controls was assessed by multiplex-PCR method. Logistic regression was used to assess the relationship between GSTM1 and GSTT1 genotypes and risk of CML. Chi-square test was used to evaluate the trend in modulating the risk to CML by one or more potential high risk genotype. Although GSTM1 null genotype frequency was higher in CML patients (41%) than in the controls (35%), it did not reached a statistical significance (OD = 1.32, 95% CI: 0.73-2.40; P value = 0.4295). The frequency of GSTT1 null genotypes was higher in the CML patients (36%) than in the controls (21%) and the difference was found to be statistically significant (OD = 2.12, 95% CI: 1.12-4.02; P value = 0.0308). This suggests that the presence of GSTT1genotype may have protective role against the CML. We found a statistically significant (OD = 3.09, 95% CI: 1.122-8.528; P value = 0.0472) interaction between the GSTM1 and GSTT1 null genotypes and thus individuals carrying null genotypes of both GSTM1 and GSTT1 genes are at elevated risk of CML.

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Section: Discussionsupporting

confidence: 78%

Polymorphic Variation in Glutathione-S-transferase Genes and Risk of Chronic Myeloid Leukaemia in the Kashmiri Population

Bhat

Bhat²,

Wani³

et al. 2012

Asian Pacific Journal of Cancer Prevention

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“…Biotransformation of toxic xenobiotics to their nontoxic forms is considered as the most important step in the processing of the potentially toxic chemical substances toward their elimination [7]. Xenobiotics are metabolized typically in a two-phase reaction: activation and deactivation.…”

Section: Discussionmentioning

confidence: 99%

“…It has been observed that GSTM1 null may affect individual susceptibility to cancer [17]. GSTT1 null has also been proved to be a risk factor for individual susceptibility to some cancers [7,18].…”

Section: Introductionmentioning

confidence: 98%

“…CYP1A1 participates in the metabolism of a vast number of xenobiotics, among which hydroxylation at a vacant position of an aromatic ring is considered to be the hallmark of the initiation of carcinogenesis; it has been reported that the formation of highly reactive intermediates can cause oncogenic mutations in experimental animals and humans [6]. It was revealed experimentally that the polymorphism of Msp I restriction site owing to a T-C variation in the 3′ non-coding region of CYP1A1 allele is associated with increased catalytic activity and increased DNA adducts in cord blood and placenta of newborns [7]. CYP2D6 is involved in the metabolism of various therapeutic drugs and is a possible susceptibility factor for certain environmental reagent-induced diseases [8].…”

Section: Introductionmentioning

confidence: 99%

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Genetic polymorphisms of metabolic enzymes—CYP1A1, CYP2D6, GSTM1, and GSTT1, and gastric carcinoma susceptibility

et al. 2010

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Genetic polymorphisms in metabolic enzymes are associated with numerous cancers. In this study, the relationships between genetic polymorphisms of phase I metabolic enzymes including cytochrome P450 1A1 (CYP1A1), CYP2D6 and phase II metabolic enzymes such as glutathione S-transferase M1 (GSTM1) and GSTT1 and gastric carcinoma susceptibility were investigated. Genomic DNA was isolated from the peripheral blood of 129 healthy controls and 123 gastric carcinoma patients from Han ethnic group of Hunan Province located in Central South China. The genetic polymorphisms of the above mentioned enzymes were analyzed using PCR-RFLP techniques. There was no significant difference among the frequencies of CYP1A1 and/or CYP2D6 gene's wild type, heterozygous or homozygous mutations between the gastric carcinoma group and control group. But the differences among the frequencies of GSTM1 and GSTT1 null genotype between the gastric carcinoma and control group were significant (both P < 0.05). Also there were significant differences in the frequencies of GSTM1 null in high/high-middle differentiated, middle differentiated, middle-low differentiated and low differentiated gastric tumor separately. GSTM1 null showed an increased risk in middle-low differentiated and low differentiated gastric carcinoma type, but GSTT1 null was not a risk factor for the four pathological types of gastric carcinoma mentioned above. We report here that the genotypes of CYP1A1 and CYP2D6 are not associated with gastric carcinoma risk; GSTM1 null, but not GSTT1 null inheritably increases risk of some pathological types of gastric carcinoma in Han ethnic population of Hunan Province.

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“…According to the inclusion criteria, 43 studies (Agúndez et al, 1994;Wundrack et al, 1994;Agúndez et al, 1996;Ladona et al1996;Legrand et al, 1996;London et al, 1997;Agúndez et al, 1998;Febbo et al, 1998; González et al, 1998; Hu et Shaw et al, 1998;Krajinovic et al, 1999;Lemos et al, 1999;Topić et al, 2000;Butler et al, 2001;Liu et al, 2002;Sobti et al, 2003;Chen et al, 2004;Fukatsu et al, 2004;Li et al, 2004;Gajecka et al, 2005;Gomes et al, 2005;Guo et al, 2005;Liang et al, 2005;Mochizuki et al, 2005;Sobti et al, 2005;Aydin-Sayitoglu et al, 2006;Bonanni et al, 2006;Li et al, 2006;Lemos et al, 2007;Chen et al, 2008;Khedhaier et al, 2008;Majumdar et al, 2008;Ouerhani et al, 2008 ;Torresan et al, 2008;Yan et al, 2008;Altayli et al, 2009;Gutman et al, 2009;Lim et al, 2011;Luo et al, 2011;Zhou et al, 2011) appeared to have met the inclusion criteria and were subjected to further examination. The flow chart of study selection is shown...…”

Section: Characteristics Of Included Studiesmentioning

confidence: 99%

Genetic Variants of CYP2D6 Gene and Cancer Risk: A HuGE Systematic Review and Meta-analysis

Zhou

Luan²,

Dong³

et al. 2012

Asian Pacific Journal of Cancer Prevention

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Genetic polymorphisms of metabolic enzymes CYP1A1, CYP2D6, GSTM1 and GSTT1 and leukemia susceptibility

Cited by 50 publications

References 48 publications

Polymorphic Variation in Glutathione-S-transferase Genes and Risk of Chronic Myeloid Leukaemia in the Kashmiri Population

Polymorphic Variation in Glutathione-S-transferase Genes and Risk of Chronic Myeloid Leukaemia in the Kashmiri Population

Genetic polymorphisms of metabolic enzymes—CYP1A1, CYP2D6, GSTM1, and GSTT1, and gastric carcinoma susceptibility

Genetic Variants of CYP2D6 Gene and Cancer Risk: A HuGE Systematic Review and Meta-analysis

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