Genetic polymorphisms of arylamine N-acetyltransferases 1 and 2 and the likelihood of developing pediatric acute lymphoblastic leukemia

Hernández-González, Oswaldo; Ortiz-Zamudio, Juan José; Rodríguez-Pinal, Cristian Jazmín; Alvarado-Morales, Ildemar; Martínez-Jiménez, Verónica; Salazar‐González, Raúl A.; Correa-González, Lourdes Cecilia; Gómez, Rocío; Portales-Pérez, Diana Patricia; Milán‐Segovia, Rosa del Carmen

doi:10.1080/10428194.2017.1406090

Cited by 8 publications

(10 citation statements)

References 30 publications

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“…Studies in Mexican children have documented a folate deficiency in 11.2% of the children aged 4 years, which could explain our results (51). Nevertheless, our findings in the control group differ of those frequencies reported in general population from different regions of Mexico (43,50,52). NAT2 gene has a high frequency of functional variation that differs among ethnically diverse populations, in fact, NAT2 functional variation contributes to high levels of diversity, illustrating how geographically and temporally fluctuating xenobiotic environments may have influenced our genome variability and susceptibility to disease (52,53).…”

Section: Discussioncontrasting

confidence: 84%

“…Previous studies have suggested that the rapid-acetylator genotype of NAT2 leads to an increased risk of various types of cancer, particularly leukemia, colorectal and bladder cancer (4,(41)(42)(43)(44)(45). As it has been reported in Caucasian and Middle Eastern populations, rapid acetylator phenotypes were less frequent than slow acetylator phenotypes (4,39,46), but no statistical significance was observed between cases and controls.…”

Section: Discussionmentioning

confidence: 87%

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Genotype-Environment Interaction Analysis of NQO1, CYP2E1, and NAT2 Polymorphisms and the Risk of Childhood Acute Lymphoblastic Leukemia: A Report From the Mexican Interinstitutional Group for the Identification of the Causes of Childhood Leukemia

et al. 2020

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Section: Discussioncontrasting

confidence: 84%

Section: Discussionmentioning

confidence: 87%

Genotype-Environment Interaction Analysis of NQO1, CYP2E1, and NAT2 Polymorphisms and the Risk of Childhood Acute Lymphoblastic Leukemia: A Report From the Mexican Interinstitutional Group for the Identification of the Causes of Childhood Leukemia

et al. 2020

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“…21 Genes encoding the NAT1 and NAT2 isoenzymes are highly polymorphic among populations, which lead to interindividual variability in N-acetylation capacity. 22 In our study, capecitabine O-acetylation was primarily catalyzed by the NAT2 isozyme. We believe that NAT1 and NAT2 polymorphic variants may influence the metabolism of capecitabine.…”

Section: Discussionmentioning

confidence: 47%

“…NAT1 is expressed in various tissues including the liver, intestine, and bladder, whereas NAT2 is locally expressed in the liver and intestine . Genes encoding the NAT1 and NAT2 isoenzymes are highly polymorphic among populations, which lead to interindividual variability in N-acetylation capacity . In our study, capecitabine O-acetylation was primarily catalyzed by the NAT2 isozyme.…”

Section: Discussionmentioning

confidence: 56%

Identification of the Novel Capecitabine Metabolites in Capecitabine-Treated Patients with Hand-Foot Syndrome

Lou

Wang

Zheng

et al. 2018

Chem. Res. Toxicol.

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Hand-foot syndrome (HFS), the most common side effect of capecitabine, is a dose-limiting cutaneous toxicity with only rare therapeutic options. The causative mechanisms of HFS are still unclear. Many studies suggested that capecitabine or its metabolites caused the toxicity. This study is attempting to determine if there are any new metabolites that may be present and be linked to toxicity. For this purpose, 25 patients who ingested capecitabine orally were enrolled and divided into HFS positive and negative groups. Urine and plasma samples were collected before administration and five cycles after administration. Eleven phase I and phase II metabolites of capecitabine were detected and identified by ultraperformance liquid chromatography coupled with quadrupole time-of-flight tandem mass spectrometry with a metabolomic approach and MetaboLynx. Nine novel metabolites of capecitabine were identified herein, which were not observed in the HFS negative group. Their structures were confirmed by chemical synthesis and nuclear magnetic resonance spectroscopy. The cytotoxities of capecitabine and its metabolites on HaCaT cells were measured. Among them, M9/10 exhibited significant inhibitory activity, and they were produced via acetylation mainly by N-acetyltransferase 2. Our study comprehensively described the metabolism of capecitabine in patients with HFS and detected the novel pathways of capecitabine, which was a positive significance for the mechanism of HFS.

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“…NAT2 is located on chromosome 8 (8p21.3-23.1 and 8p22) (Hernández-González et al, 2018) and is a Phase II drug-metabolizing enzyme. It catalyzes the detoxification of common carcinogens and the acetylation of numerous clinically used drugs eg: isoniazid, sulfonamides, procainamide, and hydrazine (Adithan and Subathra, 2016).…”

Section: Evaluation Of Genetic Polymorphisms Of N-acetyltransferase 2mentioning

confidence: 99%

Evaluation of Genetic Polymorphisms of N-acetyltransferase 2 and Relation with Chronic Myeloid Leukemia

Tebien

Khalil

Mills

et al. 2020

Asian Pac J Cancer Prev

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Objectives: The N-Acetyltransferase 2 (NAT2) gene encodes a key enzyme involved in xenobiotic metabolism, which contributes to the detoxification of numerous cancer therapy-induced products. However, the NAT2 genotype/phenotype is not fully understood and few studies have reported its relationship with CML. The aim of this study was to determine whether its polymorphisms ( C481T, G590A, 803A>G and 857G>A ) have a role in chronic myeloid leukemia susceptibility (CML) in Sudanese population. Methods: We performed a case- control study. DNA from 200 CML patients and 100 controls was analyzed for the NAT2 polymorphisms using PCR-RFLP assay. Results: The study showed NAT2 polymorphisms 803AG are associated with CML protection by a factor of 2.3, (OR = 0.044, 95% CI: 0.020-0.095, p = 0. 000). The study indicated that the heterozygous (GA) and mutant (AA) variants of the G857A genotype also offer protection, (OR = 0.002, 95% CI: 0.002-0.019, p = 0. 000) and (OR = 0.018, 95% CI: 0.002-0.133, p = 0. 000), respectively. Conclusion: There was no significant difference in CML diagnosis among Sudanese cases with the 481C→T and 590G→A polymorphisms. But patients with the compound NAT2 genotypes 481CT/803 AG, 590AG/ 803AG, 590AG/ 803GG, 590AA/ 803AG and 590GG/ 803AG were found to have a reduced risk. The current study demonstrates that polymorphisms of NAT2 A803G and G857A might also act as protective factors against developing the disease.

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Genetic polymorphisms of arylamine N-acetyltransferases 1 and 2 and the likelihood of developing pediatric acute lymphoblastic leukemia

Cited by 8 publications

References 30 publications

Genotype-Environment Interaction Analysis of NQO1, CYP2E1, and NAT2 Polymorphisms and the Risk of Childhood Acute Lymphoblastic Leukemia: A Report From the Mexican Interinstitutional Group for the Identification of the Causes of Childhood Leukemia

Genotype-Environment Interaction Analysis of NQO1, CYP2E1, and NAT2 Polymorphisms and the Risk of Childhood Acute Lymphoblastic Leukemia: A Report From the Mexican Interinstitutional Group for the Identification of the Causes of Childhood Leukemia

Identification of the Novel Capecitabine Metabolites in Capecitabine-Treated Patients with Hand-Foot Syndrome

Evaluation of Genetic Polymorphisms of N-acetyltransferase 2 and Relation with Chronic Myeloid Leukemia

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