NAD(P)H:quinone oxidoreductase 1 null genotype is not associated with pediatric de novo acute leukemia

Sırma, Sema; Ağaoğlu, Leyla; Yıldız, İnci; Cayli, Dilara; Horgusluoglu, Emrin; Anak, S.; Yüksel, Lebriz; Ünüvar, Ayşegül; Çelkan, Tiraje; Apak, Hilmi; Karakaş, Zeynep; Devecioğlu, Ömer; Özbek, Uğur

doi:10.1002/pbc.20098

Cited by 34 publications

(22 citation statements)

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“…Pooling data from all seven studies, however, provided no evidence of a relationship between NQO1 C609T genotype and risk (Online Supplementary Figure S1). Controls in the study by Sirma et al 56 showed evidence of population stratification (P=0.01). In pooling data from the six other studies (Table 2; Online Supplementary Figure S2), there was evidence for a relationship between carrier status and risk (1.24, 95% CI: 1.02-1.50, P=0.03; Phet=0.49, I2=0%) but no relationship with either hetero-or homozygosity (data not shown).…”

Section: Meta-analysismentioning

confidence: 87%

“…The majority of them [29][30][31][32][33][34][35][40][41][42][43][44][46][47][48][51][52][53][54][55][56]59,60,62,63,65,67,68,70,71,74 were DNA extracted from peripheral blood, bone marrow or buccal samples collected at the time of diagnosis at the study center or with unspecified patient status. Five studies included samples from remission and those collected at diagnosis.…”

Section: Discussionmentioning

confidence: 99%

“…Seven studies 35,36,[53][54][55][56][57] have evaluated NQO1 C609T as a risk factor for ALL (Table 2; Online Supplementary Figure S1; Online Supplementary Table S1). The study by Lanciotti et al 53 only provided data on 609T carrier status.…”

Section: Meta-analysismentioning

confidence: 99%

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Candidate gene association studies and risk of childhood acute lymphoblastic leukemia: a systematic review and meta-analysis

Vijayakrishnan¹,

Houlston²

2010

Haematologica

111

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To evaluate the contribution of candidate gene association studies to the understanding of genetic susceptibility to childhood acute lymphoblastic leukemia we conducted a systematic review and meta-analysis of published studies (January 1996-July 2009. Studies had to meet the following criteria: be case-control design, be studied by two or more studies, not be focused on HLA antigen genetic markers and be published in English. We identified 47 studies of polymorphic variation in 16 genes and acute lymphoblastic leukemia risk. To clarify the impact of individual polymorphisms on risk, pooled analyses were performed. Of the 25 polymorphic variants studied, significant associations (P<0.05) were seen in pooled analyses for eight variants: GSTM1 (OR =1.16; 95%CI: 1.04-1.30), MTRR A66G (OR=0.73, 95%CI:0.59-0.91), SHMT1 C1420T (OR=0.79, 95%CI: 0.65-0.98), RFC1 G80A (OR=1.37, 95%CI: 1.11-1.69), CYP1A1*2A (OR=1.36, 95%CI:1.11-1.66), CYP2E1*5B (OR=1.99, 95%CI:1.32-3.00) NQO1 C609T (OR=1.24, 95%CI:1.02-1.50) and XRCC1 G28152A (OR=1.78, 95%CI:1.32-2.42). These findings should, however, be interpreted with caution as the estimated false-positive report probabilities (FPRP) for each association were not noteworthy (i.e. FPRP>0.2). While candidate gene analyses are complementary to genome-wide association studies, future analyses should be based on sample sizes commensurate with the detection of small effects and attention needs to be paid to study design.Key words: polymorphisms, acute lymphoblastic leukemia, risk, meta-analysis, false positive report probabilities. -analysis. Haematologica 2010;95(8):1405-1414. doi:10.3324/haematol.2010 This is an open-access paper. Citation: Vijayakrishnan J and Houlston RS. Candidate gene association studies and risk of childhood acute lymphoblastic leukemia: a systematic review and meta IntroductionAcute leukemia is the major pediatric cancer in developed countries, affecting between 30-45 per 1,000,000 children each year.1 Dysregulated immune response to infection may be a cause of childhood acute lymphoblastic leukemia (ALL) 2 and epidemiological data are consistent with transplacental carcinogen exposure as a basis for infant leukemia associated with MLL gene fusion, 3 but the role of environmental carcinogenesis in ALL is currently undefined. It is, however, likely that the risk of ALL from environmental exposure is influenced by co-inheritance of multiple low-risk variants.The commonest method for identifying common low-risk variants is through association studies. These are based on comparing the frequency of polymorphic genotypes in cases and controls. Alleles positively associated with the disease are analogous to risk factors in epidemiology and may be causally related to disease risk or in linkage disequilibrium with disease-causing variants. There are a number of different methods of analyzing the risk associated with a specific variant. For simple bi-allelic polymorphisms, the odds ratio of disease can be derived by comparing allele frequencies in cases and controls. This ap...

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Section: Meta-analysismentioning

confidence: 87%

Section: Discussionmentioning

confidence: 99%

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Candidate gene association studies and risk of childhood acute lymphoblastic leukemia: a systematic review and meta-analysis

Vijayakrishnan¹,

Houlston²

2010

Haematologica

111

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“…Studies of Caucasian and Japanese patients have shown that the occurrence of alleles conferring lowactivity variants of NQO1 was associated with an increased risk of IAL, especially with MLL /AF4 fusion genes (51,52). Sirma et al (53) demonstrated that in pediatric ALL without MLL rearrangements, the null genotype of the NQO1 gene is not associated with the etiology of the disease. Recently, in a series of Italian IAL cases, contradictory results were obtained, with this polymorphism appearing to be associated with infant ALL without MLL rearrangements, but not with MLL-positive infants (54).…”

Section: Gene-environment Interactionmentioning

confidence: 99%

Acute leukemia in early childhood

Emerenciano

Koifman

Pombo‐de‐Oliveira

2007

Braz J Med Biol Res

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Acute leukemia in early childhood is biologically and clinically distinct. The particular characteristics of this malignancy diagnosed during the first months of life have provided remarkable insights into the etiology of the disease. The pro-B, CD10 negative immunophenotype is typically found in infant acute leukemia, and the most common genetic alterations are the rearrangements of the MLL gene. In addition, the TEL /AML1 fusion gene is most frequently found in children older than 24 months. A molecular study on a Brazilian cohort (age range 0-23 months) has detected TEL /AML1 +ve (N = 9), E2A/PBX1 +ve (N = 4), PML /RARA +ve (N = 4), and AML1/ETO +ve (N = 2) cases. Undoubtedly, the great majority of genetic events occurring in these patients arise prenatally. The environmental exposure to damaging agents that give rise to genetic changes prenatally may be accurately determined in infants since the window of exposure is limited and known. Several studies have shown maternal exposures that may give rise to leukemogenic changes. The Brazilian Collaborative Study Group of Infant Acute Leukemia has found that mothers exposed to dipyrone, pesticides and hormones had an increased chance to give birth to babies with infant acute leukemia [OR = 1.48 (95%CI = 1.05-2.07), OR = 2.27 (95%CI = 1.56-3.31) and OR = 9.08 (95%CI = 2.95-27.96)], respectively. This review aims to summarize recent clues that have facilitated the elucidation of the biology of early childhood leukemias, with emphasis on infant acute leukemia in the Brazilian population.

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“…Estudos epidemiológicos têm mostrado um risco elevado do desenvolvimento de leucemias em crianças, associado com a exposição ambiental a pesticidas (Daniels et al, 1997;Zahm;Ward, 1998), com o uso materno de drogas, tais como o cigarro e bebidas alcoólicas, e com exposição parental a pesticidas (Severson et al, 1993;Buckley et al, 1994;Ross et al, 1994;Shu et al, 1996; Lemos et al, 1999;Garte et al, 2001;Krajinovic et al, 2002b;Rossit et al, 2002;Sirma et al, 2004;Duarte et al, 2005;Joseph et al, 2005). No presente estudo, a análise multivariada considerando etnia e sexo como co-variáveis, não modificou as conclusões para todas as variantes testadas.…”

Section: Polimorfismos De Enzimas Metabolizadoras De Xenobióticos E Aunclassified

Polimorfismos genéticos, susceptibilidade e resposta ao tratamento em crianças portadoras de leucemia linfoblástica aguda

Andrade¹

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NAD(P)H:quinone oxidoreductase 1 null genotype is not associated with pediatric de novo acute leukemia

Cited by 34 publications

References 10 publications

Candidate gene association studies and risk of childhood acute lymphoblastic leukemia: a systematic review and meta-analysis

Candidate gene association studies and risk of childhood acute lymphoblastic leukemia: a systematic review and meta-analysis

Acute leukemia in early childhood

Polimorfismos genéticos, susceptibilidade e resposta ao tratamento em crianças portadoras de leucemia linfoblástica aguda

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