Paraoxonase 192 gene polymorphism and serum paraoxonase activity in high grade gliomas and meningiomas

Kafadar, Ali; Ergen, Arzu; Zeybek, Ümit; Ağaçhan, Bedia; Kuday, Cengiz; İsbır, Turgay

doi:10.1002/cbf.1284

Cited by 33 publications

(21 citation statements)

References 22 publications

(28 reference statements)

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“…Our review indicated that currently available studies do not provide enough supportive information to establish genes involved in metabolism for PBT risk assessment (Table 3 [71][72][73][74][75][76][77][78][79][80][81][82][83] ). Contradictory results were observed for MTHFR, MTRR, NAT2, and PON1 for glioma.…”

Section: Pbts Molecular Epidemiologic Studies With Focus On Metabolismmentioning

confidence: 99%

Molecular Epidemiology of Primary Brain Tumors

Liu

Kyritsis

et al. 2009

Neurotherapeutics

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Summary:Although primary brain tumors (PBTs) are generally considered to be a multifactorial disorder, understanding the genetic basis and etiology of the disease is essential for PBT risk assessment. Understanding of the genetic susceptibility for PBT has come from studies of rare genetic syndromes, linkage analysis, family aggregation, early-onset pediatric cases, and mutagen sensitivity. There are currently no effective markers to assess biological dose of exposures and genetic heterogeneity. The priorities recently recommended by the Brain Tumor Epidemiology Consortium emphasized the need for expanding research in genetics and molecular epidemiology. In this article, we review the literature to identify molecular epidemiologic case-control studies of PBTs that were hypothesis-driven and focused on four hypothesized candidate pathways: DNA repair, cell cycle, metabolism, and inflammation. We summarize the results in terms of genetic associations of single nucleotide polymorphisms of these pathways. We also discuss future research directions based on available evidence and technologies, and conclude that high resolution whole genome approach with significantly large sample size could rapidly advance our understanding of the genetic etiology of PBTs. Literature searches were done on PubMed in March 2009 with the terms glioma, glioblastoma, brain tumor, association, and polymorphism, and we only reviewed English language publications.

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Section: Pbts Molecular Epidemiologic Studies With Focus On Metabolismmentioning

confidence: 99%

Molecular Epidemiology of Primary Brain Tumors

Liu

Kyritsis

et al. 2009

Neurotherapeutics

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“…Although the activities of these enzymes are assessed in some types The results of recent studies investigating the association between serum PON activity and various forms of cancer are highly variable. In a study conducted by Kafadar et al, serum PON1 activities of patients with high grade glioma and menegioma were significantly lower than controls (20). Similarly, Akçay et al reported decreased serum PON activities in patients with gastric and pancreatic cancers (10,11).…”

Section: Discussionmentioning

confidence: 95%

Serum Paraoxonase and Arylesterase Activities in Esophageal Cancer: A Controlled Study

et al. 2010

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“…In studies evaluating the effect of PON1 192 genotyping on lipid levels, it has been reported that the PON1 192 gene polymorphism is not a major inhibitor in the oxidation of low-density lipoprotein, and for this reason, it may not affect lipid levels (Kafadar et al, 2006;Kucukali et al, 2008). In the present study, there was no significant difference in serum lipid 7 (29) 15 (63) 2 (8) 38 (79) 10 (21) Heterozygote and no mutation (N = 20) 4 (20) 11 (55) 5 (25) 30 (75) 10 (25) Control (N = 51)…”

Section: Discussionmentioning

confidence: 99%

Genetic polymorphisms of paraoxonase1 192 and glutathione peroxidase1 197 enzymes in familial Mediterranean fever

Öktem¹,

Anıl²,

Sütçü³

et al. 2014

Genet. Mol. Res.

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ABSTRACT. Familial Mediterranean fever (FMF) is an autosomal recessive disorder and is the most frequent of the periodic febrile inflammatory syndromes. The pathogenesis of the disease is not completely understood, even though the FMF gene has been identified. Oxidative stress and inflammation may play a role in the pathogenesis of FMF. We investigated gene polymorphisms of the antioxidative enzymes, glutathione peroxidase (GPX) and paraoxonase (PON) in FMF patients, and possible associations with FMF pathogenesis. Sixty FMF patients during an attack-free period and 51 healthy children as the control group were included in our study. PON1 Q/R192 and GPX1 Pro197Leu gene polymorphisms were assayed. Blood urea nitrogen, creatinine and serum lipid profile were also measured. PON1 Q/R192 genotype distribution was 52% QQ, 46% QR and 2% RR in the FMF group and 45% QQ, 45% QR and 10% RR in the control group (P > Familial Mediterranean fever 0.05). GPX1 Pro197Leu genotype distribution was 28% PP, 57% PL, 15% LL in the FMF group and 18% PP, 53% PL, 29% LL in the control group (P > 0.05). Blood urea nitrogen, serum creatinine, lipid levels, and the distribution of PON1 Q/R192 and GPX1 Pro197Leu genotypes were similar in the two groups. We conclude that the PON1 Q/R192 and GPX1 Pro197Leu gene polymorphisms are not important risk factors in the development of FMF. However, larger studies are warranted to validate these conclusions.

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Paraoxonase 192 gene polymorphism and serum paraoxonase activity in high grade gliomas and meningiomas

Cited by 33 publications

References 22 publications

Molecular Epidemiology of Primary Brain Tumors

Molecular Epidemiology of Primary Brain Tumors

Serum Paraoxonase and Arylesterase Activities in Esophageal Cancer: A Controlled Study

Genetic polymorphisms of paraoxonase1 192 and glutathione peroxidase1 197 enzymes in familial Mediterranean fever

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