Prognostic value of TP53 Pro47Ser and Arg72Pro single nucleotide polymorphisms and the susceptibility to gliomas in individuals from Southeast Brazil

Pinto, Giovanny R.; Yoshioka, Fumi; Silva, R L L; Clara, Carlos Afonso; Santos, Marcelo José dos; Almeida, J. R. W.; Burbano, Rommel Rodrı́guez; Rey, Juan A.; Casartelli, Cacilda

doi:10.4238/vol7-1gmr415

Cited by 46 publications

(31 citation statements)

References 34 publications

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“…Studies that looked at the correlations between cell cycle genes and glioma risk did not generate a clear pattern (Table 2 43,. The positive association between EGF/EGFR and glioma risk was observed in majority of the case-control studies published.…”

Section: Pbts Molecular Epidemiologic Studies With Focus On Cell Cyclementioning

confidence: 99%

“…We have listed about 20 epidemiological studies reporting positive associations between DNA repair polymorphisms and cancer risk (Table 1 [29][30][31][32][33][34][35][36][37][38][39][40][41][42][43][44][45] ). Only a small proportion of studies were large (five studies were more than 500 pair cases and controls) and population based; however, some consistencies in results are apparent.…”

Section: Pbts Molecular Epidemiologic Studies With Focus On Dna Repairmentioning

confidence: 99%

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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 Cell Cyclementioning

confidence: 99%

Section: Pbts Molecular Epidemiologic Studies With Focus On Dna Repairmentioning

confidence: 99%

Molecular Epidemiology of Primary Brain Tumors

Liu

Kyritsis

et al. 2009

Neurotherapeutics

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“…15 Finally, the low frequency of the S47 polymorphism (1-5% of African Americans and Brazilians) precludes the ability to associate this polymorphism with cancer risk in a statistically significant way. 16,17 These facts constitute a compelling argument for modeling these polymorphisms in the mouse.…”

Section: Introductionmentioning

confidence: 99%

Tissue-specific apoptotic effects of the p53 codon 72 polymorphism in a mouse model

Azzam¹,

Frank²,

Hollstein³

et al. 2011

Cell Cycle

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Currently there are several dozen human polymorphisms that have been loosely associated with cancer risk. Correlating such variants with cancer risk has been challenging, primarily due to factors such as genetic heterogeneity, contributions of diet and environmental factors, and the difficulty in obtaining large sample sizes for analysis. Such difficulties can be circumvented with the establishment of mouse models for human variants. Recently, several groups have modeled human cancer susceptibility polymorphisms in the mouse. Remarkably, in each case these mouse models have accurately reflected human phenotypes, and clarified the contribution of these variants to cancer risk. We recently reported on a mouse model for the codon 72 polymorphism in p53, and found that this polymorphism regulates the ability to cooperate with NFκB and induce apoptosis. Here-in we present evidence that this polymorphism impacts the apoptotic function of p53 in a tissue-specific manner; such tissue-specific effects of polymorphic variants represent an added challenge to human cancer risk association studies. The data presented here support the premise that modeling human polymorphisms in the mouse represents a powerful tool to assess the impact of these variants on cancer risk, progression and therapy.

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“…We identified 10 reports that evaluated the association of p53 Arg72Pro and glioma susceptibility (Wang et al, 2004;Parhar et al, 2005;Malmer et al, 2005Malmer et al, , 2007Rajaraman et al, 2007;Idbaih et al, 2008;Lima-Ramos et al, 2008;Pinto et al, 2008;El Hallani et al, 2009;and Jha et al, 2011;see Table 1). Included were 2587 cases and 4061 controls, and all data were used in the current meta-analysis.…”

Section: Association Between P53 Arg72pro and Glioma Susceptibilitymentioning

confidence: 99%

Association of p53 Arg72Pro and MDM2 SNP309 polymorphisms with glioma

Sh²,

Xh³

et al. 2012

Genet. Mol. Res.

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ABSTRACT. Epidemiological studies of the association of variants p53 Arg72Pro and MDM2 single-nucleotide polymorphism 309 (SNP309) with glioma risk have produced inconsistent results. The aim of the current study was to evaluate the association of these 2 variants with glioma susceptibility using a meta-analysis approach. For p53 Arg72Pro, 10 case-control studies including 2587 glioma patients and 4061 unrelated controls were identified. The pooled odds ratios (ORs) for Arg/Pro heterozygotes and Pro/Pro homozygotes were 1.08 [95% confidence interval (95%CI) = 0.85-1.37] and 1.08 (95%CI = 0.85-1.36), respectively, when compared to Arg/Arg carriers. Under the dominant effect model, Pro allele carriers also showed no significantly elevated glioma risk (pooled OR = 1.11, 95%CI = 3619 ©FUNPEC-RP www.funpecrp.com.br Genetics and Molecular Research 11 (4): 3618-3628 (2012) p53 and MDM2 polymorphisms and glioma susceptibility 0.90-1.38), and similar results were found under the recessive-effect model (pooled OR = 1.17, 95%CI = 0.85-1.61). For variant MDM2 SNP309, 3 case-control studies including 606 cases and 309 controls were identified. A marginal association with glioma risk was found for heterozygous G/T carriers (pooled OR = 1.95, 95%CI = 1.00-3.81), whereas homozygous G/G carriers showed an increased but not significantly elevated risk of glioma (pooled OR = 2.14, 95%CI = 0.71-6.45) compared with that of T/T homozygotes. We also found no significant association between the MDM2 SNP309 polymorphism and glioma risk (pooled OR = 1.86, 95%CI = 0.94-3.67 and pooled OR = 1.25, 95%CI = 0.62-2.56, respectively) under the dominant and recessive models. Taken together, the current data suggested that the 2 polymorphisms may not contribute to glioma susceptibility.

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Prognostic value of TP53 Pro47Ser and Arg72Pro single nucleotide polymorphisms and the susceptibility to gliomas in individuals from Southeast Brazil

Cited by 46 publications

References 34 publications

Molecular Epidemiology of Primary Brain Tumors

Molecular Epidemiology of Primary Brain Tumors

Tissue-specific apoptotic effects of the p53 codon 72 polymorphism in a mouse model

Association of p53 Arg72Pro and MDM2 SNP309 polymorphisms with glioma

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