Polymorphisms in the matrix metalloproteinase-9 promoters and susceptibility to glial tumors in turkey

Ozden, Mahmut; Katar, Salim; Hanımoğlu, Hakan; Ulu, Mustafa Onur; İşler, Cihan; Baran, Oğuz; Antar, Veysel; Ekmekçi, Cumhur Gökhan; Kaynar, Mehmet Yaşar

doi:10.5137/1019-5149.jtn.17960-16.1

Cited by 3 publications

(4 citation statements)

References 23 publications

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“…The genotyping for three SNPs was carried out according to previous studies. 14 The blind DNA duplicates were used to control the quality of genotyping for random samples. Twenty samples were also randomly chosen for each genotype and the amplicons were sequenced in CEQ, 8000 System (Beckman Coulter, England); 100% consistency was observed between genotyping assays.…”

Section: Methodsmentioning

confidence: 99%

Matrix metalloproteinase-9 gene polymorphisms and their interaction with environment on subarachnoid hemorrhage risk

Wang

Song

et al. 2018

Exp Biol Med (Maywood)

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The current study aimed to investigate the relations of three single nucleotide polymorphisms of matrix metalloproteinase-9 gene, and single nucleotide polymorphisms-smoking interaction to subarachnoid hemorrhage risk. The optimal pattern of the interaction among single nucleotide polymorphisms and smoking was selected by generalized multifactor dimensionality reduction. The association between the three single nucleotide polymorphisms within the matrix metalloproteinase-9 gene was analyzed by logistic regression test. As well as genetic risk of subarachnoid hemorrhage interactions with smoking, the risk of subarachnoid hemorrhage in carriers with the rs3918242 (T) was significantly higher than in carriers carrying CC (genotype: CT + TT vs. CC), adjusted OR (95% CI) = 1.58 (1.25-2.03), and in carriers carrying rs17576- (genotype: AG + GG vs. AA), adjust OR (95% CI) = 1.62 (1.19-2.13). However, after adjusting for covariates, we did not find any direct association between rs17577 and subarachnoid hemorrhage risk. The generalized multifactor dimensionality reduction model shows a potential relation between rs3918242 and smoking risk for subarachnoid hemorrhage ( P = 0.0010). After covariates adjustment, current smokers with rs3918242-CT or TT genotype, compared to never-smokers with rs3918242-CC genotype, OR (95% CI) = 2.57 (1.74-3.46), have a higher subarachnoid hemorrhage risk. Our study showed that the rs3918242 (T) and rs17576 (G), the cross reaction between rs3918242 and smoking increased the risk of subarachnoid hemorrhage. Impact statement Matrix metalloproteinase-9 ( MMP-9) is a possible candidate gene for some diseases, including metabolic syndrome, stroke, coronary artery disease (CAD). But to date, limited data focused on the relationship between MMP-9 gene SNPs and SAH susceptibility. The purpose of this study was to evaluate SNPs of MMP-9 gene and their interaction with environmental factors with SAH risk based on a Chinese population.

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Section: Methodsmentioning

confidence: 99%

Matrix metalloproteinase-9 gene polymorphisms and their interaction with environment on subarachnoid hemorrhage risk

Wang

Song

et al. 2018

Exp Biol Med (Maywood)

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“…Numerous SNPs have been reported in different genes in gliomas (4). A few of these reported SNPs (rs1052576, rs55705857, and rs17577) have been investigated to find if they are associated with gliomas, in studies performed in the Turkish population (12)(13)(14)(15). According to human genome studies, EGFR gene SNPs may both be protective against glioma and offer a risk for it.…”

Section: Ozcan Et Al Egfr Snp Rs1468727 In Gliomamentioning

confidence: 99%

Association of EGFR Gene Polymorphism with Glioma Susceptibility in Turkish Population

Özcan¹,

Akdeniz²,

Yılmaz³

et al. 2023

experimed

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Objective: Gliomas are devastating adult brain tumors of unknown etiology, occupying 8 out of 10 primary brain tumors. Epidermal growth factor receptor (EGFR) as a tyrosine kinase family member is encoded by the EGFR gene located in chromosome 7p12-13. Various studies have identified numerous SNPs, including those in the EGFR gene, as linked to gliomas. The objective of the investigation was to determine whether the genotype and allele frequencies of the EGFR may have a role in glioma susceptibility. Materials and Methods:To examine the association of EGFR SNP rs1468727 with glioma susceptibility in a case-control study from Türkiye (34 cases, 36 controls), genotyping and statistical analyses were performed by using real-time-polymerase chain reaction (RT-PCR) and SPSS version 25.0, respectively.Results: A significant relationship was found between the study groups EGFR SNP rs1468727 genotypes (p = 0.028). The CC genotype frequency was significantly greater in the control group compared to the glioma group (p=0.005). When compared with the control group, the frequency of mutant type T allele carriers was significantly higher in glioma patients (p=0.012). Conclusion:As a result of the preliminary findings, having the mutant T allele may increase risk by 3.36 times, whereas having the ancestral homozygote CC genotype lowers the risk for glioma in Turkish population.

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“…The main linking substances able to relate inflammation to tumorigenesis through the oxidative/nitrosative stress, are prostaglandins and cytokines [61,83]. Therefore, long-term lack of oxygen on immature glial cells is the primary cause in the genesis of gliomas; that is of the uncontrollable growth of glioma cells, expressed as astrocyte proliferation (Figure 1).…”

Section: Genesis Of Gliomas In the Encephalonmentioning

confidence: 99%

“…Therefore, peri-ependymal ischemia is the primary cause of syringomyelia and syringobulbia, while hypoxia in moderate to severe degree causes ependymomas. Both pathologies related to localized atheromatous plaques at the mouths of the vertebral arteries [21,24,27,43], trauma in the spinal cord [96] and anatomical variants of the antero-ventral spinal arteries, postero-lateral spinal arteries, radicular arteries and anterior spinal artery [36,[98][99][100] as well as of circulating environmental chemicals in the bloodstream [11,12,62,[82][83][84].…”

Section: Syringomyelia and Ependymomasmentioning

confidence: 99%

Etiopathogenesis of Central Nervous System Gliomas

Rafael¹

2017

J Oncol Transl Res

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There is much evidence that gliomas are caused by progressive ischemia, followed by increasing and prolonged hypoxia very close to the subventricular zone. In this way, hypoxia on immature glial cells is the primary cause in gliomas genesis. The ischemic process caused by atherosclerosis, anatomical variants of the arteries in the affected area and associated with carcinogenic agents are the harmful factors. While cytotoxic hypoxia triggers a reactive oxygen species (ROS) overproduction in the glial progenitor cells. Consequently, cellular impairment caused by ROS alters the cell cycle phases and provokes genesis of low-grade glioma. Subsequently, its progression causes angiogenesis and higher-grade cancer cells. Then, the vascular recanalization through aspirin is the indicated therapy to reduce the ischemic process by increasing blood flow and oxygen in the affected zone. Therefore, we must fight against the genesis of atherosclerosis and thus decrease the incidence of "neurodegenerative" diseases and cancer.

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Polymorphisms in the matrix metalloproteinase-9 promoters and susceptibility to glial tumors in turkey

Cited by 3 publications

References 23 publications

Matrix metalloproteinase-9 gene polymorphisms and their interaction with environment on subarachnoid hemorrhage risk

Matrix metalloproteinase-9 gene polymorphisms and their interaction with environment on subarachnoid hemorrhage risk

Association of EGFR Gene Polymorphism with Glioma Susceptibility in Turkish Population

Etiopathogenesis of Central Nervous System Gliomas

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