Unveiling the etiological impact of GST-M1, GST-T1, and P53 genotypic variations on brain carcinogenesis

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dc.authoridhttps://orcid.org/0000-0003-0511-6611en_US
dc.authoridhttps://orcid.org/0000-0002-8861-7106en_US
dc.authoridhttps://orcid.org/0000-0001-5772-2838en_US
dc.contributor.authorDirican, Onur
dc.contributor.authorKaygın, Pınar
dc.contributor.authorOğuztüzün, Serpil
dc.contributor.authorHusseini, Abbas Ali
dc.contributor.authorYılmaz Sarıaltın, Sezen
dc.contributor.authorYılmaz, Can
dc.contributor.authorÜnlü, Nihan
dc.contributor.authorİzci, Yusuf
dc.date.accessioned2024-03-13T01:51:48Z
dc.date.available2024-03-13T01:51:48Z
dc.date.issued2024en_US
dc.departmentSağlık Hizmetleri Meslek Yüksekokuluen_US
dc.description.abstractBackground Functional variants of glutathione-S-transferase (GST)-M1, GST-T1, p53 might modulate brain cancer risk by altering the rate of metabolism and clearance of carcinogens from the brain tissue. In this study, the role of GST-M1, GSTT1, p53 polymorphisms on brain tumor was investigated. Methods and results Brain tumor tissues of 143 patients were obtained from the Gulhane Training and Research Hospital, Department of Neurosurgery between 2019 and 2020. In the xenobiotic mechanism, the null allele frequency in the GST-T1, GST-M1 gene regions of Phase II enzymes by qPCR method were investigated. Single nucleotide polymorphism encoding Arg/Pro conversion in the p53 gene region was analyzed in 120 cases by sequence analysis method. The data were analyzed statistically with patient’s demographic and clinical data. GST-M1, GST-T1, p53 genotypes of the patient group were determined. The most frequent genotype was null genotype (0/0) for GST-M1 (?2=39.756, p<0.001). GST-M1 genotype frequencies were 30.8%, 23.1%, 44.3% for 1/1, 1/0, 0/0, respectively. The most frequent genotype was GST-T1 1/1 following by GST-T1 1/0 (?2=0.335, p=0.846). GST-T1 genotype frequencies were 64.3%, 30.8%, 4.9% for 1/1, 1/0, 0/0, respectively. GST-M1 null genotype might be associated with the development of brain tumors. Genotype distribution obtained in p53 exon 4 codon 72; Arg/Arg was determined as 31 (25.8%), Arg/Pro 70 (58.3%), and Pro/Pro 19 (15.8%) in the case group, while there were 18 (38.3%), 23 (48.9%), and 6 (12.8%) respectively in the control group. However, the genotype distribution of p53 exon 4 codon 72 among tumorous tissue did not significantly vary from healthy control tissues (?²=2.536, p=0.281). Conclusion The null allele frequency encountered in the GST-M1, GST-T1 gene regions is consistent with the rates in the gene pool called Caucasian in the literature. GST-M1 gene polymorphism may play a crucial role in brain carcinogenesis in Turkish patients. This study based on clinical data is thought to help to understand the important epidemiological features of brain tumors.en_US
dc.identifier.doi10.1007/s11033-023-08985-2en_US
dc.identifier.endpage8en_US
dc.identifier.issn0301-4851
dc.identifier.issn1573-4978
dc.identifier.issue1en_US
dc.identifier.pmid38158432en_US
dc.identifier.scopus2-s2.0-85181224591en_US
dc.identifier.scopusqualityQ2en_US
dc.identifier.startpage1en_US
dc.identifier.urihttps://hdl.handle.net/11363/7194
dc.identifier.urihttps://doi.org/
dc.identifier.volume51en_US
dc.identifier.wosWOS:001132269100003en_US
dc.identifier.wosqualityN/Aen_US
dc.indekslendigikaynakWeb of Scienceen_US
dc.indekslendigikaynakScopusen_US
dc.indekslendigikaynakPubMeden_US
dc.institutionauthorDirican, Onur
dc.institutionauthorHusseini, Abbas Ali
dc.institutionauthorÜnlü, Nihan
dc.language.isoenen_US
dc.publisherSPRINGERVAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDSen_US
dc.relation.ispartofMOLECULAR BIOLOGY REPORTSen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/openAccessen_US
dc.subjectBrain tumorsen_US
dc.subjectGST-T1en_US
dc.subjectGST-M1en_US
dc.subjectp53en_US
dc.subjectPolymorphismen_US
dc.titleUnveiling the etiological impact of GST-M1, GST-T1, and P53 genotypic variations on brain carcinogenesisen_US
dc.typeArticleen_US

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