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Association of FV G1691A, FV H1299R, and FII G20210A variations with thrombosis and coronary artery disease (CAD): A population-based study

dc.contributor.authorÖzmen, Sevda Ünallı
dc.contributor.authorÖzarda, Yeşim
dc.contributor.authorKöseler, Aylin
dc.contributor.authorSabırlı, Ramazan
dc.contributor.authorKaynak, Derya Sucu
dc.contributor.authorKoç, İbrahim
dc.contributor.buuauthorÖzmen, Sevda Unallı
dc.contributor.departmentSağlık Bilimleri Enstitüsü
dc.contributor.departmentTranslasyonel Tıp Ana Bilim Dalı
dc.contributor.researcheridKYR-0994-2024
dc.contributor.researcheridKLY-3251-2024
dc.contributor.researcheridAAD-8992-2019
dc.date.accessioned2025-11-06T16:58:59Z
dc.date.issued2025-01-01
dc.description.abstractBackground: Thrombosis and coronary artery disease (CAD) are complex disorders influenced by genetic factors. Specific gene variations, such as Factor V (FV) G1691A (Leiden), FV H1299R, and Prothrombin (FII) G20210A, have been implicated in thrombotic events and CAD. However, their precise role in CAD development remains controversial. This study investigated the prevalence and association of these gene variations with thrombosis and CAD in the Turkish population. Methods: A case-control study included 406 healthy individuals and 64 CAD patients. Genotyping for FV G1691A, FV H1299R, and FII G20210A was performed using a strip assay. Fisher's exact test compared allele and genotype frequencies between the CAD and control groups. Results: No significant differences were observed in genotype frequencies of FV G1691A, FV H1299R, and FII G20210A between the CAD and control groups (p>0.05). Similarly, allele frequencies did not differ significantly between the two groups (p>0.05). Conclusions: The findings suggest that FV G1691A, FV H1299R, and FII G20210A variations may not play a significant role in the development of CAD in the Turkish population studied. These results are consistent with the existing conflicting literature on the association between these gene variations and CAD. Further research with larger sample sizes and diverse populations is warranted to elucidate the role of these variations in CAD pathogenesis.
dc.identifier.doi10.5937/jomb0-39668
dc.identifier.endpage452
dc.identifier.issn1452-8258
dc.identifier.issue3
dc.identifier.scopus2-s2.0-105008403513
dc.identifier.startpage447
dc.identifier.urihttps://doi.org/10.5937/jomb0-39668
dc.identifier.urihttps://hdl.handle.net/11452/56722
dc.identifier.volume44
dc.identifier.wos001574102700001
dc.indexed.wosWOS.SCI
dc.language.isoen
dc.publisherSociety of Medical Biochemists of Serbia
dc.relation.journalJournal of Medical Biochemistry
dc.subjectFactor V Leiden
dc.subjectProthrombin gene polymorphism
dc.subjectHR2 haplotype
dc.subjectMyocardial infarction
dc.subjectMutation
dc.subjectRisk
dc.subjectPrevalence
dc.subjectFrequency
dc.subjectThromboembolism
dc.subjectMeta-analysis
dc.subjectThrombosis
dc.subjectCoronary artery disease
dc.subjectFactor V gene
dc.subjectProthrombin gene
dc.subjectGene variations
dc.subjectAllele frequencies
dc.subjectScience & technology
dc.subjectLife sciences & biomedicine
dc.subjectBiochemistry & molecular biology
dc.titleAssociation of FV G1691A, FV H1299R, and FII G20210A variations with thrombosis and coronary artery disease (CAD): A population-based study
dc.typeArticle
dspace.entity.typePublication
local.contributor.departmentSağlık Bilimleri Enstitüsü/Translasyonel Tıp Ana Bilim Dalı
local.indexed.atWOS
local.indexed.atScopus

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