Publication: Yüksek grade glial tümör hastalarinda anjiotensin konverting enzim (ACE) gen polimorfizminin incelenmesi
Abstract
Amaç: Bu çalışmanın amacı ACE I/ D polimorfizmi ile glioblastoma arasındaki ilişkiyi değerlendirmek ve terapötik bir hedef olarak potansiyelini araştırmaktır. Gereç ve Yöntem: Çalışmaya 35 glioblastoma hastası ve 36 sağlıklı kontrol dahil edildi. Periferik kan örneklerinden DNA çıkarıldı ve TaqMan SNP Genotipleme Analizleri kullanılarak genotip belirlendi. İstatistiksel analizler IBM SPSS Statistics (v23) kullanılarak, ki-kare ve Fisher'ın kesin testleri genotip ve alel dağılım farklılıklarını değerlendirerek gerçekleştirildi. Olasılık oranları (OR) ve %95 güven aralıkları (CI) hesaplandı. Bulgular: Genotip dağılımı glioblastoma ve kontrol grupları arasında anlamlı bir fark göstermedi (p=0,171). Ancak D aleli glioblastoma hastalarında (%43,7) kontrollerden (%33,8) anlamlı derecede daha yaygındı (p=0,027), bu da glioblastoma riskinin dört kat arttığını gösteriyordu (OR=0,258, %95 CI=0,074–0,901). I aleli anlamlı olmayan bir koruyucu eğilim gösterdi. Sonuç: Bulgular, ACE I/ D polimorfizminin D alelinin glioblastoma riskine katkıda bulunduğunu ve ACE'nin potansiyel bir terapötik hedef olduğunu vurguladığını ileri sürmektedir. Bu sonuçları doğrulamak ve glioblastoma yönetiminde ACE inhibitörlerinin klinik faydasını araştırmak için daha fazla çalışmaya ihtiyaç vardır.
Objective: This study aims to evaluate the association between ACE I/ D polymorphism and glioblastoma and to explore its potential as a therapeutic target. Materials and Methods: The study included 35 glioblastoma patients and 36 healthy controls. DNA was extracted from peripheral blood samples and genotyped using TaqMan SNP Genotyping Assays. Statistical analyses were conducted using IBM SPSS Statistics (v23), with chi-square and Fisher's exact tests assessing genotype and allele distribution differences. Odds ratios (OR) and 95% confidence intervals (CI) were calculated. Results: Genotype distribution showed no significant differences between glioblastoma and control groups (p=0.171). However, the D allele was significantly more prevalent in glioblastoma patients (43.7%) than in controls (33.8%) (p=0.027), indicating a fourfold increased risk of glioblastoma (OR=0.258, 95% CI=0.074–0.901). The I allele exhibited a non-significant protective trend. Conclusion: The findings suggest that the D allele of the ACE I/ D polymorphism contributes to glioblastoma risk, highlighting ACE as a potential therapeutic target. Further studies are needed to confirm these results and investigate the clinical utility of ACE inhibitors in glioblastoma management.
Objective: This study aims to evaluate the association between ACE I/ D polymorphism and glioblastoma and to explore its potential as a therapeutic target. Materials and Methods: The study included 35 glioblastoma patients and 36 healthy controls. DNA was extracted from peripheral blood samples and genotyped using TaqMan SNP Genotyping Assays. Statistical analyses were conducted using IBM SPSS Statistics (v23), with chi-square and Fisher's exact tests assessing genotype and allele distribution differences. Odds ratios (OR) and 95% confidence intervals (CI) were calculated. Results: Genotype distribution showed no significant differences between glioblastoma and control groups (p=0.171). However, the D allele was significantly more prevalent in glioblastoma patients (43.7%) than in controls (33.8%) (p=0.027), indicating a fourfold increased risk of glioblastoma (OR=0.258, 95% CI=0.074–0.901). The I allele exhibited a non-significant protective trend. Conclusion: The findings suggest that the D allele of the ACE I/ D polymorphism contributes to glioblastoma risk, highlighting ACE as a potential therapeutic target. Further studies are needed to confirm these results and investigate the clinical utility of ACE inhibitors in glioblastoma management.