Key result
ACE I/D polymorphism D allele linked to ~4-fold higher glioblastoma risk.
Why the study?
High recurrence rates in glioblastoma multiforme highlight the need for new therapeutic targets, and ACE's involvement in angiogenesis and proliferation suggests it may play a role in pathogenesis.
Is the ACE I/D polymorphism associated with an increased risk of glioblastoma in the Turkish population?
Case-Control (n=71)
Is the ACE I/D polymorphism associated with an increased risk of glioblastoma in the Turkish population?
The D allele of the ACE I/D polymorphism is associated with an increased risk of glioblastoma in the Turkish population, suggesting ACE as a potential therapeutic target.
Should not alter ACEi prescribing; leaves open possible glioblastoma risk association pending validation in prospective cohorts.
BACKGROUND/AIM: Glioblastoma multiforme (GBM) is the most aggressive primary brain tumor, with limited survival despite standard treatments such as surgery, radiotherapy, and chemotherapy. High recurrence rates after gross total resection underline the need for identifying new therapeutic targets. Angiotensin-converting enzyme (ACE) plays a role in angiogenesis and cellular proliferation, making it a potential marker in glioblastoma pathogenesis. This study aimed to evaluate the association between ACE I/D polymorphism and glioblastoma in the Turkish population and explore its potential as a therapeutic target. PATIENTS AND METHODS: The study included 35 patients with glioblastoma 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. The I allele exhibited a non-significant protective trend. CONCLUSION: 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.
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Türk et al. (2026) conducted a case-control in Glioblastoma multiforme (GBM) (n=71). ACE I/D polymorphism (D allele) vs. Healthy controls was evaluated on Glioblastoma risk (OR 0.258, 95% CI 0.074-0.901, p=0.027). The D allele of the ACE I/D polymorphism was associated with a fourfold increased risk of glioblastoma (OR 0.258; 95% CI 0.074-0.901; p=0.027).
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