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Glioblastoma multiforme (GBM) is the most common form of primary brain tumors. Although mutations in isocitrate dehydrogenase‐1 (IDH1) have been identified in a number of cancers, their role in tumor development has not been fully elucidated. In this preliminary study we aimed to investigate the association between IDH1 mutations, tumor tissue HIF‐1 alpha and serum VEGF levels in patients with primary GBM.32 patients (mean age, years: 58 ± 14.0) diagnosed with primary glioblastoma multiforme were screened for IDH1 mutations (R132H, R132S, R132C and R132L) by direct sequencing. Serum VEGF and tumor tissue HIF1‐alpha levels were measured by ELISA. Associations between categoric variables were determined using chi‐square tests. Differences between two groups were compared with t test for continuous variables. Two patients were heterozygous for R132H mutation (6%). Tumor HIF1‐alpha and serum VEGF levels were found to be significantly increased in IDH1‐mutated tumor tissues. Wild Type IDH1 (n=30) Mutant IDH1 (n=2) p Serum VEGF (ng/ml) 0.189 ± 0.08 0.309 ± 0.016 0.0454 Tumor HIF1‐α (ng/ml) 0.710 ± 0.835 5.058 ± 3.75 < 0.0001 Our preliminary results suggest that mutated IDH1 may contributes to carcinogenesis via induction of HIF‐1 alpha pathway in primary GBM.

Amaç: Bu çalışmada, izositrat dehidrogenaz (IDH) molekülünün bibliyometrik göstergeler kullanılarak WoS veri tabanında incelenmesi ve yapılan çalışmaların Türkiye ölçeğinde de değerlendirilmesi amaçlanmıştır.

Objective: This investigation aimed to detect the possible protective impacts of naringenin (NAR) on vancomycin (VCM)-induced liver toxicity through measuring caspase-3, -8 and -9 activities as markers of apoptosis and the levels of tumor necrosis factor-alpha, cyclooxygenase-2 and vascular endothelial growth factor as inflammation markers and assessing the histopathological alterations in rats. Methods:The rats were allocated into seven groups as, the control group (saline, intraperitoneally (i.p.)), VCM group (400 mg/kg/day, i.p.), carboxymethyl cellulose (CMC) group (0.5%, orally), NAR100 group (100 mg/kg/day, orally), VCM+NAR25 group (25 mg/kg/day, orally), VCM+NAR50 group (50 mg/kg/day, orally), VCM+NAR100 group (100 mg/kg/day, orally). The caspase enzyme activities and inflammation markers were measured using colorimetric methods and ELISA, respectively. Histopathological examinations were performed. Results:The caspase activities and levels of inflammation markers were significantly higher in the VCM group as opposed to the other groups. The caspase activities were significantly ameliorated in the VCM+NAR25 group compared to the VCM+NAR50 and VCM+NAR100 groups, but the levels of inflammation markers were significantly reduced in the VCM+NAR50 group and, especially, the VCM+NAR100 group compared to the VCM+NAR25 group. Conclusion:NAR has potential protective impact on liver injury caused by VCM, and the protective impacts of NAR at distinct doses may occur via different molecular mechanisms.