New 3,5-disubstituted-2-pyrazoline derivatives (4-6), their boron-fluorine complexes (boron (3-(2'-aminophenyl),5-(2'-/3'-/4'-pyridyl)pyrazoline, BOAPPY) (7-9) and boron 1,2'-diazaflavone complex (BODAF) (11) were synthesized starting from azachalcones (1-3) to diazaflavone (10), respectively. Biological evaluation of compounds 4-9 and 11 showed remarkable antioxidant, antibacterial, and acetylcholinesterase and tyrosinase enzyme inhibition activities. All newly synthesized compounds 4-9 and 11 showed respectable antibacterial effect with minimum inhibitory concentrations in the range of 4.7-150 μg/mL.

Aim: Glioblastoma multiforme (GBM) is the most malignant glial tumor. Angiogenesis which provides nutrient and oxygen support to proliferating cells plays an essential role in GBM development, proliferation, and metastasis. The development of antiangiogenetic agents is a promising treatment approach as blood vessels are essential for the vitality of tumor cells. For this purpose, in this study, the effects of bevacizumab on cell viability and apoptosis were analyzed using glioblastoma cells. Material and method: U-87 MG and T98G cells were treated with various concentrations of bevacizumab for 24 hours, 48 hours, and 72 hours. Cell viability was analyzed after administration of bevacizumab. Cytotoxicity was determined using MTT. Apoptosis rate was determined with cell death detection kit. Results: Cell viability analysis showed that when 8 mg / ml bevacizumab was administered to glioblastoma cells for 48 hours and 72 hours, cell proliferation was only 50% compared to proliferation of cells without bevacizumab. Additionally, apoptosis rates for U-87 MG and T98G cell lines treated with various concentrations of bevacizumab for 48 hours and 72 hours showed results similar to those of cell viability. Conclusions: This study showed that while high concentration treatment of U-87 MG cells caused an increase in cell viability in a time-dependent manner, high dose treatment of T98G cells resulted in a decrease in cell viability in a time-dependent manner. This means that some glioblastoma cells can still survive under high doses of bevacizumab. This, in turn, demonstrated that glioblastoma cells developed resistance against bevacizumab.

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Purpose: Brain tumors are a group of diseases in which different genotypes result in different phenotypes at the molecular level. Although there have been a number of studies related to the role of alterations in nuclear genes, such as oncogenes and tumor suppressor genes, in the development of brain tumors, the effects of mitochondrial genes on tumorigenesis have not been well elucidated. Methods: It is thought that mitochondrial DNA plays an important role in the tumorogenesis process due to the fact that it is more susceptible to mutations than the nuclear DNA and the repair mechanisms are weaker. Mitochondrial DNA mutations have been extensively studied for their use as biomarkers since they can reach high copy number in clonal characterization. Results: MtDNA mutations play an important role in cancer developmental stages, but the mechanisms of cancer development and progression of these mutations are not fully explained. Conclusion: The identification of mitochondrial DNA defects is anticipated earlier in the diagnosis of brain tumors, and more effective treatment protocols will be regulated.