Scopus İndeksli Yayınlar Koleksiyonu / Scopus Indexed Publications Collection
Permanent URI for this collectionhttps://hdl.handle.net/11147/7148
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Article Chemosensitizing Effect of Apigenin on T-ALL Cell Therapy(Frontiers Media SA, 2025) Huseynova, N.; Baran, Z.; Khalilov, R.; Mammadova, A.; Baran, Y.T-cell acute lymphoblastic leukemia (T-ALL) is an aggressive hematological malignancy with limited therapeutic options and frequent treatment-associated toxicities. L-asparaginase, a cornerstone in T-ALL therapy, is often restricted by hypersensitivity reactions and systemic side effects, highlighting the need for safer strategies to enhance its efficacy. This study investigated the potential of apigenin, a naturally occurring flavonoid with antioxidant and pro-apoptotic properties, to act as a chemosensitizer for L-asparaginase in MOLT-4 T-ALL cells. Cytotoxicity was assessed using the MTT assay, apoptosis by Annexin V/PI staining, cell cycle distribution by flow cytometry, and mitochondrial membrane potential by JC-1 staining. Both apigenin and L-asparaginase produced dose- and time-dependent cytotoxicity, with combination treatment resulting in reduced IC<inf>50</inf> values. Apoptotic analysis showed significantly higher apoptosis in the combination-treated groups than in single-agent groups. Cell cycle analysis revealed that apigenin induced S-phase arrest and L-asparaginase induced G1-phase arrest, while the combination disrupted cell cycle progression at multiple checkpoints. JC-1 assay further demonstrated enhanced mitochondrial depolarization, with up to a 29.2-fold increase in cytoplasmic-to-mitochondrial fluorescence ratio in combination therapy compared to L-asparaginase alone. These findings indicate that apigenin potentiates L-asparaginase-induced cytotoxicity through mitochondrial dysfunction and intrinsic apoptotic signaling. The combined use of apigenin and L-asparaginase may provide a novel strategy to improve therapeutic efficacy in T-ALL while potentially reducing the toxicity associated with high-dose L-asparaginase monotherapy. © © 2025 Huseynova, Baran, Khalilov, Mammadova and Baran.Article Citation - WoS: 19Citation - Scopus: 20Use of Micrornas in Personalized Medicine(Humana Press Inc., 2014) Avci, C.B.; Baran, Y.Personalized medicine comprises the genetic information together with the phenotypic and environmental factors to yield healthcare tailored to an individual and removes the limitations of the "one-size-fits-all" therapy approach. This provides the opportunity to translate therapies from bench to clinic, to diagnose and predict disease, and to improve patient-tailored treatments based on the unique signatures of a patient's disease and further to identify novel treatment schedules. Nowadays, tiny noncoding RNAs, called microRNAs, have captured the spotlight in molecular biology with highlights like their involvement in DNA translational control, their impression on mRNA and protein expression levels, and their ability to reprogram molecular signaling pathways in cancer. Realizing their pivotal roles in drug resistance, they emerged as diagnostic targets orchestrating drug response in individualized therapy examples. It is not premature to think that researchers could have the US Food and Drug Administration (FDA)-approved kit-based assays for miRNA analysis in the near future. We think that miRNAs are ready for prime time. © Springer Science+Business Media New York 2014.Review Citation - WoS: 10Citation - Scopus: 11An Update on Molecular Biology and Drug Resistance Mechanisms of Multiple Myeloma(Elsevier Ireland Ltd, 2015) Mutlu, P.; Kiraz, Y.; Gündüz, U.; Baran, Y.Multiple myeloma (MM), a neoplasm of plasma cells, is the second most common hematological malignancy. Incidance rates increase after age 40. MM is most commonly seen in men and African-American population. There are several factors to this, such as obesity, environmental factors, family history, genetic factors and monoclonal gammopathies of undetermined significance (MGUS) that have been implicated as potentially etiologic. Development of MM involves a series of complex molecular events, including chromosomal abnormalities, oncogene activation and growth factor dysregulation. Chemotherapy is the most commonly used treatment strategy in MM. However, MM is a difficult disease to treat because of its marked resistance to chemotherapy. MM has been shown to be commonly multidrug resistance (MDR)-negative at diagnosis and associated with a high incidence of MDR expression at relapse. This review deals with the molecular aspects of MM, drug resistance mechanisms during treatment and also possible new applications for overcoming drug resistance. © 2015 Elsevier Ireland Ltd.