Person: ERZİK, CAN
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ERZİK
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CAN
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Publication Metadata only Toward Precision Oncology in Glioblastoma with a Personalized Cancer Genome Reporting Tool and Genetic Changes Identified by Whole Exome Sequencing(2023-09-01) ERDOĞAN, ONUR; ERZİK, CAN; ARĞA, KAZIM YALÇIN; BAYRAKLI, FATİH; ERDOĞAN O., Özkaya Ş. Ç., ERZİK C., Bilguvar K., ARGA K. Y., BAYRAKLI F.Precision/personalized medicine in oncology has two key pillars: molecular profiling of the tumors and personalized reporting of the results in ways that are clinically contextualized and triangulated. Moreover, neurosurgery as a field stands to benefit from precision/personalized medicine and new tools for reporting of the molecular findings. In this context, glioblastoma (GBM) is a highly aggressive brain tumor with limited treatment options and poor prognosis. Precision/personalized medicine has emerged as a promising approach for personalized therapy in GBM. In this study, we performed whole exome sequencing of tumor tissue samples from six newly diagnosed GBM patients and matched nontumor control samples. We report here the genetic alterations identified in the tumors, including single nucleotide variations, insertions or deletions (indels), and copy number variations, and attendant mutational signatures. Additionally, using a personalized cancer genome-reporting tool, we linked genomic information to potential therapeutic targets and treatment options for each patient. Our findings revealed heterogeneity in genetic alterations and identified targetable pathways, such as the PI3K/AKT/mTOR pathway. This study demonstrates the prospects of precision/personalized medicine in GBM specifically, and neurosurgical oncology more generally, including the potential for genomic profiling coupled with personalized cancer genome reporting. Further research and larger studies are warranted to validate these findings and advance the treatment options and outcomes for patients with GBM.Publication Open Access Exosomes' profile in ankylosing spondylitis: A preliminary study(2023-01-01) ABACAR, KEREM YİĞİT; ATAGÜNDÜZ, MEHMET PAMİR; ERZİK, CAN; Karakaya E., Deniz R., ABACAR K. Y., ATAGÜNDÜZ M. P., ERZİK C.Objective: Ankylosing spondylitis (AS) is a chronic systemic inflammatory disease that leads to structural and functional im-pairments and reduced quality of life, with heterogeneous manifestations. The origin and possible role of extracellular vesicles represented by exosomes (EVexo) in the pathogenesis of AS were examined in this study. Materials and Methods: Extracellular vesicles (EVs) were isolated from serum from ten AS patients and ten healthy controls through Izon qEV2/35 nm columns. After assessing the isolate purity by bicinchoninic acid assay (BCA) and Enzyme-Linked ImmunoSorbent Assay (ELISA), the relationship between EVexo concentration and AS was tested by the BCA method. The EVexo surface markers were analyzed by flow cytometry (FC) to verify EVexo presence and reveal its origin. Results: In FC analysis, CD86+TSG101+ and CD3+TSG101+ exosome percentages of AS group were significantly higher than the control group (p<0.05). A significant difference was found between the AS and control groups in terms of CD3+IL17+ and CD3+IFNg+ and CD86+TNF alpha+ and CD86+IL12(p35)+ exosome percentages (p<0.01). Conclusion: The exosomes whose ratio increased in the AS process were derived from T cells expressing increased levels of IL-17A and IFNg in their membranes, and macrophages expressing increased levels of TNF alpha and IL-12(p35) in their membranes. The EVexo profile did not change according to the AS course.Publication Metadata only Response Assessment With Molecular Characterization of Circulating Tumor Cells and Plasma MicroRNA Profiling in Patients With Locally Advanced Breast Cancer During Neoadjuvant Chemotherapy(CIG MEDIA GROUP, LP, 2020) ERZİK, CAN; Akkiprik, Mustafa; Koca, Sinan; Ugurlu, M. Umit; Ekren, Ruchan; Eyuboglu, Irem Peker; Alan, Ozkan; Erzik, Can; Amuran, Gokce Gullu; Telli, Tugba Akin; Gulluoglu, M. Bahadir; Sezerman, Ugur; Yumuk, Perran FuldenPeripheral blood samples from 36 patients with locally advanced breast cancer who had undergone neoadjuvant chemotherapy were collected for circulating tumor cell (CTC) and plasma microRNA (miR) analysis. Pretreatment CTC and ALDH1 positivity (P = .0245) correlated, with miR-146b-5p and miR-199a-5p accompanied by CTC positivity. CTC and miR profiling of serial samples during neoadjuvant chemotherapy appears to be a very useful in predicting cure and clinical course. Background: Cells detaching from the primary tumor site are metastasis initiator cells, and the detection of CTC, known as liquid biopsy, is an important test of biomarkers of cancer progression. We investigated the molecular characterization of circulating tumor cells (CTCs), profiled the plasma microRNA (miR) content, and analyzed the relationship with the clinical outcomes by sampling the peripheral blood from patients with locally advanced breast cancer before and after neoadjuvant chemotherapy. Patients and Methods: Markers of breast cancer, epithelial-mesenchymal transition (EMT), drug resistance, and stem cells were used for CTC isolation and characterization. Plasma miR profiles were obtained from selected patients with CTC positivity determined using next-generation sequencing. Resutts: The proportion of CTC, EMT, and stem cell marker positivity was 16.7%, 8.3%, and 25% before and 18.2%, 15.2%, and 9.1% after treatment, respectively. A significant correlation was found between the pretreatment CTCs and ALDH1 positivity (P= .0245). These CTCs with stemness properties were observed in most hormone receptor-positive, human epidermal growth factor receptor 2 -negative cases and were also present with a high incidence in cases of early metastasis. miR-146b-5p and miR-199a-5p, which are involved in metastasis, invasion, and EMT, were accompanied by CTC positivity, and miR-4646-3p was associated with the development of early metastasis. Conclusions: Molecular characterization of CTCs and miR profiling of serial samples from patients with locally advanced breast cancer during neoadjuvant chemotherapy appears to be a very useful in predicting cure and clinical course and might be a key to developing new targeted therapies. (C) 2020 Elsevier Inc. All rights reserved.Publication Metadata only The impact of vitamin B12 deficiency on infant gut microbiota(SPRINGER, 2020) ERZİK, CAN; Boran, Perran; Baris, Hatice Ezgi; Kepenekli, Eda; Erzik, Can; Soysal, Ahmet; Dinh, Duy M.Although physiologic and neurologic consequences of micronutrient deficiencies have been addressed extensively, less is known about their impact on developing gut microbiota. Vitamin B12 deficiency is a common micronutrient deficiency in infants. We aimed to analyze the gut microbial composition of exclusively breastfed infants aged between 4 and 6 months with and without vitamin B12 deficiency by 16S rRNA gene sequencing. In a subgroup of infants with vitamin B12 deficiency, stool samples are recollected and reanalyzed after vitamin B12 supplementation. A total of 88 infants' stool samples (median age 4 months [IQR 4-5], 50% males) were analyzed, of which 28 (31.8%) were vitamin B12 sufficient and 60 (68.2%) were vitamin B12 insufficient. Comparisons between vitamin B12-sufficient and vitamin B12-insufficient infants revealed no evidence of differences in the microbiota. Proteobacteria, Firmicutes, Actinobacteria, and Bacteroidetes were the most abundant phyla in all groups. There was no difference between the pre- and post-treatment composition of gut microbiota. Conclusion: Vitamin B12-deficient infants have similar gut microbial composition as vitamin B12-sufficient infants. Since the samples were collected at an early period of life and the exposure to deficiency was relatively short, it may be possible that the effects were not fully established.Publication Metadata only Neuroprotective Effect of Plasminogen Activator Inhibitor-1 Antagonist in the Rat Model of Mild Traumatic Brain Injury(SPRINGER/PLENUM PUBLISHERS, 2021) ERZİK, CAN; Kuru Bektasoglu, Pinar; Koyuncuoglu, Turkan; Akbulut, Selin; Akakin, Dilek; Eyuboglu, Irem Peker; Erzik, Can; Yuksel, Meral; Kurtel, HizirPlasminogen activator inhibitor-1 (PAI-1) antagonists are known for their neuroprotective effects. In this study, it was aimed to investigate the possible protective effects of PAI-1 antagonists in a rat mild traumatic brain injury (TBI) model. Sprague-Dawley male rats were grouped as sham (n = 7), TBI (n = 9), and TBI + PAI-1 antagonist (5 and 10 mg/kg TM5441 and TM5484; n = 6-7). Under anesthesia, TBI was induced by dropping a metal 300-g weight from a height of 1 m on the skull. Before and 24-h after trauma neurological examination, tail suspension, Y-maze, and novel object recognition tests were performed. Twenty-four hours after TBI, the rats were decapitated and activities of myeloperoxidase, nitric oxide release, luminol-, and lucigenin-enhanced chemiluminescence were measured. Also, interleukin-1 beta, interleukin-6, tumor necrosis factor, interleukin-10, tumor growth factor-beta, caspase-3, cleaved caspase-3, and PAI levels were measured with the ELISA method in the brain tissue. Brain injury was graded histopathologically following hematoxylin-eosin staining. Western blot and immunohistochemical investigation for low-density lipoprotein receptor, matrix metalloproteinase-3, and nuclear factor-kappa B were also performed. Data were analyzed using GraphPad Prism 8.0 (GraphPad Software, San Diego, CA, USA) and expressed as means +/- SEM. Values of p < 0.05 were considered to be statistically significant. Higher levels of myeloperoxidase activity in the TBI group (p < 0.05) were found to be suppressed in 5 and 10 mg/kg TM5441 treatment groups (p < 0.05-p < 0.01). The tail suspension test score was increased in the TBI group (p < 0.001) and decreased in all treatment groups (p < 0.05-0.001). The histologic damage score was increased statistically significantly in the cortex, dentate gyrus, and CA3 regions in the TBI group (p < 0.01-0.001), decreased in the treatment groups in the cortex and dentate gyrus (p < 0.05-0.001). PAI antagonists, especially TM5441, have antioxidant and anti-inflammatory properties against mild TBI in the acute period. Behavioral test results were also improved after PAI antagonist treatment after mild TBI.Publication Open Access Rethinking large group lectures – how far in this format(2022-05-01) SEVİM, MUSTAFA; ERZİK, CAN; YEGEN, BERRAK; GÜLPINAR, MEHMET ALİ; AKTURAN S., SEVİM M., ERZİK C., YEGEN B., GÜLPINAR M. A.Objective: The aim of this study is to determine the perceptions, attitudes, and behaviour of medical students and lecturers regarding the lectures and their effects on students’ learning behaviour. Materials and Methods: This was a qualitative study including multi-methods. Researchers observed lecture ambiance and activities in two courses. Lectures were observed and slide-presentations were evaluated. Additionally, in-depth and focus group interviews were conducted. Results: Two researchers attended and observed 75 lectures. The average number of attendees was 51.21. Eighty percent of lecturers did not introduce any activities to attract attention and prepare students for the lecture. Only 12% of lectures were taught interactively. Of the evaluated 43 (69.80%) slide-presentations, sufficient association or integration was not made between clinical and basic sciences. Conclusion: This study revealed that the lectures created negative feelings and thoughts in students and lecturers, and led to undesirable attitudes and behaviour. It is essential to focus on giving interactive lectures which aim at developing reasoning, decision-making, and evaluation competencies. The most significant factors determining students’ attendance and appraisal of the lectures were related to the preparation of the lecturers, the intensity of the content, integration between basic science and clinical science, and the presentation skills.Publication Metadata only Adenosine-receptor antagonists improve intestinal motility and oxidative injury due to post-operative ileus in rats: Role of vagus nerve(2023-09-14) KAHRAMAN, MERVE MERİÇ; ERZİK, CAN; PEKER EYÜBOĞLU, İREM; ŞEN L. S., KAHRAMAN M. M., Sezen Mermer K., Toraman A. E., Tiftikci E., Harlak M., Recai M. S., Akkurt Z. N., ERZİK C., PEKER EYÜBOĞLU İ., et al.Publication Metadata only Phoenixin 14 ameloriates pancreatic injury in streptozotocin-induced diabetic rats by alleviating oxidative burden(2022-09-01) ÖZDEMİR KUMRAL, ZARİFE NİGAR; YÜKSEL, MERAL; AKAKIN, DİLEK; ERZİK, CAN; HAKLAR, GONCAGÜL; ÖZDEMİR KUMRAL Z. N. , Sen E., Yapici H. B. , Atakul N., Domruk O. F. , Aldag Y., Sen L. S. , Mustafaoglu F. K. , YÜKSEL M., AKAKIN D., et al.Phoenixin-14 (PNX) is a neuropeptide that has been shown to prevent oxidative damage and stimulates insulin secretion. We investigated the effects of PNX on pancreatic injury induced by streptozotocin (STZ), and nicotinamide (NAD). Male Sprague-Dawley rats, in control (C) and diabetic (STZ) groups, were treated with either saline, or PNX (0.45 nmol/kg, or 45 nmol/kg) daily for 3 days 1 week after STZ injection. Fasting blood glucose (FBG) and gastric emptying rate (GER) were measured. Tissue and blood samples were collected. PNX treatments prevented pancreatic damage and beta cell loss. Increased luminol and lucigenin levels in the pancreas, ileum and liver tissues of STZ groups were alleviated by PNX treatment in pancreatic and ileal tissues. PNX0.45 decreased FBG without any change in insulin blood level and pancreatic mRNA. GER increased in all diabetic rats while PNX0.45 delayed GER only in the C group. PNX diminishes pancreatic damage and lowers FBG by reducing oxidative load.Publication Metadata only Flavonoid ile Kombine Edilmiş Kemoterapi İlaçlarının Kolorektal Kanser Hücrelerine Etkisi(2022-12-09) AYDIN OMAY, BANU; ERZİK, CAN; ARĞA, KAZIM YALÇIN; CABADAK, HÜLYA; Kanlı Z., Aydın Omay B., Erzik C., Arğa K. Y. , Cabadak H.Publication Open Access Anti-inflammatory, antioxidant and neuroprotective effects of niacin on mild traumatic brain injury in rats(2023-01-01) KOYUNCUOĞLU, TÜRKAN; AKAKIN, DİLEK; ERZİK, CAN; YÜKSEL, MERAL; YEGEN, BERRAK; Ozaydin D., Bektasoglu P. K., Koyuncuoglu T., Ozkaya S. C., Koroglu A. K., AKAKIN D., ERZİK C., YÜKSEL M., YEGEN B., Gurer B.AIM: To study the effects of niacin, a water-soluble vitamin, on inflammation, oxidative stress and apoptotic processes observed after mild traumatic brain injury (TBI). MATERIAL and METHODS: A total of 25 Wistar albino male rats were randomly divided into control (n=9), TBI + Placebo group (n=9), TBI + niacin (500 mg/kg; n=7) groups. Mild TBI was performed under anesthesia by dropping a 300 g weight from a height of 1 meter onto the skull. Behavioral tests were applied before and 24 hours after TBI. Luminol and lucigenin levels and tissue cytokine levels were measured. Histopathological damage was scored in brain tissue. RESULTS: After mild TBI, luminol and lucigenin levels were increased (p<0.001), and their levels were decreased with niacin treatment (p<0.01-p<0.001). An increased score was obtained with trauma in the tail suspension test (p<0.01), showing depressive behavior. The number of entries to arms in Y-maze test were decreased in TBI group compared to pre-traumatic values (p<0.01), while discrimination (p<0.05) and recognition indices (p<0.05) in object recognition test were decreased with trauma, but niacin treatment did not change the outcomes in behavioral tests. Levels of the anti-inflammatory cytokine IL-10 were decreased with trauma, and increased with niacin treatment (p<0.05). The histological damage score was increased with trauma (p<0.001), and decreased with niacin treatment in the cortex (p<0.05), and hippocampal dentate gyrus region (p<0.01). CONCLUSION: Niacin treatment after mild TBI inhibited trauma-induced production of reactive oxygen derivatives and elevated the anti-inflammatory IL-10 level. Niacin treatment ameliorated the histopathologically evident damage.