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Öğe Alterations in Promoter Methylation Status of Tumor Suppressor HIC1, SFRP2, and DAPK1 Genes in Prostate Carcinomas(MARY ANN LIEBERT INC, 2012) Kilinc, Devran; Ozdemir, Oztuerk; Ozdemir, Semra; Korgali, Esat; Koksal, Binnur; Uslu, Atilla; Gultekin, Yener E.Hypermethylated genomic DNA is a common feature in tumoral tissues, although the prevalence of this modification remains poorly understood. We aimed to determine the frequency of five tumor suppressor (TS) genes in prostate cancer and the correlation between promoter hypermethylation of these genes and low and high grade of prostate carcinomas. A total of 30 prostate tumor specimens were investigated for promoter methylation status of TS hypermethylated in cancer 1 (HIC1), death-associated protein kinase 1 (DAPK1), secreted frizzled-related protein 2 (SFRP2), cyclin-dependent kinase inhibitor 2A (p16), and O-6-methylguanine-DNA methyltransferase (MGMT) genes by using bisulfite modifying method. A high frequency of promoter hypermethylation was found in HIC1 (70.9%), SFRP2 (58.3%), and DAPK1 (33.3%) genes in tumor samples that were examined. The current data show high frequency of hypermethylation changes in HIC1, SFRP2, and DAPK1 genes in prostate carcinomas of high Gleason Score (GS).Öğe Antitumoral effects of Allium sivasicum on breast cancer in vitro and in vivo(SPRINGER, 2013) Tepe, Bektas; Tuncer, Ersin; Saraydin, Serpil Unver; Ozer, Hatice; Sen, Metin; Karadayi, Kursat; Inan, Deniz Sahin; Karadayi, Sule; Polat, Zubeyde; Akpulat, Askin; Duman, Mustafa; Koksal, Binnur; Turan, MustafaThis work aims to investigate the antiproliferative properties of Allium sivasicum (AS) on breast cancer. AS extracts were studied for cytotoxicity against the breast cancer cell lines. In vitro apoptosis studies of breast cancer cells were performed by annexin V staining in flow cytometry analyses. AS showed cytotoxicity to three cancer cell lines. Annexin-positive cells level in AS treated cell lines were higher than the untreated control cells. The expressions of caspase-7 protein and TUNEL positive cells were much higher for the rats treated by AS, compared with the untreated control group. The expressions of the Ki-67 decreased in treatment groups compared with the control group. In vivo studies showed that mean tumor volume inhibition ratio in AS treated group was 38 % compared with the untreated rats. These results indicate that A. sivasicum has antitumoral potential against breast cancer.Öğe Antitumoral effects of Salvia absconditiflora Greuter & Burdet syn. Salvia cryptantha Montbret & Aucher ex Benth. on Breast cancer(NATL INST SCIENCE COMMUNICATION-NISCAIR, 2013) Ozer, Hatice; Altun, Ahmet; Saraydin, Serpil Unver; Soylu, Sinan; Goktas, Selcuk; Tuncer, Ersin; Inan, Deniz Sahin; Koksal, Binnur; Temiz, Tijen Kaya; Tepe, Bektas; Sen, Metin; Karadayi, Kursat; Turan, MustafaThis work aims to investigate the antiproliferative properties of Salvia cryptantha on breast cancer. Salvia cryptantha (SC) extracts were studied for cytotoxicity against the breast cancer cell lines. In-vitro apoptosis studies of breast cancer cells were performed by nnexin V staining in flow cytometry analyses Immunohistochemistry studies for Ki-67 and p16 in the tumoral tissue sections of Dimethyl Benzanthracene (DMBA) induced mammary tumor in rats were performed. In-vivo anticancer activity testing was carried out by inhibiting the growth of mammary tumor in rats. SC showed cytotoxicity to three cancer cell lines. Annexin-positive cells level in SC treated cell lines were higher than the untreated control cells. The expression of the Ki-67 decreased in treatment groups compared with the control group. The expression of p16 protein was much higher for the rats treated by SC, compared with the untreated control group. In vivo studies showed that mean tumor volume inhibition ratio in SC treated group was 38 % compared with the untreated rats. These results indicate that Salvia cryptantha has antitumoral potential against breast cancer.Öğe Bcii-RFLP profiles for serum amiloid A1 and mutated MEFV gene prevalence in chronic renal failure patients requiring long-term hemodialysis(TAYLOR & FRANCIS LTD, 2015) Ozdemir, Ozturk; Kayatas, Mansur; Cetinkaya, Selma; Yildirim, Malik Ejder; Silan, Fatma; Kurtulgan, Hande Kucuk; Koksal, Binnur; Urfali, Mine; Candan, FerhanBackground and aim: There is an increased mortality risk in long-term hemodialysis patients of renal failure due to the chronic inflammation. The relationship between the chronic renal failure (CRF) and the role of familial genetic markers remains incompletely understood. In the current study, it was aimed to find out the prevalence of common MEFV gene mutations and BcII polymorphism in serum amyloid A1 (SAA1) gene in chronic renal patients (CRF) who require long-term hemodialysis. Method: Current cohort includes 242 CRF patients and 245 healthy individuals from the same population. Total genomic DNA was isolated from peripheral blood-EDTA samples and genotyping of target MEFV gene was carried out by reverse hybridization Strip Assay and real-time techniques. The SAA1 gene was genotyped by the BcII-RFLP method. Results: Increased mutated MEFV genotypes were found in current CRF patients when compared with the control group from the same ethnicity and the difference was statistically significant (Table 2) (OR: 4.9401, 95% CI: 3.0694-7.9509), p < 0.0001. The most frequent point mutations were M694V and E148Q. The mutated T allel frequency in the SAA1 gene was also different when compared with the healthy controls and the difference was found to be statistically significant (chi(2) : 13.18; p = 0.000). Conclusions: The current results indicate the germline mutations in both genetic biomarkers (MEFV and SAA1 genes) that are related to inflammation and amyloidosis processes may play a crucial role in CRF pathogenesis due to the long-term chronic inflammation.Öğe CCR2 Polymorphism in Chronic Renal Failure Patients Requiring Long-Term Hemodialysis(JAPAN SOC INTERNAL MEDICINE, 2011) Sezgin, Ilhan; Koksal, Binnur; Bagci, Gokhan; Kurtulgan, Hande Kucuk; Ozdemir, OzturkObjective A number of chemokines and chemokine receptors are produced by intrinsic renal cells as well as by infiltrating cells during renal inflammation. The CCR2 chemokine receptor mediates leukocyte chemoattraction in the initiation and amplification phase of renal inflammation. The polymorphism, CCR2-V64I, changes valine 64 of CCR2 to isoleucine. We aimed to determine the frequency of CCR2-V64I polymorphism in patients with chronic renal failure requiring long-term hemodialysis. Methods and Patients The PCR-based restriction fragment length polymorphism (PCR-RFLP) technique was used to assess the gene frequencies of CCR2-641 in CRF patients (n=210) and healthy controls (n=139) in the current study. Results The frequencies of the CCR2 genotype were 0.68 for V/V, 0.28 for V/I, and 0.4 for I/I in the CRF patients and 0.81 for V/V, 018 for V/I and 0.1 for I/I in healthy controls. The distribution of the CCR2-V64I mutant genotype was significantly different between subjects with CRF and healthy control subjects (X2=7.197 and p=0.027). Conclusion We found that the CCR2-V64I polymorphism was significantly high in CRF patients. In addition to the contribution to disease pathogenesis, it was recently found that chemokines have therapeutic importance in chronic renal failure. The frequency of CCR2-V64I and other chemokine and chemokine receptor polymorphisms in renal pathologies must be further investigated in larger study populations and in different renal diseases.Öğe Clinical and molecular analysis of common MEFV gene mutations in familial Mediterranean fever in Sivas population(SPRINGER, 2009) Koksal, Binnur; Nur, Naim; Sari, Musa; Candan, Ferhan; Acemoglu, Mursit; Kocak, Nadir; Ozen, Filiz; Ozdemir, OzturkFamilial Mediterranean fever (FMF) is the most frequent hereditary inflammatory disease characterized by self-limited recurrent attacks of fever and serositis. The aim of the current study is to determine the frequency of the mutations in 365 suspected FMF patients and to reveal whether there is a correlation between genotype and phenotype of these patients. All patients were clinically examined according to Tell-Hashomer FMF criteria and were screened genetically in terms of common 12 Mediterranean fever gene (MEFV) mutations. Various point mutations were detected in 270 (74%) patients. The most frequent mutation was M694V (26.85% of the alleles) and was followed by E148Q (15.55%), M680I (G/C) (9.62%) and V726A (7.96%). Patients who bear M694V homozygous mutation had most severe disease phenotype and high risk for amyloidosis (P = 0.04). Our results indicate that Sivas population has a wide range of heterozygous mutated carriers of MEFV gene and there is a high frequency of E148Q allele when compared to the other Mediterranean groups.Öğe Cytochrome P450 2D6 and MDR1 Gene Mutation in Relation to Mortality in Patients with Crimean-Congo Hemorrhagic Fever: A Preliminary Study(ORTADOGU AD PRES & PUBL CO, 2009) Engin, Aynur; Koksal, Binnur; Dogan, Omer Tamer; Elaldi, Nazif; Dokmetas, Ilyas; Bakir, Mehmet; Ozdemir, OzturkObjective: The aim of this study was to investigate the role of multidrug transporter P-glycoprotein 1 (MDR1), cytochrome P450 isozyme 2D6 (CYP2D6) and C-C chemokine receptor 5 (CCR5) genes in the mortality of patients with Crimean-Congo Hemorrhagic Fever (CCHF). Material and Methods: Fifteen patients under drug therapy and conventional supportive measures were investigated. Diagnosis of the patients was confirmed by ELISA and/or reverse transcription-polymerase chain reaction (RT-PCR) technique. Clinical and laboratory features of three cases with fatal outcomes were compared with those of twelve patients with non-fatal CCHF. Genomic DNA was isolated from pheripheral blood samples and PCR based reverse hybridization strip assay was used for the genotyping. Results: The mortality rate was 20% (3/15) in this study. In two fatal cases the MDR1 gene had homozygous point mutation and in one fatal case heterozygous point mutation. All the fatal cases had poor drug metabolizer genotypes of CYP2D6 gene. Of the twelve surviving patients, three had heterozygous mutation in the MDR gene while only one had homozygous mutation of the same gene. Drug metabolizer genotypes of CYP450 gene were normal in all surviving patients. In fatal cases, ratios of mutable MDR1 and poor drug metabolizer genotypes of CYP450 genes were higher than those in non-fatal cases. The CCR5 gene was normal in all cases. Conclusion: Hypoexpression of CYP2D6 alleles and mutation in MDR I gene could cause impaired drug metabolism and/or lead to therapeutic failure in the CCHF patients. MDR1 and CYP2D6 genes may play a crucial role in pharmacokinetics, immunological response and drug metabolism in the management of CCHF infection. Further studies are necessary to substantiate these findings.Öğe The endemic RTL80V/I and RTM204V/I YMDD mutation profiles in a case of chronic hepatitis B(SPRINGER, 2011) Ozdemir, Ozturk; Alagozlu, Hakan; Timucin, Meryem; Ozdemir, Semra; Korkmaz, Mehmet; Koksal, Binnur; Ozen, Ozen…Öğe Epigenetic alterations and oncogenes mutations in urinary bladder carcinomas(SPRINGER, 2009) Ozdemir, Oztuerk; Yildiz, Esin; Ayan, Semih; Gul, Eylem; Gokce, Goekhan; Yildiz, Fazilet; Koksal, Binnur; Goze, Fahrettin; Gultekin, E. Yener…Öğe Epigenetic Inactivation of Tumor Suppressor SFRP2 and Point Mutation in KRAS Proto-Oncogene in Fistula - Associated Mucinous Type Anal Adenocarcinoma: Report of Two Cases(JAPAN SOC INTERNAL MEDICINE, 2010) Sen, Metin; Ozdemir, Oztuerk; Turan, Mustafa; Arici, Sema; Yildiz, Fazilet; Koksal, Binnur; Goze, FahrettinThe secreted frizzled-related proteins (SFRPs) genes are unmethylated in normal colorectal mucosa tissue but abberant methylation profiles can be detected in colorectal cancer (CRC), adenomas, and in aberrant crypt foci. The aim of the current study was to clarify whether SFRP2 methylation and K-ras structural mutation in fecal DNA can be found in stool and tumoral tissues of individuals with fistula-associated mucinous type anal adenocarcinomas (MTAA). Two man patients (68 and 56 years old) were treated for anorectal fistula in the surgical department. Patients were evaluated for clinical findings, tumoural tissue samples were examined histopathologically and DNA from fecal and tumoral tissue samples were isolated. K-ras mutation and promoter hypermethylation of SFRP2 gene in tumoral tissues were assessed by methylation-specific PCR based stripAssay hybridisation technique (Me-PCR) and compared to the healthy controls. Fecal and tumoural tissue samples from both patients were found to be fully hypermethylated profiles for SFRP2 gene and combined point mutations were detected in codon 12 and 13 of K-ras proto-oncogene. The current results showed that the combined effects of somatic mutations in K-ras and epigenetic alterations in SFRP2 genes may play an active role in the development of mucinous type anal adenocarcinoma.Öğe Epigenetic silencing of the tumor suppressor HIC1 and SFRP2 genes in prostate carcinomas(SPRINGER, 2011) Kilic, Davran; Ozdemir, Oziurk; Korgali, Esat; Ozdemir, Semra; Koksal, Binnur; Gultekin, Yener…Öğe A Frame-Shift Mutation in the SLC34A2 Gene in Three Patients with Pulmonary Alveolar Microlithiasis in an Inbred Family(JAPAN SOC INTERNAL MEDICINE, 2010) Dogan, Omer Tamer; Ozsahin, Sefa Levent; Gul, Eylem; Arslan, Sulhattin; Koksal, Binnur; Berk, Serdar; Ozdemir, Ozturk; Akkurt, IbrahimPulmonary alveolar microlithiasis (PAM) is a rare disease characterized by the presence of small calculi in the alveolar space. The SLC34A2 is thought to be responsible for the disease. We encountered three siblings of an inbred family who have PAM. We examined the family of the proband who was admitted with dyspnea on exertion and cough, and eventually was diagnosed with PAM. Genetic analysis revealed that both parents (a consanguineous marriage) of the proband were carriers with heterozygous mutation of SLC34A2 gene, and three of their children were diagnosed with PAM with homozygous mutation in the SLC34A2 gene. These findings suggest that impaired activity of the SLC34A2 gene may be responsible for familial PAM.Öğe Heterozygous Deletion of Exon 8 in WFS1 Gene in Two Wolfram Syndrome Probands with Hearing Loss: Case Report(ORTADOGU AD PRES & PUBL CO, 2011) Altuntas, Emine Elif; Ozdemir, Ozturk; Bora, Adem; Koksal, Binnur; Kurtulgan, Hande Kucuk; Muderris, SuphiPoint mutations in the Wolfram syndrome 1 gene (WFS1) are attributed the autosomal dominant and/or recessive mild type sensorineural hearing loss in first degree relatives. Total genomic DNA was isolated from peripheral blood of affected probands and controls, Multiplex polymerase chain reaction was performed and followed by multiplex ligated probe amplification analysis. Sensorineural hearing loss was moderate in a 48-year-old male patient (case 1) and sensorineural hearing loss and optic atrophy were evident in his 16 year old daughter (case 2). We identified heterozygous deletion in exon 8 of WFS1 gene (Wolframin protein) in father and in one of his affected daughters with hearing loss and optic atrophy. The genetic results demonstrate the necessity of screening for the possible point mutation and/or larger deletions in WFS1 gene in cases with non-syndromic mild type sensorineural hearing loss. This study emphasizes the need for careful molecular evaluation in cases with impaired hearing, insulin-dependent diabetes mellitus and optic atrophy for the diagnosis of Wolfram syndrome. Proper genetic counseling must be given accordingly to patients and their other family members since it is important for their next generation.Öğe Homozygous hypermethylation of tumor suppressor SFRP2 gene in a case with mucinous anal adenocarcinoma(SPRINGER, 2009) Sen, Metin; Ozdemir, Oztuerk; Colak, Ahmet; Turan, Mustafa; Arici, Sema; Oezcan, Dogan; Yildirim, Yesim; Koksal, Binnur…Öğe Predictive significance of KRAS point mutation in patients with non-small cell lung carcinoma relation to smoking and asbestos exposure in middle Anatolia population(DRUNPP-SARAJEVO, 2010) Arslan, Sulhattin; Akkurt, Ibrahim; Koksal, Binnur; Karadayi, Sule; Ozdemir, OzturkPersons who have been occupationally exposed to environmental mutagens have a substantially increased risk for somatic oncogene mutations. Structural mutation in viral kristen rat sarcoma oncogene homolog 2 (KRAS; v-Ki-ras 2) has been assessed as a mechanism of de-novo resistance to epidermal growth factor receptor (EGFR) tyrosine-kinase inhibition in patients with non-small-cell lung cancer (NSCLC). The aim of the current study was to investigate the predictive significance of KRAS mutations in patient with NSCLC in relation to cigarette smoking and asbestos exposure. We have investigated 42 fresh tumoral tissue samples of cases that were histopathologically diagnosed as lung carcinomas. Patients were evaluated for clinical findings; tumoral tissue samples were examined histopathologically and genomic DNA from tumoral tissue samples were isolated. The KRAS point mutations were assessed by strip-Assay reverse hybridization method and compared with the healthy controls. A total of 24 patients (57%) demonstrated KRAS point mutations in their tumoral tissues, while 18 (43%) patients did not. Mutations were accumulated in current cases of NSCLC, which were active smokers and exposed to the asbestos. Current results showed that the combined effects of somatic mutations in KRAS may play an active role in development of primary lung carcinomas due to heavy smoke and asbestos exposure. Results also may have important implications for molecular diagnosis and targeted therapies in NSCLC.Öğe Predictive significance of KRAS point mutation in patients with nonsmall cell lung carcinoma relation to smoking and asbestos exposure in middle anatolia population(2010) Arslan, Sulhattin; Akkurt, Ibrahim; Koksal, Binnur; Karadayi, Sule; Ozdemir, OztürkPersons who have been occupationally exposed to environmental mutagens have a substantially increased risk for somatic oncogene mutations. Structural mutation in viral kristen rat sarcoma oncogene homolog 2 (KRAS; v-Ki-ras 2) has been assessed as a mechanism of de-novo resistance to epidermal growth factor receptor (EGFR) tyrosine-kinase inhibition in patients with non-smallcell lung cancer (NSCLC). The aim of the current study was to investigate the predictive significance of KRAS mutations in patient with NSCLC in relation to cigarette smoking and asbestos exposure. We have investigated 42 fresh tumoral tissue samples of cases that were histopathologically diagnosed as lung carcinomas. Patients were evaluated for clinical findings; tumoral tissue samples were examined histopathologically and genomic DNA from tumoral tissue samples were isolated. The KRAS point mutations were assessed by stripAssay reverse hybridization method and compared with the healthy controls. A total of 24 patients (57%) demonstrated KRAS point mutations in their tumoral tissues, while 18 (43%) patients did not. Mutations were accumulated in current cases of NSCLC, which were active smokers and exposed to the asbestos. Current results showed that the combined effects of somatic mutations in KRAS may play an active role in development of primary lung carcinomas due to heavy smoke and asbestos exposure. Results also may have important implications for molecular diagnosis and targeted therapies in NSCLC.Öğe Prevalence of known mutations in the MEFV gene in a population screening with high rate of carriers(SPRINGER, 2011) Ozdemir, Ozturk; Sezgin, Ilhan; Kurtulgan, Hande Kucuk; Candan, Ferhan; Koksal, Binnur; Sumer, Haldun; Icagasioglu, Dilara; Uslu, Atilla; Yildiz, Fazilet; Arslan, Sulhattin; Cetinkaya, Selma; Citli, Senol; Oztemur, Zekeriya; Kayatas, MansurThe Familial Mediterranean Fever (FMF) shows an autosomal recessive pattern of inheritance and affects certain ethnic groups. Disease is caused by mutations in MEFV gene and more than 180 mutations have been defined in affected individuals. Current study aimed to determine the frequency-type of the mutations for MEFV gene in Sivas-middle Anatolian city. The cohort was composed of 3340 patients. MEFV gene mutations were studied by multiplex PCR based reverse hybridization stripAssay method. Patients' clinical features were; family history: 68%, erysipelas-like erythema: 17.6%, fever: 89.9%, abdominal pain: 84.2%, peritonitis: 90.2%, arthritis: 33%, pleuritis: 14.2%, parental consanguinity: 21.2%. Current results revealed that M694V is the most frequent mutation (43.12%), followed by E148Q (20.18), M680I(G/C) (15.00%) and V726A (11.32%). The study population has a high rate of carriers and the E148Q mutation frequency was found to be highest when compared to the other regions of Turkey and other Mediterranean groups.Öğe Prevelance of Common YMDD Motif Mutations in Long Term Treated Chronic HBV Infections in a Turkish Population(ASIAN PACIFIC ORGANIZATION CANCER PREVENTION, 2013) Alagozlu, Hakan; Ozdemir, Ozturk; Koksal, Binnur; Yilmaz, Abdulkerim; Coskun, MahmutIn the current study we aimed to show the common YMDD motif mutations in viral polymerase gene in chronic hepatitis B patients during lamivudine and adefovir therapy. Forty-one serum samples obtained from chronic hepatitis B patients (24 male, 17 female; age range: 34-68 years) were included in the study. HBV-DNA was extracted from the peripheral blood of the patients using an extraction kit (Invisorb, Instant Spin DNA/RNA Virus Mini Kit, Germany). A line probe assay and direct sequencing analyses (INNO-LIPA HBV DR v2; INNOGENETICS N.V, Ghent, Belgium) were applied to determine target mutations of the viral polymerase gene in positive HBV-DNA samples. A total of 41 mutations located in 21 different codons were detected in the current results. In 17 (41.5%) patients various point mutations were detected leading to lamivudin, adefovir and/or combined drug resistance. Wild polymerase gene profiles were detected in 24 (58.5%) HBV positive patients of the current cohort. Eight of the 17 samples (19.5%) having rtM204V/I/A missense transition and/or transversion point mutations and resistance to lamivudin. Six of the the mutated samples (14.6%) having rtL180M missense transversion mutation and resistance to combined adefovir and lamivudin. Three of the mutated samples (7.5%) having rtG215H by the double base substituation and resistance to adefovir. Three of the mutated samples (7.5%) having codon rtL181W due to the missense transversion point mutations and showed resistance to combined adefovir and lamivudin. Unreported novel point mutations were detected in the different codons of polymerase gene region in the current HBV positive cohort from Turkish population. The current results provide evidence that rtL180M and rtM204V/I/A mutations of HBV-DNA may be associated with a poor antiviral response and HBV chronicity during conventional therapy in Turkish patients.Öğe Recurrent Pregnancy Loss and Its Relation to Combined Parental Thrombophilic Gene Mutations(MARY ANN LIEBERT, INC, 2012) Ozdemir, Ozturk; Yenicesu, Gonca Imir; Silan, Fatma; Koksal, Binnur; Atik, Sinem; Ozen, Filiz; Gol, Mert; Cetin, AliBackground and Aim: Recurrent pregnancy loss (RPL) is a heterogeneous disorder that has been associated with antiphospholipid syndrome and other prothrombotic parameters. We aimed to investigate the prevalence of 12 thrombophilic gene mutations in RPL couples in the current results. Method: In a total of 543 Turkish women with RPL and 327 of their male partners (870 individuals with RPL), and a control group of 106 fertile couples (control) were analyzed for factor V leiden (FVL), factor V H1299R, factor II prothrombin G20210A, FXIII V34L, b-fibrinogen -455G>A, plasminogen activator inhibitor-1 (PAI-1), GPIIIa L33P (HPA-1 a/b L33P), methylenetetrahydrofolate reductase (MTHFR) C677T, MTHFR A1298C, ACE I/D, Apo B R3500Q, and Apo E genes. Results: The overall, heterozygous and/or homozygous point mutations in FVL -FVR2, ApoE2, PAI-1, MTHFR C677T - A1298C, and ACE genes were associated with RPL. There was no meaningful association between RPL and other studied genes. Conclusion: The homozygosity of 4G in PAI-1 and MTHFR C677T genes in women with RPL, and heterozygosity of FVL, FVR2, ACE, and ApoE2 genes in both parents play crucial role in RPL and should be considered as a risk factor in RPL. Current results showed that RPL is related to combined parental (not only maternal) thrombophilic gene mutations.Öğe Tumoral tissue specific promoter hypermethylation of(SPRINGER, 2009) Arslan, Sulhattin; Dogan, Tamer; Koksal, Binnur; Yildirim, Malik Ejder; Gumus, Cesur; Elagoz, Sahenda; Akkurt, Ibrahim; Ozdemir, Oztuerk…
