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Öğe Effect of trail C1595T variant and gene expression on the pathogenesis of non-small cell lung cancer(TAYLOR & FRANCIS LTD, 2-4 PARK SQUARE, MILTON PARK, ABINGDON OR14 4RN, OXON, ENGLAND, 2019) Koç Erbaşoğlu, Öncü; Horozoğlu, Cem; Ercan, Şeyda; Kara, Hasan Volkan; Turna, Akif; Farooqi, Ammad Ahmad; Yaylım, İlhanIt is known that disorders in apoptosis function play an important role in the pathogenesis of many types of cancer, including lung cancer. Tumor necrosis factor related apoptosis inducing ligand (TRAIL), a type II transmembrane protein, is a death ligand capable of inducing apoptosis by activating distinctive death receptor. Our purpose in this study is to investigate the gene polymorphisms in TRAIL molecular pathway and TRAIL gene expression levels in non-small cell lung cancer (NSCLC) patients in terms of pathogenesis and prognosis of the disease. In this study, TRAIL C1595T polymorphism was genotyped using polymerase chain reaction-restriction fragment length polymorphism analysis in 158 patients with NSCLC and 98 healthy individuals. Surgically resected tissues were examined and classified histopathologically. In addition, TRAIL gene expression levels in tumor tissue and tumor surrounding tissue samples of 48 patients with NSCLC were determined using real-time polymerase chain reaction. TRAIL gene expression levels of NSCLC patients were detected significantly 28.8 fold decrease in the tumor tissue group compared to the control group (p=0.026). When patients were compared to tumor stage, expression of TRAIL gene in advanced tumor stage was found to be significantly 7.86 fold higher than early tumor stage [p=0.028]. No significant relationship was found between NSCLC predisposition and prognostic parameters of NSCLC with TRAIL genotypes, but the frequency of TRAIL gene 1595 CT genotype was observed to be lower in the patients compared to the other genotypes, and the difference was found to be very close to statistical significance (p=0.07). It can be suggested that TRAIL may play an important role in the development of NSCLC and may be an effective prognostic factor in tumor progression.: It is known that disorders in apoptosis function play an important role in the pathogenesis of many types of cancer, including lung cancer. Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL), a type II transmembrane protein, is a death ligand capable of inducing apoptosis by activating distinctive death receptor. Our purpose in this study is to investigate the gene polymorphisms in TRAIL molecular pathway and TRAIL gene expression levels in non-small cell lung cancer (NSCLC) patients in terms of pathogenesis and prognosis of the disease.Öğe Gene variants of TCF7L2 are histopathologically important in colorectal cancers but do not have direct association with MYC expression(C M B ASSOC, 34 BOULEVARD SOLFERINO, 86000 POITIERS, FRANCE, 2019) Küçük, Nazlı Ezgi Özkan; Horozoğlu, Cem; Timirci Kahraman, Özlem; Arıkan, Soykan; Farooqi, Ammad Ahmad; Sürmen, Saime; Korkmaz, Gurbet; Kelten Talu, Esra Canan; Sabitaliyevich, Uteuliyev Yerzhan; Yaylım, İlhanRapidly accumulating preclinical and clinical studies have helped us to unveil underlying mechanisms of colorectal cancer development and progression. Deregulated signaling pathways play instrumental role in carcinogenesis, drug resistance and metastasis. Wnt signaling cascade has attracted considerable attention in colorectal cancer as many ground-breaking researches have highlighted central role of Wnt pathway in pathogenesis of colorectal cancer. T-Cell Transcription Factors (TCFs) have been shown to work synchronously with beta-catenin to fuel colorectal cancer development and progression. Chromatin immunoprecipitation coupled with high-throughput sequencing (ChIP-Seq) data sets has deepened our knowledge about critical role of risk-associated SNPs. Increasingly it is being reported that many risk-associated SNPs are located within binding sites for transcription factors and consequently risk status of these SNPs may modify binding pattern of transcriptional factors and thus rewire the transcriptional regulation. DNA was extracted from peripheral blood samples of 117 colorectal cancer patients and 127 healthy subjects. TCF7L2 variants (rs6983267, rs7903146) were examined by the PCR-RFLP method. Tumor and the surrounding tissues were dissected from 37 CRC patients and RNA isolation was performed. The gene expression of c-myc was determined by RT-PCR. T allele carriage of rs6983267 variant was found to be associated with CRC (p=0.042). TT genotype of rs7903146 was associated with late tumor stage (T3+T4) (p=0.037) and presence of mucinous component (p-0.031). 'MT haplotype was found to be statistically higher in CRC compared to the control group (p-0.007). Mere was no statistically significant difference in c-myc gene expression. TCF7L2 gene variants may play an important role in histopathologic aspects associated with CRC and it is independent of c-myc gene expression.Öğe The Importance of Programmed Death Ligand 1 Gene Expression, Epidermal Growth Factor Receptor Gene Mutations and Serum Epidermal Growth Factor Receptor Levels in Turkish Non-Small Cell Lung Cancer Patients(Editor of the Journal of Turkish Thoracic and Cardiovascular Surgery, 2018-03-12) Turna, Akif; Horozoğlu, Cem; Koç Erbaşoğlu, Öncü; Ercan, Şeyda; Küçükhüseyin, Özlem; Turan, Saime; Hakan, Mehmet Tolgahan; Kara, Hasan Volkan; Hekimoğlu, Elvin; Zeybek, Ümit; Coşkunpınar, Ender; Cacına, Canan; Ergen, Arzu; Yaylım, İlhanThis study aims to investigate the possible relationships between epidermal growth factor receptor gene mutations, serum epidermal growth factor receptor levels, programmed death ligand gene expression levels and the risks and survivals of resectable nonsmall cell lung cancer patients. Deoxyribonucleic acid isolation was performed from peripheral blood samples and tumor tissues. The mutation analysis was performed for epidermal growth factor receptor. Programmed death ligand 1 gene expression levels were examined pathologically and histopathologically following the tissue tracing of 36 non-small cell lung cancer patients (29 males, 7 females; mean age 60.1 years; range, 41 to 79 years) and analyzed using real-time polymerase chain reaction. Epidermal growth factor receptor serum levels were assessed in all patients. As a result of mutation analyses in 21 patients (28.5% of all adenocarcinoma patients), epidermal growth factor receptor mutation was determined in at least one exon in six patients. In epidermal growth factor receptor mutation detected patients, programmed death ligand 1 gene expression levels were associated with lymph node metastasis (p=0.036). However, epidermal growth factor receptor mutations were not statistically significantly associated according to histopathological examination (p>0.05). Of patients carrying exon 20 (c.2303G>T) mutations, 25% had tumors with perineural invasion. There was a statistically significant association between exon 20 insertions and c.2303G>T and lymphatic invasion (p=0.02), lymph node metastasis and exon 20 insertions (p=0.03). Patients with lower serum epidermal growth factor receptor levels (<400 pg/mL) had better survival time than those with higher serum epidermal growth factor receptor levels (p=0.04). Programmed death ligand 1 gene expression and epidermal growth factor receptor mutation might have a combined effect on non-small cell lung cancer. Programmed death ligand 1 gene expression in tumor pathology may also be a significant feature for tumor progression and tumorigenesis. Serum epidermal growth factor receptor levels seem to be associated with survival.Öğe Investigation of The Vitamin D Receptor (VDR) Gene Polymorphisms in Lumbar Disc Herniation in Turkish Patients(Istanbul University Press, 2019) Hekimoğlu, Bahar Toptaş; Eraltan, Hakan; Sarı, Hidayet; Hakan, Mehmet Tolgahan; Sönmez, Dilara; Horozoğlu, Cem; Zeybek, ÜmitObjective: Lumbar disc herniation (LDH) is a common degenerative disease. It is still not clear if there is a possible association between the vitamin D pathway and the etiopathogenesis of the disease. In this study, we investigated certain VDR polymorphisms which are known to affect vitamin D levels in patients with lumbar disc herniation. Material and Method: TaqI (rs731236) and Fok-I (rs2228570) poly-morphisms were studied by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) in 72 LDH patients and 81 healthy controls. Results: After evaluation of our results, the frequency of LDH patients who have VDR Taq-I Tt genotype was significantly higher than the controls and carriers of Taq-I Tt genotype and t allele who had an increased risk for lumbar disc hernia cases, respectively p=0.002, OR:1.688, 95%CI:1.206-2.360; p=0.006, OR:1.420, 95%CI:1.104-1.825. VDR Fok-I genotypes did not differ significantly between lumbar disc herniation and control cases. (p=0.079). But, Ff genotype and f allele carriers had a higher risk for lumbar disk hernia than those with other genotypes, respectively p=0.025, OR:1.594, 95%CI:1.052-2.414; p=0.037, OR:1.514, 95%CI:1.019-2.250. Conclusion: Our study contributes to the identification of genetic risk factors for specific subgroups of patients with LDH, and em-phasizes the contribution of these biomarkers to the detailed clinical evaluation of patients with genetic biomarkers. © 2019, Istanbul University Press. All rights reserved.Öğe A Study of Short- and Long-term mRNA Levels of the Retn, Iapp, and Drd5 Genes in Obese Mice Induced with High-fat Diet(INT INST ANTICANCER RESEARCH, EDITORIAL OFFICE 1ST KM KAPANDRITIOU-KALAMOU RD KAPANDRITI, PO BOX 22, ATHENS 19014, GREECE, 2018) Tımırcı Kahraman, Özlem; Yılmaz, Ümit; Yılmaz, Nesibe; Çevik, Aydın; Horozoğlu, Cem; Çelik, Faruk; Gökçe, Muhammed Oğuz; Ergen, Arzu; Melekoğlu, Abdullah; Zeybek, ÜmitBackground/Aim: Adipocyte gene expression is altered in obese individuals through multiple metabolic and biochemical pathways. In this study, we aimed to examine the expression of resistin (Retn), amylin (Iapp), and dopamine receptor domain 5 (Drd5) genes previously suggested to contribute to the pathogenesis of obesity, albeit controversially. We also aimed to determine the effects on short and long-term mRNA levels of these genes in obese mice, induced with high-fat diet (HFD). Materials and Methods: Two obesity models were created in our study: group T1 (20 mice) was fed with HFD (60% fat) for 3 months, and group T2 (20 mice) was fed with HFD (60% fat) for 6 months. The control group T0 (20 mice) was fed with a diet of 10% kcal fat supplement for 6 months. At the end of the experiment, their adipose tissues were dissected surgically. Tissue samples of each group were pooled for RNA isolation, cDNA synthesis was carried out and the mRNA levels were examined by quantitative real-time polymerase chain reaction. Serum resistin levels were measured using multiplex bead (luminex) technology for validation. Results: In T2 mice, the mRNA expression of Retn showed a moderate up-regulation (fold change=8.32; p=0.0019) in the adipose tissues. Iapp expression was also significantly up-regulated (fold change=9.78; p=0.012). Moreover, a 6.36-fold upregulation for Drd5 was observed in the adipose tissues of T2 mice (p<0.001). At the same time, serum levels of resistin were found to be high in T1 and T2 mice compared to the control group (p<0.001 and p=0.024, respectively). Conclusion: Our study demonstrated that the mRNA levels of the genetic markers considered to play a role in adipogenesis were different in short- and long-term obesity models formed in C57BL/6J mice using HFD.
