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Background/Aims: Lymphocyte function-associated antigen 1 (LFA-1) is a transmembrane glycoprotein expressed on the surface of leukocytes and containing the binding domain for junctional adhesion molecule-A (JAM-A). The aim of the present study was to evaluate the effects of JAM-A and LFA-1 variants on the formation of colorectal cancer and metastasis.Materials and Methods: A total of 82 subjects with colorectal cancer and 67 healthy subjects were studied. DNA was isolated from blood samples, and variations were determined using the polymerase chain reaction and restriction fragment length polymorphism method. Results: JAM-A rs790056 CC genotype and C allele were found to be higher in the colorectal cancer group (p<0.05), and approximately 3-fold increased colorectal cancer risk with CC genotype was determined (p=0.029). Haplotype analysis showed that GC haplotype (LFA-1 rs8058823G and JAM-A rs790056C) frequency was significantly higher in the patient group (p=0.041) than in controls. Conclusion: JAM-A rs790056 variation may be effective in the development of colorectal cancer.

The Wingless/INT (WNT) signaling network has roles in renal cancer development. It was shown that the tumor-suppressor microRNA-124 (miR-124) is associated with the Wnt pathway. Thus, we aimed to measure miR-124 expression levels to evaluate whether it is a prognostic marker or a potential treatment strategy. Thirty tumor and 30 surrounding healthy kidney tissues from the same subjects diagnosed with renal cell carcinoma (RCC), were included in the study. The expression levels of miR-124 were measured with real-time polymerase chain reaction (qPCR) and determined by the 2–ΔΔCT method. The Statistical Package for Social Science (SPSS) version 22 program was used for statistical analyses and a p value of 0.05 was considered to be statistically significant. The expression levels of miR-124 was found to be about 3-fold lower in tumors than in healthy tissues (p 0.001) and decreased expression levels correlated with tumor stage, tumor diameter, body mass index (BMI) and neutrophil values (p 0.05). Our results showed that miR-124 expression levels are associated with RCC. MicroRNA-124 may be assessed as a biomarker in prognosis and the restoration of miR-124 expression might be effective in the treatment of RCC.

BackgroundThe proteolytic activities of matrix metalloproteinases (MMP), cell surface enzymes degrading extracellular matrix, is inhibited by matrix metalloproteinase tissue inhibitors (TIMP). We aim to detect the effects of MMP-9 rs3918242 and TIMP-2 rs8179090 gene variations in renal cell cancer transformation.MethodsOne hundred tumor and 100 adjacent healthy tissues were obtained from the patients with renal cell cancer. Polymerase chain reaction (PCR) and restriction fragment length polymorphism (RFLP) was performed and the products carried out in agarose gel electrophoresis were visualized under UV light. Statistical analyses were performed using SPSS 22 and p-values of less than 0.05 were considered as statistically significant.ResultsMMP-9 rs3918242 T allele was higher in tumor tissues (36.5%) than adjacent tissues (17%) and odds ratio was found 2.8 in T allele (p<0.001). Odds ratio values were found 3.325 in the carriers of TT genotype and 3.5 in the carriers of CT genotype compared to the carriers of CC genotype (p<0.01). The polymorphism of TIMP-2 rs8179090 was not found statically significant in tumor and adjacent tissues (p>0.05).ConclusionMMP-9 rs3918242 T allele, TT and CT genotypes can be used as biomarkers in determining of renal cell carcinoma.

Aim Metabolic syndrome (MS) is associated with dyslipidemia such as hypertriglyceridemia and high-density lipoprotein (HDL) levels. Scavenger receptor BI (SR-BI) is the transmembrane receptor that regulates selective intake of cholesterol esters by the liver and it binds to HDL with high affinity. This study was aimed to determine the effects of SR-BI gen variations upon proatherogenic and antiatherogenic lipid profiles in the patients with metabolic syndrome. Methods The patient group was consisted of 104 (30–65 years) male subjects who were diagnosed with MS and 100 healthy male subjects were included in control group. DNA was isolated from blood samples. SR-BI gene rs4238001 and rs5888 variants were examined by SNaPshot multiplexing system. SPSS 18 was used for statistical analysis and p<0.05 considered as statistically significant. Results It was found that SR-BI gene rs4238001 T allele increased the risk of metabolic syndrome 1.61 fold (p=0.02). Subjects with TT genotype 2.847 fold increased the risk of metabolic syndrome according to subjects with CC genotype (p=0.017). Conclusions SR-BI rs4238001 variation may be related to an increased risk of metabolic syndrome.

Background Scavenger receptor class B, type I (SR-BI), involved in reverse cholesterol pathway, is a multilipoprotein receptor and capable of binding HDL, LDL and VLDL. SR-BI may contribute to the development of hypertension due to accumulation of cholesterol in the vessel wall via transporting lipoproteins. Therefore, it was aimed to investigate the relationship between SR-BI rs5888 and rs4238001 variants in the patient with hypertension. Materials and methods Seventy three subjects diagnosed with hypertension and 76 healthy subjects constituted the patient and control group, respectively. Genomic DNA was isolated from peripheral blood samples and a real-time quantitative polymerase chain reaction protocol was performed to detect variations of rs5888 and rs4238001. The results were analyzed with the SPSS 22 program and p < 0.05 was considered statistically significant. Results and discussion SR-BI rs4238001 variation did not show significant difference between patient and control group (p > 0.05). In the SR-BI rs5888 variation; normal homozygous CC and heterozygous CT carriers had an average 2-fold lower risk of hypertension than those carrying the TT genotype (p < 0.05). Conclusion SR-BI rs5888 TT variant may increase hypertension risk by reducing lipid transport to the liver from the vessel wall.

Introductıon While kidney cancer is the third most common cancer among urogenital cancers, it ranks seventeen among the most common cancers (1). Although kidney cancer patients usually have good outcomes after surgical intervention, less than 20% of individuals with advanced disease have a 2-year survival. Kidney cancer is seen twice in men than in women (2). Kidney cancer is not a single type of cancer and it has genetically and histologically different types responding to therapy differently due to mutations in various genes (3). 5,10-methylenetetrahydrofolate reductase (MTHFR) is the key enzyme in folate metabolism. MTHFR catalyzes the reduction of MTHF to 5-methyl THF using 5,10 FAD as a cofactor that acts as a regulator of folate coenzymes for purine, pyrimidine and methionine synthesis (4). Fivemethyl THF provides the methyl group for the synthesis of methionine (5)

Background Aortic aneurysm occurs in the thoracic and abdominal sections of the aorta and is a deadly late-age-at-onset disease. Thoracic aortic aneurysms (TTAs) are characterized by progressive smooth muscle cell rarefaction due to impaired extracellular matrix. The aim of this study was to investigate fibrillin-1 (FBN-1), fibronectin-1 (FN-1) and tissue inhibitors of metalloproteinases-3 (TIMP-3) gene expression levels in patients with TTA. Materials and methods The data were analyzed for 16 patients treated for TAA and nine control subjects. Tissue samples obtained during surgery were frozen immediately in liquid nitrogen and stored at −80°C until RNA isolation. Gene expression analysis was performed by quantitative reverse transcription polymerase chain reaction for each gene and Beta actin was used as control gene. 2−ΔΔCT method was used for the determining expression levels of the genes. Results According to the results of this study, TIMP-3 gene was nine-fold higher expressed in TAA tissues (p = 0.034). Furthermore, TIMP-3 expression levels were found associated with fasting blood glucose, red blood cells and ejection fraction. The gene expression levels of FBN-1 and FN-1 were not statistically significant (p > 0.05). Conclusion In this clinical trial, we concluded that TIMP-3 expression increases in dilated aorta.