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Abstract Background The bladder cancer (BC) pathology is caused by both exogenous environmental and endogenous molecular factors. Several genes have been implicated, but the molecular pathogenesis of BC and its subtypes remains debatable. The bioinformatic analysis evaluates high numbers of proteins in a single study, increasing the opportunity to identify possible biomarkers for disorders. Methods The aim of this study is to identify biomarkers for the identification of BC using several bioinformatic analytical tools and methods. BC and normal samples were compared for each probeset with T test in GSE13507 and GSE37817 datasets, and statistical probesets were verified with GSE52519 and E-MTAB-1940 datasets. Differential gene expression, hierarchical clustering, gene ontology enrichment analysis, and heuristic online phenotype prediction algorithm methods were utilized. Statistically significant proteins were assessed in the Human Protein Atlas database. GSE13507 (6271 probesets) and GSE37817 (3267 probesets) data were significant after the extraction of probesets without gene annotation information. Common probesets in both datasets (2888) were further narrowed by analyzing the first 100 upregulated and downregulated probesets in BC samples. Results Among the total 400 probesets, 68 were significant for both datasets with similar fold-change values (Pearson r: 0.995). Protein-protein interaction networks demonstrated strong interactions between CCNB1, BUB1B, and AURKB. The HPA database revealed similar protein expression levels for CKAP2L, AURKB, APIP, and LGALS3 both for BC and control samples. Conclusion This study disclosed six candidate biomarkers for the early diagnosis of BC. It is suggested that these candidate proteins be investigated in a wet lab to identify their functions in BC pathology and possible treatment approaches.

Abstract Our aim was to identify the differentially expressed genes (DEGs) in peripheral blood mononuclear cells (PBMC) of Parkinson’s disease (PD) patients and healthy controls by microarray technology and analysis of related molecular pathways by functional annotation. Thirty PD patients and 30 controls were enrolled. Agilent Human 8X60 K Oligo Microarray was used for gene level expression identification. Gene ontology and pathway enrichment analyses were used for functional annotation of DEGs. Protein–protein interaction analyses were performed with STRING. Expression levels of randomly selected DEGs were quantified by real time quantitative polymerase chain reaction (RT-PCR) for validation. Flow cytometry was done to determine frequency of regulatory T cells (Tregs) in PBMC. A total of 361 DEGs (143 upregulated and 218 downregulated) were identified after GeneSpring analysis. DEGs were involved in 28 biological processes, 12 cellular components and 26 molecular functions. Pathway analyses demonstrated that upregulated genes mainly enriched in p53 (CASP3, TSC2, ATR, MDM4, CCNG1) and PI3K/Akt (IL2RA, IL4R, TSC2, VEGFA, PKN2, PIK3CA, ITGA4, BCL2L11) signaling pathways. TP53 and PIK3CA were identified as most significant hub proteins. Expression profiles obtained by RT-PCR were consistent with microarray findings. PD patients showed increased proportions of CD49d+ Tregs, which correlated with disability scores. Survival pathway genes were upregulated putatively to compensate neuronal degeneration. Bioinformatics analysis showed an association between survival and inflammation genes. Increased CD49d+ Treg ratios might signify the effort of the immune system to suppress ongoing neuroinflammation.

Detection of the circulating tumour cells (CTC) in dogs with a mammary tumour is a useful tool to reveal the micrometastases long before metastases are recognised clinically. The aim of this study was to evaluate the association of the epidermal growth factor receptor (EGFR), claudin 7 (CLND7) and epithelial cell adhesion molecule (EPCAM) with the clinical indices and to reveal the diagnostic importance of these biomarkers in canine mammary tumours (CMTs). Peripheral blood (PB) samples were collected from 45 bitches (group MT) which had single mass with malignant epithelial tumours and 9 healthy bitches (group H). Real time PCR (rt-PCR) was performed to determine the expression levels of EGFR, CLDN7, and EPCAM. Mean values of EGFR and CLDN7 expressions were significantly higher in group MT compared to group H (P < 0.01 and P < 0.001, respectively). The expression level of CLDN7 was positively correlated with EGFR and EPCAM (P < 0.001 and P < 0.05, respectively). The EPCAM expression was associated with increased tumour size (P < 0.05) and EPCAM tended to decrease in the presence of skin ulceration on tumour (P = 0.05). Furthermore, expression levels of EGFR in intact dogs were significantly higher compared to spayed dogs in group MT (P < 0.01). The EGFR expression was significantly higher in the presence of metastases (P < 0.05). Also, increased EGFR was determined in grade 2 compared to grade 1 (P < 0.05). In conclusion, these results show that EGFR, CLDN7, EPCAM markers are measureable in PB and they may provide valuable information about the clinical pathophysiology of CMT. [ABSTRACT FROM AUTHOR]

Our aim was to identify the differentially expressed genes (DEGs) in peripheral blood mononuclear cells (PBMC) of Parkinson's disease (PD) patients and healthy controls by microarray technology and analysis of related molecular pathways by functional annotation. Thirty PD patients and 30 controls were enrolled. Agilent Human 8X60 K Oligo Microarray was used for gene level expression identification. Gene ontology and pathway enrichment analyses were used for functional annotation of DEGs. Protein–protein interaction analyses were performed with STRING. Expression levels of randomly selected DEGs were quantified by real time quantitative polymerase chain reaction (RT-PCR) for validation. Flow cytometry was done to determine frequency of regulatory T cells (Tregs) in PBMC. A total of 361 DEGs (143 upregulated and 218 downregulated) were identified after GeneSpring analysis. DEGs were involved in 28 biological processes, 12 cellular components and 26 molecular functions. Pathway analyses demonstrated that upregulated genes mainly enriched in p53 (CASP3, TSC2, ATR, MDM4, CCNG1) and PI3K/Akt (IL2RA, IL4R, TSC2, VEGFA, PKN2, PIK3CA, ITGA4, BCL2L11) signaling pathways. TP53 and PIK3CA were identified as most significant hub proteins. Expression profiles obtained by RT-PCR were consistent with microarray findings. PD patients showed increased proportions of CD49d+ Tregs, which correlated with disability scores. Survival pathway genes were upregulated putatively to compensate neuronal degeneration. Bioinformatics analysis showed an association between survival and inflammation genes. Increased CD49d+ Treg ratios might signify the effort of the immune system to suppress ongoing neuroinflammation. [ABSTRACT FROM AUTHOR]

Background/aim: Leptin is a hormone that is known to be related to weight gain and obesity. The soluble leptin receptor has been found in plasma as an important determinant of leptin sensitivity. In this study, our goal was to investigate the association between leptin levels and leptin receptor polymorphisms in a Turkish population. Materials and methods: The sample pool of this study consisted of 202 subjects. G2548A variant in the promoter region of the leptin gene and Q223R polymorphism of the leptin receptor gene were evaluated by using PCR-RFLP. Leptin levels were determined by ELISA. Results: Leptin levels were significantly higher in subjects with the A allele than in subjects without the A allele. Leptin receptor levels were lower in subjects with the AA genotype than in those with the AG genotype. There was a higher prevalence of the leptin-2548 AA genotype among subjects with a BMI ≤ 25 kg/m² than in those with a BMI < 25 kg/m². Conclusion: The leptin-2548A allele might be a predisposing factor for obesity. [ABSTRACT FROM AUTHOR]

Background/aim: Oxidative stress plays a role on the development of colorectal cancer. Manganese superoxide dismutase (MnSOD) and glutathione peroxidase 1 (GPX1) are crucial in regulating oxidative balance and its stabilization. Possible mechanisms of action of these enzymes in various types of cancers require further investigation. We aimed to determine expression levels of these genes and their effects on protein levels in serum of patients with colorectal cancer., Materials and Methods: Expression levels of genes were determined using Real Time-Polymerase chain reaction in 35 patients with colorectal cancer. We used enzyme-linked immunosorbent assay to determine MnSOD and GPX1 levels., Results: We found significant differences in GPX1 expression between tumor and normal tissues, with a 2-fold decrease in tumor tissues (p<0.05). However, although no significant difference was found between the expression of MnSOD gene in tumor and that in normal tissues, there was a 1.13-fold change in expression. We observed no relationship between expressions of either gene and their levels in serum., Conclusion: The GPX1 gene may play a critical role in the development of colorectal cancer., (Copyright© 2015 International Institute of Anticancer Research (Dr. John G. Delinassios), All rights reserved.)

Background: The aim of this study was to investigate a possible association of the CYP1A1 Ile462Val and GSTM1 null polymorphisms with the risk of developing bladder cancer in a Turkish population., Patients and Methods: The study constituted 176 patients with bladder cancer and 97 healthy individuals. Evaluation of CYP1A1 Ile462Val gene polymorphism was performed by polymerase chain reaction (PCR) and restriction fragment length polymorphism (RFLP). GSTM1 null gene polymorphism was exclusively determined by PCR. Our results were examined by statistical analyses., Results: There were no significant differences in CYP1A1 genotype frequencies between patients and controls. Furthermore, the frequency of GSTM1 null genotype was higher in patients compared to controls, but it did not reach significance (p=0.622 χ(2)=0.243 OR=0.94 95% CI=0.75-1.18). Significance was discovered in combined analysis of CYP1A1 and GSTM1 genotypes. In the present study, GSTM1 null genotype with CYP1A1 Ile/Ile genotype combination was significantly more frequent in the patient group than in controls (p=0,04, χ(2)=4.217). At the same time, possessing both GSTM1 null genotype and CYP1A1 Val variants (Ile/Val+Val/Val) were significantly higher in control group than in patients (p=0.017, χ(2)=5.468). When the pathological tumor grades were assessed, the frequency of CYP1A1 Val mutant variant with GSTM1 null genotype combination was higher in patients with medium and high-grade tumors than in those with low-grade tumors (p=0.06, χ(2)=3.527, OR=1.36 95% CI=1.03-1.78)., Conclusion: We suggest that the CYP1A1 Ile/Ile genotype with GSTM1 null genotype combination may contribute to the development of bladder cancer in this Turkish population.