A majority of patients with bladder cancer present with superficial disease and subsequently, some patients show progression to muscle invasive or metastatic disease. Bladder cancer has a complex genetic process and identification of the genetic alterations which occur during progression may lead to the understanding of the nature of the disease and provide the possibility of early treatment. The aim of the present study was to compare the structural and numerical chromosomal differences and changes in the p16 and p53 genes between low‑grade (LG) and high‑grade (HG) bladder cancer (BC) using cytogenetic and molecular cytogenetic methods. Between March 2009 and March 2010, cytogenetic analyses were carried out on tumor and blood samples in 34 patients with transitional cell type BC, and on blood samples of 34 healthy patients as a control group. Fluorescence in situ hybridization probes for the p16 and p53 genes were also used to screen the alterations in these genes in 32 patients with BC. The patients were divided into two groups (LG and HG) and the findings were compared. A total of 11 (32.3%) patients exhibited LGBC, 22 (64.7%) exhibited HGBC and one (3%) patient exhibited carcinoma in situ. There were no differences between the LGBC and HGBC groups according to the number of chromosomal aberrations (P=0.714); however, differences between alterations of the p16 and p53 genes were significant (P=0.002 and P=0.039). Almost all structural abnormalities were found to be located to the 1q21, 1q32, 3p21 and 5q31 regions in patients with HG tumors. In conclusion, the p16 and p53 genes were altered more prominently in patients with HG tumors compared with LG tumors. The structural abnormalities in the 1q21, 1q32, 3p21 and 5q31 regions were observed more frequently in patients with HG tumors. These regions may play significant roles in the progression of BC, but further studies are required to find candidate genes for a panel of BC.

Several studies have shown that rs9939609 and rs1421085 in fat mass and obesity-associated (FTO) gene rs17782313 and rs12970134 in melanocortin-4 receptor (MC4R) gene influence obesity. In the present study, we aimed to determine association between rs9939609, rs1421085, rs17782313, and rs12970134 polymorphism, and their relation with body mass index (BMI), glucose, insulin, homeostasis model assessment of insulin resistance (HOMA-IR) and lipid values in obese children. We included 100 newly diagnosed obese children and 100 healthy children. The rs1421085 (CC/CT) (p = 0.019) and rs9939609 (AA/AT) (p = 0.002) polymorphism regions were higher in the obese group. Additionally, we found that both the rs1421085 (CC/CT) and rs9939609 (AA/AT) polymorphism associated with high-density lipoprotein cholesterol (p = 0.011 and p = 0.003) and triglycerides (p = 0.01 and p = 0.004) level, respectively. Further, the rs9939609 and rs1421085 variants of FTO gene associated with HDL-cholesterol and triglycerides levels in obese children; however, updated studies with a large sample size are required to establish strong links with genetic variants and risk factors in childhood obesity.