The assessment of NDRG1 expression offers valuable prognostic information for patients with colorectal cancer, especially for those with stage II disease. We propose that NDRG1 expression level could be used to select patients with stage II disease who are at increased risk of unfavorable outcome, and who may benefit from adjuvant therapy.

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The exact function of the protein product of N-myc downstream regulated 1 gene (NDRG1) is unclear. Depending on the tissue type the NDRG1 protein is localized in the cytoplasm, nucleus, mitochondrion or membranes. Moreover, the expression of NDRG1 may be altered by several factors such as hypoxia, heavy metals, DNA damage, hormones, oncogene, and tumor-suppressor genes. A number of studies emphasize the role of NDRG1 in cancerogenesis. Presumably NDRG1 participates in angiogenesis, metastases, and mechanisms leading to anti-cancer drug resistance. This review summarizes current knowledge about the NDRG1 gene and the position of NDRG1 protein in the cellular machinery. The role of NDRG1 in cancer pathogenesis and its possible usefulness as a prognostic factor for patients with cancer is also discussed.

Evaluation of CAV1 expression offers valuable prognostic information for patients with colorectal cancer, and could be used to select patients with stage I or II disease, who are at increased risk of unfavorable outcomes.

Glucocorticoids are a group of hormones with a particularly significant effect on hemostasis. In hypercortisolemic patients increased concentrations of II, VIII, and von Willebrand factors were reported. Considerably fewer studies were concerned with factor XII (FXII). There are reports of decreased FXII concentrations in both venous and arterial thrombosis patients. Also, it was determined that FXII C46T promoter gene polymorphism leads to changes of its concentration. The aim of the study was to determine the C46T polymorphism of FXII promoter gene in hypercortisolemic patients. Thirty hypercortisolemic patients were enrolled in the study. Twenty-nine healthy individuals served as controls. Genomic DNA was isolated from peripheral blood leukocytes. To analyse the polymorphism, PCR products were digested by Hga I at 37°C for 23 h, subjected to 2% agarose gel, and stained with ethidium bromide. In all subjects FXII activity was determined using a clot-based method. All statistical calculations were performed using STATA 12.0 software. A p-value lower than 0.05 was considered statistically significant. Prevalence of FXII C46T polymorphism did not differ significantly between hypercortisolemic patients and controls. No correlation was found between FXII activity and its gene promoter polymorphism in the hypercortisolemic group; however, a clear trend was recorded toward higher FXII activities in 46C homozygotes, and lower in 46T homozygotes. Mean FXII activities did not differ significantly between hypercortisolemic patients and the control group. It seems that in hypercortisolemic patients no significant disorders are present concerning FXII concentrations due to the C46T polymorphism of its gene promoter.