The present study is the first to evaluate the relevance of the TGFBR2-875G>A functional polymorphism in CRPC patients. The concordance index was used to compare the predictive ability of different prognostic variables associated with CR development; the predictive value was assessed with Harrell’s concordance indexes, where a c-index of 1 indicates perfect concordance. Tumor stage is a well-known prognostic factor for cancer progression. Worldwide, PC is the most prevalent malignancy in men. Prostate cancer is a complex, multifactorial and heterogeneous disease. A better understanding of the mechanisms involved in this disease may contribute to early diagnosis and to the establishment of new therapeutic targets to increase survival and improve the quality of patients’ life. The PC progression to CR has been associated with the cell insensitivity to antiproliferative signals and consequent disruption of the balance between cell growth rate and apoptosis. The CRPC is an invariably lethal condition, with chemotherapy being the sole treatment option with only palliative benefits. Therefore, it is important to understand the mechanisms involved in CR progression. In the present study, we describe that the functional TGFBR2 polymorphism influences the development of CRPC. Our results suggest that small changes in TGFBR2 expression levels, due to functional SNPs, may contribute to a disequilibrium in the TGF1 signaling pathway activation and thus to a higher risk for an earlier development of resistance to ADT. TGF1 signaling pathway mediates growth, mainly by inhibiting cell cycle progression through G1-arrest, suppressing c-myc, and stimulating cyclin-dependent kinases inhibitors including p21WAF1 and p15Ink4b, but also by inducing apoptosis, through the induction of DAP kinase and others. Several studies demonstrated that TGF1 signaling components, including TGFRII, are often lost in human cancer. In PC, the TGF1 is frequently up-regulated and the loss of TGFRI and RII has been detected. Is has been hypothesized, that TGFBR2 AbMole Isoforskolin repression is responsible for most of the tumor associated TGF1 resistance observed in vivo. Studies performed by Rojas and co-workers showed that TGFBR2 expression levels can regulate the intensity of activation of the Smad and non-Smad signaling pathways. The inactivation of TGFBR2 gene in mouse fibroblasts has been associated with prostate intraepithelial neoplasia and invasive squamous cell carcinoma of forestomach development.After AbMole Povidone iodine correcting SAS/SDS, the decreased GMD of the insula still existed. The results suggested that psychological factors did not have a significant impact on the microstructure of the insula. However, the decreased GMD in the insula didn’t show a significant correlation with durations and symptoms of FD patients no matter whether anxiety and depression were controlled for or not. It indicated that the GMD changes in the insula might be induced by multiple factors and need further investigation.