In the present study, hCG is associated with AMN-107 molecular weight Elevated VD in testicular tumors. hCG has been associated with angiogenesis in normal tissues; this has been confirmed in vivo and in

vitro by increasing capillary formation and endothelial cell migration [16, 18], and in regulation of placental angiogenesis [24]. Elevated hCG serum levels are present in pregnancy; thus, similarities between tumor invasion and its vascularization and blastocyst implantation and placental development have been described [25, 26]. In addition, it has been proposed that hCG could induce VEGF production in tissues such as 4SC-202 price placenta [17] and granulosa cells [18, 19]. hCG administration to women undergoing in vitro fertilization increases urinary [27], serum, and follicular-fluid VEGF concentrations [28]. Furthermore, hCG exerts a direct angiogenic effect on hCG/LH receptor-expressing uterine endothelial cells, which respond with increased capillary formation in vitro [16, 29]. hCG receptors have been detected in breast carcinoma tissue, which indicates a probable link to a worse breast-cancer prognosis during pregnancy, which we previously hypothesized [30]. We found that predominantly in patients with hCG serum levels ≥ 25 mIU/mL there was increased tumoral

vascular neoformation, suggesting that hCG could be involved in angiogenic processes during tumor JQ-EZ-05 ic50 development. Intrinsic hCG activity is clinically relevant when serum concentrations are high, for instance, during pregnancy or under certain pathological conditions that might be associated to the carcinogenesis of testicular germ cells [6, 7]. In this study, a prominent VD (median, 19.0 ± 28.9) was observed in all tumors, especially non-seminomas, which would be expected as hCG is elevated in this subtype of germ tumors. Angiogenesis is essential for malignant Acyl CoA dehydrogenase neoplasm progression and is correlated with poor prognosis in numerous solid tumors [31], including germ cell testicular cancer [32, 33]. Particularly in normal testis, the endothelial cell proliferation rate is considerably higher than in other stationary

organs. It has been shown that this rate can be increased via hCG stimulation of Leydig cells [34]. In addition, a correlation between hCG and VEGF has been confirmed in rat models and transformed mouse Leydig cell lines (MA-10 cells) [35, 36]. In our results, VEGF expression was limited to 56% of the tumors studied, showing no clinical or histopathological association; nevertheless, tissue availability comprised a factor that could render the data less significant. VEGF expression in germ cell testicular tumors was previously found to be significantly higher than in normal testis and was correlated with microvessel density [11, 37]; it was also described as an indicator of metastatic disease [12].