One hundred twelve patients (76 men, 36 LY3039478 concentration women; age range, 25-88 years; mean age, 58.1 years) underwent MR imaging of

113 renal masses (mean diameter, 5.4 cm) with pathologic diagnoses of clear cell (n = 75), papillary (n = 28), or chromophobe (n = 10) RCC. A 1.5-T clinical MR protocol was used before and after (corticomedullary and nephrographic phases) intravenous administration of contrast agent. Region-of-interest measurements within tumor and uninvolved renal cortex were used to calculate percentage signal intensity change and tumor-to-cortex enhancement index. Subtype groups were compared by using linear mixed-effects models. Receiver operating characteristic (ROC) curve analysis was performed for the comparison of clear cell and papillary RCCs.

Results: On both the corticomedullary and nephrographic

phase images, clear cell RCCs showed greater signal intensity change (205.6% and 247.1%, respectively) than did papillary RCCs (32.1% and 96.6%, respectively) (P < .001). Chromophobe RCCs showed intermediate change (109.9% and 192.5%, respectively). The tumor-to-cortex enhancement indexes at corticomedullary and nephrographic phases were largest for clear cell RCCs (1.4 and 1.2, respectively), smallest for papillary Fedratinib order RCCs (0.2 and 0.4, respectively), and intermediate for chromophobe RCCs (0.6 and 0.8, respectively). Signal intensity changes on corticomedullary phase images were the most effective parameter for distinguishing clear cell and papillary RCC (area under ROC curve, 0.99); a threshold value of 84% permitted distinction with 93% sensitivity

and 96% specificity.

Conclusion: Clear cell, papillary, and chromophobe RCCs demonstrate different patterns of enhancement on two-time point clinical dynamic contrast-enhanced MR images, allowing their differentiation with high sensitivity and specificity. (c) RSNA, 2009″
“The epithelial-mesenchymal transition (EMT) is a SB203580 research buy crucial event that occurs during cancer metastasis and can be induced by transforming growth factor-beta (TGF-beta) in various tumor cells in vitro. However, little is known about the effects of TGF-beta in canine mammary gland tumors (CMGTs). Here, we investigated the role of TGF-beta in CMGT. We observed that treatment of the CMGT cell line CHMp13a with TGF-beta 1 leads to transient induction of the mesenchymal marker vimentin. Real-time measurements of cellular electrical impedance also showed that CMGT invasiveness is transiently increased by TGF-beta 1 treatment, but is reversed after prolonged stimulation. This phenomenon is similar to the mesenchymal-epithelial transition (MET, the reverse phenomenon of EMT), and a process that is implicated in the establishment of secondary metastatic lesions. (C) 2012 Elsevier Ltd. All rights reserved.