Use my Search Websuite to scan PubMed, PMCentral, Journal Hosts and Journal Archives, FullText. Kick-your-searchterm to multiple Engines kick-your-query now !>

A dictionary by aggregated review articles of nephrology, medicine and the life sciences Your one-stop-run pathway from word to the immediate pdf of peer-reviewed on-topic knowledge.

10.1158/0008-5472.CAN-15-1293 http://scihub22266oqcxt.onion/10.1158/0008-5472.CAN-15-1293 C4873388!4873388 !26980767     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=26980767 &cmd=llinks): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 215       Cancer+Res 2016 ; 76 (9 ): 2525-39 Nephropedia Template TP {{tp|p=26980767 |t=2016. TGF? Signaling in the Pancreatic Tumor Microenvironment Promotes Fibrosis and Immune Evasion to Facilitate Tumorigenesis |pdf=|usr=}}{{26980767 }} gab.com Text TGF Signaling in the Pancreatic Tumor Microenvironment Promotes Fibrosis and Immune Evasion to Facilitate Tumorigenesis JO: Cancer Res http://www.kidney.de/pget.php?&tw=1&pmid=26980767 #FOAvip In early pancreatic carcinogenesis, TGF? acts as a tumor suppressor due to its growth-inhibitory effects in epithelial cells. However, in advanced disease, TGF? appears to promote tumor progression. Therefore, to better understand the contributions of TGF? signaling to pancreatic carcinogenesis, we generated mouse models of pancreatic cancer with either epithelial or systemic TGFBR deficiency. We found that epithelial suppression of TGF? signals facilitated pancreatic tumorigenesis, whereas global loss of TGF? signaling protected against tumor development via inhibition of tumor-associated fibrosis, stromal TGF?1 production, and the resultant restoration of antitumor immune function. Similarly, TGFBR-deficient T cells resisted TGF?-induced inactivation ex vivo, and adoptive transfer of TGFBR-deficient CD8(+) T cells led to enhanced infiltration and granzyme B-mediated destruction of developing tumors. These findings paralleled our observations in human patients, where TGF? expression correlated with increased fibrosis and associated negatively with expression of granzyme B. Collectively, our findings suggest that, despite opposing the proliferation of some epithelial cells, TGF? may promote pancreatic cancer development by affecting stromal and hematopoietic cell function. Therefore, the use of TGFBR inhibition to target components of the tumor microenvironment warrants consideration as a potential therapy for pancreatic cancer, particularly in patients who have already lost tumor-suppressive TGF? signals in the epithelium. Cancer Res; 76(9); 2525-39. ©2016 AACR. Twit Text FOAVip TGF Signaling in the Pancreatic Tumor Microenvironment Promotes Fibrosis and Immune Evasion to Facilitate Tumorigenesis ????Cancer Res http://www.kidney.de/pget.php?&tw=1&pmid=26980767 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26980767 #FOAvip English Wikipedia <ref>{{Cite pmid|26980767 }}</ref> TGF? Signaling in the Pancreatic Tumor Microenvironment Promotes Fibrosis and Immune Evasion to Facilitate Tumorigenesis #MMPMID26980767 Principe DR ; DeCant B ; Mascariñas E ; Wayne EA ; Diaz AM ; Akagi N ; Hwang R ; Pasche B ; Dawson DW ; Fang D ; Bentrem DJ ; Munshi HG ; Jung B ; Grippo PJ Cancer Res 2016[May]; 76 (9 ): 2525-39 PMID26980767 show ga In early pancreatic carcinogenesis, TGF? acts as a tumor suppressor due to its growth-inhibitory effects in epithelial cells. However, in advanced disease, TGF? appears to promote tumor progression. Therefore, to better understand the contributions of TGF? signaling to pancreatic carcinogenesis, we generated mouse models of pancreatic cancer with either epithelial or systemic TGFBR deficiency. We found that epithelial suppression of TGF? signals facilitated pancreatic tumorigenesis, whereas global loss of TGF? signaling protected against tumor development via inhibition of tumor-associated fibrosis, stromal TGF?1 production, and the resultant restoration of antitumor immune function. Similarly, TGFBR-deficient T cells resisted TGF?-induced inactivation ex vivo, and adoptive transfer of TGFBR-deficient CD8(+) T cells led to enhanced infiltration and granzyme B-mediated destruction of developing tumors. These findings paralleled our observations in human patients, where TGF? expression correlated with increased fibrosis and associated negatively with expression of granzyme B. Collectively, our findings suggest that, despite opposing the proliferation of some epithelial cells, TGF? may promote pancreatic cancer development by affecting stromal and hematopoietic cell function. Therefore, the use of TGFBR inhibition to target components of the tumor microenvironment warrants consideration as a potential therapy for pancreatic cancer, particularly in patients who have already lost tumor-suppressive TGF? signals in the epithelium. Cancer Res; 76(9); 2525-39. ©2016 AACR. |Adoptive Transfer [MESH] |Animals [MESH] |Blotting, Western [MESH] |Carcinogenesis/*metabolism/pathology [MESH] |Disease Models, Animal [MESH] |Enzyme-Linked Immunosorbent Assay [MESH] |Fibrosis/metabolism/pathology [MESH] |Flow Cytometry [MESH] |Humans [MESH] |Immunohistochemistry [MESH] |Mice [MESH] |Mice, Mutant Strains [MESH] |Pancreatic Neoplasms/*pathology [MESH] |Signal Transduction/physiology [MESH] |Transforming Growth Factor beta/*metabolism [MESH] |Tumor Escape/*physiology [MESH]TGF? Signaling in the Pancreatic Tumor Microenvironment Promotes Fibro(epmc).pdf DeepDyve Pubget Overpricing