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10.3390/cancers12102785 http://scihub22266oqcxt.onion/10.3390/cancers12102785 32998363!7601465!32998363     free     free     free Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\32998363.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Cancers+(Basel) 2020 ; 12 (10): ä Nephropedia Template TP {{tp|p=32998363|t=2020. Angiotensin Inhibition, TGF-beta and EMT in Cancer |pdf=|usr=}}{{32998363}} gab.com Text Angiotensin Inhibition, TGF-beta and EMT in Cancer JO: Cancers (Basel) http://www.kidney.de/pget.php?&tw=1&pmid=32998363 #FOAvip Angiotensin inhibitors are standard drugs in cardiovascular and renal diseases that have antihypertensive and antifibrotic properties. These drugs also exert their antifibrotic effects in cancer by reducing collagen and hyaluronan deposition in the tumor stroma, thus enhancing drug delivery. Angiotensin II signaling interferes with the secretion of the cytokine TGF-beta-a known driver of malignancy. TGF-beta stimulates matrix production in cancer-associated fibroblasts, and thus drives desmoplasia. The effect of TGF-beta on cancer cells itself is stage-dependent and changes during malignant progression from inhibitory to stimulatory. The intracellular signaling for the TGF-beta family can be divided into an SMAD-dependent canonical pathway and an SMAD-independent noncanonical pathway. These capabilities have made TGF-beta an interesting target for numerous drug developments. TGF-beta is also an inducer of epithelial-mesenchymal transition (EMT). EMT is a highly complex spatiotemporal-limited process controlled by a plethora of factors. EMT is a hallmark of metastatic cancer, and with its reversal, an important step in the metastatic cascade is characterized by a loss of epithelial characteristics and/or the gain of mesenchymal traits. Twit Text FOAVip Angiotensin Inhibition, TGF-beta and EMT in Cancer ????Cancers (Basel) http://www.kidney.de/pget.php?&tw=1&pmid=32998363 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=32998363 #FOAvip English Wikipedia <ref>{{Cite pmid|32998363}}</ref> Angiotensin Inhibition, TGF-beta and EMT in Cancer #MMPMID32998363 Pallasch FB; Schumacher U Cancers (Basel) 2020[Sep]; 12 (10): ä PMID32998363show ga Angiotensin inhibitors are standard drugs in cardiovascular and renal diseases that have antihypertensive and antifibrotic properties. These drugs also exert their antifibrotic effects in cancer by reducing collagen and hyaluronan deposition in the tumor stroma, thus enhancing drug delivery. Angiotensin II signaling interferes with the secretion of the cytokine TGF-beta-a known driver of malignancy. TGF-beta stimulates matrix production in cancer-associated fibroblasts, and thus drives desmoplasia. The effect of TGF-beta on cancer cells itself is stage-dependent and changes during malignant progression from inhibitory to stimulatory. The intracellular signaling for the TGF-beta family can be divided into an SMAD-dependent canonical pathway and an SMAD-independent noncanonical pathway. These capabilities have made TGF-beta an interesting target for numerous drug developments. TGF-beta is also an inducer of epithelial-mesenchymal transition (EMT). EMT is a highly complex spatiotemporal-limited process controlled by a plethora of factors. EMT is a hallmark of metastatic cancer, and with its reversal, an important step in the metastatic cascade is characterized by a loss of epithelial characteristics and/or the gain of mesenchymal traits. äAngiotensin Inhibition, TGF-beta and EMT in Cancer (epmc).pdf DeepDyve Pubget Overpricing