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10.1073/pnas.1703431114 http://scihub22266oqcxt.onion/10.1073/pnas.1703431114 C5692529!5692529 !29078273     free     free     free Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 267.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 267.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\29078273 .jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Proc+Natl+Acad+Sci+U+S+A 2017 ; 114 (45 ): E9635-E9644 Nephropedia Template TP {{tp|p=29078273 |t=2017. Off-tumor targets compromise antiangiogenic drug sensitivity by inducing kidney erythropoietin production |pdf=|usr=}}{{29078273 }} gab.com Text Off-tumor targets compromise antiangiogenic drug sensitivity by inducing kidney erythropoietin production JO: Proc Natl Acad Sci U S A http://www.kidney.de/pget.php?&tw=1&pmid=29078273 #FOAvip Anti-VEGF drugs are commonly used for treatment of a variety of cancers in human patients, and they often develop resistance. The mechanisms underlying anti-VEGF resistance in human cancer patients are largely unknown. Here, we show that in mouse tumor models and in human cancer patients, the anti-VEGF drug-induced kidney hypoxia augments circulating levels of erythropoietin (EPO). Gain-of-function studies show that EPO protects tumor vessels from anti-VEGF treatment and compromises its antitumor effects. Loss of function by blocking EPO function using a pharmacological approach markedly increases antitumor activity of anti-VEGF drugs through inhibition of tumor angiogenesis. Similarly, genetic loss-of-function data shows that deletion of EpoR in nonerythroid cells significantly increases antiangiogenic and antitumor effects of anti-VEGF therapy. Finally, in a relatively large cohort study, we show that treatment of human colorectal cancer patients with bevacizumab augments circulating EPO levels. These findings uncover a mechanism of desensitizing antiangiogenic and anticancer effects by kidney-produced EPO. Our work presents conceptual advances of our understanding of mechanisms underlying antiangiogenic drug resistance. Twit Text FOAVip Off-tumor targets compromise antiangiogenic drug sensitivity by inducing kidney erythropoietin production ????Proc Natl Acad Sci U S A http://www.kidney.de/pget.php?&tw=1&pmid=29078273 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=29078273 #FOAvip English Wikipedia <ref>{{Cite pmid|29078273 }}</ref> Off-tumor targets compromise antiangiogenic drug sensitivity by inducing kidney erythropoietin production #MMPMID29078273 Nakamura M ; Zhang Y ; Yang Y ; Sonmez C ; Zheng W ; Huang G ; Seki T ; Iwamoto H ; Ding B ; Yin L ; Foukakis T ; Hatschek T ; Li X ; Hosaka K ; Li J ; Yu G ; Wang X ; Liu Y ; Cao Y Proc Natl Acad Sci U S A 2017[Nov]; 114 (45 ): E9635-E9644 PMID29078273 show ga Anti-VEGF drugs are commonly used for treatment of a variety of cancers in human patients, and they often develop resistance. The mechanisms underlying anti-VEGF resistance in human cancer patients are largely unknown. Here, we show that in mouse tumor models and in human cancer patients, the anti-VEGF drug-induced kidney hypoxia augments circulating levels of erythropoietin (EPO). Gain-of-function studies show that EPO protects tumor vessels from anti-VEGF treatment and compromises its antitumor effects. Loss of function by blocking EPO function using a pharmacological approach markedly increases antitumor activity of anti-VEGF drugs through inhibition of tumor angiogenesis. Similarly, genetic loss-of-function data shows that deletion of EpoR in nonerythroid cells significantly increases antiangiogenic and antitumor effects of anti-VEGF therapy. Finally, in a relatively large cohort study, we show that treatment of human colorectal cancer patients with bevacizumab augments circulating EPO levels. These findings uncover a mechanism of desensitizing antiangiogenic and anticancer effects by kidney-produced EPO. Our work presents conceptual advances of our understanding of mechanisms underlying antiangiogenic drug resistance. |Angiogenesis Inhibitors/*pharmacology [MESH] |Animals [MESH] |Antineoplastic Agents/*pharmacology [MESH] |Bevacizumab/pharmacology [MESH] |Cohort Studies [MESH] |Colorectal Neoplasms/*drug therapy/metabolism [MESH] |Erythropoietin/*metabolism [MESH] |Humans [MESH] |Kidney/*drug effects/metabolism [MESH] |Mice [MESH] |Neovascularization, Pathologic/*drug therapy/metabolism [MESH]Off-tumor targets compromise antiangiogenic drug sensitivity by induci(epmc).pdf DeepDyve Pubget Overpricing