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10.1158/1078-0432.CCR-15-2389 http://scihub22266oqcxt.onion/10.1158/1078-0432.CCR-15-2389 C4896088!4896088!27250929     free     free     free Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Clin+Cancer+Res 2016 ; 22 (11): 2605-10 Nephropedia Template TP {{tp|p=27250929|t=2016. Molecular Pathways: Targeting the PI3K Pathway in Cancer?BET Inhibitors to the Rescue |pdf=|usr=}}{{27250929}} gab.com Text Molecular Pathways: Targeting the PI3K Pathway in Cancer BET Inhibitors to the Rescue JO: Clin Cancer Res http://www.kidney.de/pget.php?&tw=1&pmid=27250929 #FOAvip The phosphoinositide 3-kinase (PI3K) signaling pathway is a complex and tightly regulated network that is critical for many physiological processes such as cell growth, proliferation, metabolism and survival. Aberrant activation of this pathway can occur through mutation of almost any of its major nodes and has been implicated in a number of human diseases including cancer. The high frequency of mutations in this pathway in multiple types of cancer has led to the development of small molecule inhibitors of PI3K, several of which are currently in clinical trials. However, several feedback mechanisms either within the PI3K pathway or in compensatory pathways can render tumor cells resistant to therapy. Recently, targeting proteins of the bromodomain and extra-terminal (BET) family of epigenetic readers of histone acetylation has been shown to effectively block adaptive signaling response of cancer cells to inhibitors of the PI3K pathway, which at least in some cases can restore sensitivity. BET inhibitors also enforce blockade of the MAPK, JAK/STAT and ER pathways suggesting they may be a rational combinatorial partner for divergent oncogenic signals that are subject to homeostatic regulation. Here, we review the PI3K pathway as a target for cancer therapy and discuss the potential use of BET inhibition to enhance clinical efficacy of PI3K inhibitors. Twit Text FOAVip Molecular Pathways: Targeting the PI3K Pathway in Cancer BET Inhibitors to the Rescue ????Clin Cancer Res http://www.kidney.de/pget.php?&tw=1&pmid=27250929 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27250929 #FOAvip English Wikipedia <ref>{{Cite pmid|27250929}}</ref> Molecular Pathways: Targeting the PI3K Pathway in Cancer?BET Inhibitors to the Rescue #MMPMID27250929 Stratikopoulos EE; Parsons RE Clin Cancer Res 2016[Jun]; 22 (11): 2605-10 PMID27250929show ga The phosphoinositide 3-kinase (PI3K) signaling pathway is a complex and tightly regulated network that is critical for many physiological processes such as cell growth, proliferation, metabolism and survival. Aberrant activation of this pathway can occur through mutation of almost any of its major nodes and has been implicated in a number of human diseases including cancer. The high frequency of mutations in this pathway in multiple types of cancer has led to the development of small molecule inhibitors of PI3K, several of which are currently in clinical trials. However, several feedback mechanisms either within the PI3K pathway or in compensatory pathways can render tumor cells resistant to therapy. Recently, targeting proteins of the bromodomain and extra-terminal (BET) family of epigenetic readers of histone acetylation has been shown to effectively block adaptive signaling response of cancer cells to inhibitors of the PI3K pathway, which at least in some cases can restore sensitivity. BET inhibitors also enforce blockade of the MAPK, JAK/STAT and ER pathways suggesting they may be a rational combinatorial partner for divergent oncogenic signals that are subject to homeostatic regulation. Here, we review the PI3K pathway as a target for cancer therapy and discuss the potential use of BET inhibition to enhance clinical efficacy of PI3K inhibitors. äMolecular Pathways: Targeting the PI3K Pathway in Cancer?BET Inhibitor(epmc).pdf DeepDyve Pubget Overpricing