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10.15252/emmm.201808928 http://scihub22266oqcxt.onion/10.15252/emmm.201808928 C5887904!5887904!29572264     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       EMBO+Mol+Med 2018 ; 10 (4): ä Nephropedia Template TP {{tp|p=29572264|t=2018. Co?targeting driver pathways in prostate cancer: two birds with one stone |pdf=|usr=}}{{29572264}} gab.com Text Co targeting driver pathways in prostate cancer: two birds with one stone JO: EMBO Mol Med http://www.kidney.de/pget.php?&tw=1&pmid=29572264 #FOAvip Co?targeting strategies strive to improve cancer outcomes by combining therapies under contextualized genetic and environmental conditions that selectively target exploitable alterations in tumor cells. Adaptive survival pathways triggered by inhibition of driver genes in the androgen receptor (AR) or PI3K/AKT pathways are of great interest, since they are among the most frequently altered in castrate?resistant prostate cancer (CRPC). Unfortunately, negative feedback loops exist between the AR and PI3K/AKT pathways such that targeting AR leads to activation of PI3K/AKT signaling, while PI3K/AKT pathway inhibition leads to increased AR transcriptional activity. Hence, targeting both pathways provides an opportunity for conditional lethality and a high therapeutic index. In this issue of EMBO Molecular Medicine, Yan et al (2018) present an elegant study showing that histone deacetylase 3 (HDAC3) acts as a common upstream activator of both AR and AKT signaling pathways, and use HDAC3 inhibitors as a monotherapy to co?target two major pathways driving CRPC growth. Twit Text FOAVip Co targeting driver pathways in prostate cancer: two birds with one stone ????EMBO Mol Med http://www.kidney.de/pget.php?&tw=1&pmid=29572264 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=29572264 #FOAvip English Wikipedia <ref>{{Cite pmid|29572264}}</ref> Co?targeting driver pathways in prostate cancer: two birds with one stone #MMPMID29572264 Zoubeidi A; Gleave ME EMBO Mol Med 2018[Apr]; 10 (4): ä PMID29572264show ga Co?targeting strategies strive to improve cancer outcomes by combining therapies under contextualized genetic and environmental conditions that selectively target exploitable alterations in tumor cells. Adaptive survival pathways triggered by inhibition of driver genes in the androgen receptor (AR) or PI3K/AKT pathways are of great interest, since they are among the most frequently altered in castrate?resistant prostate cancer (CRPC). Unfortunately, negative feedback loops exist between the AR and PI3K/AKT pathways such that targeting AR leads to activation of PI3K/AKT signaling, while PI3K/AKT pathway inhibition leads to increased AR transcriptional activity. Hence, targeting both pathways provides an opportunity for conditional lethality and a high therapeutic index. In this issue of EMBO Molecular Medicine, Yan et al (2018) present an elegant study showing that histone deacetylase 3 (HDAC3) acts as a common upstream activator of both AR and AKT signaling pathways, and use HDAC3 inhibitors as a monotherapy to co?target two major pathways driving CRPC growth. äCo?targeting driver pathways in prostate cancer: two birds with one st(epmc).pdf DeepDyve Pubget Overpricing