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10.3390/ijms160921138 http://scihub22266oqcxt.onion/10.3390/ijms160921138 C4613246!4613246!26404259     free     free     free Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\26404259.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Int+J+Mol+Sci 2015 ; 16 (9): 21138-52 Nephropedia Template TP {{tp|p=26404259|t=2015. PI3K and AKT: Unfaithful Partners in Cancer |pdf=|usr=}}{{26404259}} gab.com Text PI3K and AKT: Unfaithful Partners in Cancer JO: Int J Mol Sci http://www.kidney.de/pget.php?&tw=1&pmid=26404259 #FOAvip The phosphatidylinositol 3-kinase (PI3K)/AKT signaling pathway regulates multiple cellular processes. An overactivation of the pathway is frequently present in human malignancies and plays a key role in cancer progression. Hence, its inhibition has become a promising approach in cancer therapy. However, the development of resistances, such as the abrogation of negative feedback mechanisms or the activation of other proliferative signaling pathways, has considerably limited the anticancer efficacy of PI3K/AKT inhibitors. In addition, emerging evidence points out that although AKT is acknowledged as the major downstream effector of PI3K, both PI3K and AKT can operate independently of each other in cancer, revealing another level of complexity in this pathway. Here, we highlight the complex relationship between PI3K and AKT in cancer and further discuss the consequences of this relationship for cancer therapy. Twit Text FOAVip PI3K and AKT: Unfaithful Partners in Cancer ????Int J Mol Sci http://www.kidney.de/pget.php?&tw=1&pmid=26404259 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26404259 #FOAvip English Wikipedia <ref>{{Cite pmid|26404259}}</ref> PI3K and AKT: Unfaithful Partners in Cancer #MMPMID26404259 Faes S; Dormond O Int J Mol Sci 2015[Sep]; 16 (9): 21138-52 PMID26404259show ga The phosphatidylinositol 3-kinase (PI3K)/AKT signaling pathway regulates multiple cellular processes. An overactivation of the pathway is frequently present in human malignancies and plays a key role in cancer progression. Hence, its inhibition has become a promising approach in cancer therapy. However, the development of resistances, such as the abrogation of negative feedback mechanisms or the activation of other proliferative signaling pathways, has considerably limited the anticancer efficacy of PI3K/AKT inhibitors. In addition, emerging evidence points out that although AKT is acknowledged as the major downstream effector of PI3K, both PI3K and AKT can operate independently of each other in cancer, revealing another level of complexity in this pathway. Here, we highlight the complex relationship between PI3K and AKT in cancer and further discuss the consequences of this relationship for cancer therapy. äPI3K and AKT: Unfaithful Partners in Cancer (epmc).pdf DeepDyve Pubget Overpricing