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10.1101/cshperspect.a014241 http://scihub22266oqcxt.onion/10.1101/cshperspect.a014241 C4031954!4031954!24890832     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       Cold+Spring+Harb+Perspect+Med 2014 ; 4 (6): ä Nephropedia Template TP {{tp|p=24890832|t=2014. MYC Activation Is a Hallmark of Cancer Initiation and Maintenance |pdf=|usr=}}{{24890832}} gab.com Text MYC Activation Is a Hallmark of Cancer Initiation and Maintenance JO: Cold Spring Harb Perspect Med http://www.kidney.de/pget.php?&tw=1&pmid=24890832 #FOAvip The MYC proto-oncogene has been implicated in the pathogenesis of most types of human tumors. MYC activation alone in many normal cells is restrained from causing tumorigenesis through multiple genetic and epigenetically controlled checkpoint mechanisms, including proliferative arrest, apoptosis, and cellular senescence. When pathologically activated in a permissive epigenetic and/or genetic context, MYC bypasses these mechanisms, enforcing many of the ?hallmark? features of cancer, including relentless tumor growth associated with DNA replication and transcription, cellular proliferation and growth, protein synthesis, and altered cellular metabolism. MYC mandates tumor cell fate, by inducing stemness and blocking cellular senescence and differentiation. Additionally, MYC orchestrates changes in the tumor microenvironment, including the activation of angiogenesis and suppression of the host immune response. Provocatively, brief or even partial suppression of MYC back to its physiological levels of activation can result in the restoration of intrinsic checkpoint mechanisms, resulting in acute and sustained tumor regression, associated with tumor cells undergoing proliferative arrest, differentiation, senescence, and apoptosis, as well as remodeling of the tumor microenvironment, recruitment of an immune response, and shutdown of angiogenesis. Hence, tumors appear to be ?addicted? to MYC because of both tumor cell?intrinsic, cell-autonomous and host-dependent, immune cell?dependent mechanisms. Both the trajectory and persistence of many human cancers require sustained MYC activation. Multiscale mathematical modeling may be useful to predict when tumors will be addicted to MYC. MYC is a hallmark molecular feature of both the initiation and maintenance of tumorigenesis. Twit Text FOAVip MYC Activation Is a Hallmark of Cancer Initiation and Maintenance ????Cold Spring Harb Perspect Med http://www.kidney.de/pget.php?&tw=1&pmid=24890832 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=24890832 #FOAvip English Wikipedia <ref>{{Cite pmid|24890832}}</ref> MYC Activation Is a Hallmark of Cancer Initiation and Maintenance #MMPMID24890832 Gabay M; Li Y; Felsher DW Cold Spring Harb Perspect Med 2014[Jun]; 4 (6): ä PMID24890832show ga The MYC proto-oncogene has been implicated in the pathogenesis of most types of human tumors. MYC activation alone in many normal cells is restrained from causing tumorigenesis through multiple genetic and epigenetically controlled checkpoint mechanisms, including proliferative arrest, apoptosis, and cellular senescence. When pathologically activated in a permissive epigenetic and/or genetic context, MYC bypasses these mechanisms, enforcing many of the ?hallmark? features of cancer, including relentless tumor growth associated with DNA replication and transcription, cellular proliferation and growth, protein synthesis, and altered cellular metabolism. MYC mandates tumor cell fate, by inducing stemness and blocking cellular senescence and differentiation. Additionally, MYC orchestrates changes in the tumor microenvironment, including the activation of angiogenesis and suppression of the host immune response. Provocatively, brief or even partial suppression of MYC back to its physiological levels of activation can result in the restoration of intrinsic checkpoint mechanisms, resulting in acute and sustained tumor regression, associated with tumor cells undergoing proliferative arrest, differentiation, senescence, and apoptosis, as well as remodeling of the tumor microenvironment, recruitment of an immune response, and shutdown of angiogenesis. Hence, tumors appear to be ?addicted? to MYC because of both tumor cell?intrinsic, cell-autonomous and host-dependent, immune cell?dependent mechanisms. Both the trajectory and persistence of many human cancers require sustained MYC activation. Multiscale mathematical modeling may be useful to predict when tumors will be addicted to MYC. MYC is a hallmark molecular feature of both the initiation and maintenance of tumorigenesis. äMYC Activation Is a Hallmark of Cancer Initiation and Maintenance (epmc).pdf DeepDyve Pubget Overpricing