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10.1016/j.mam.2015.05.001 http://scihub22266oqcxt.onion/10.1016/j.mam.2015.05.001 C4780421!4780421!26024970     free     free     free Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 245.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Mol+Aspects+Med 2015 ; 45 (ä): 3-13 Nephropedia Template TP {{tp|p=26024970|t=2015. Turning the headlights on novel cancer biomarkers: Inspection of mechanics underlying intratumor heterogeneity |pdf=|usr=}}{{26024970}} gab.com Text Turning the headlights on novel cancer biomarkers: Inspection of mechanics underlying intratumor heterogeneity JO: Mol Aspects Med http://www.kidney.de/pget.php?&tw=1&pmid=26024970 #FOAvip Although the existence of intratumoral heterogeneity (ITH) in the expression of common biomarkers has been described by pathologists since the late 1890s, we have only recently begun to fathom the staggering extent and near ubiquity of this phenomenon. From the tumor?s perspective, ITH provides a stabilizing diversity that allows for the evolution of aggressive cancer phenotypes. As the weight of the evidence correlating ITH to poor prognosis burgeons, it has become increasingly important to determine the mechanisms by which a tumor acquires ITH, find clinically-adaptable means to quantify ITH and design strategies to deal with the numerous profound clinical ramifications that ITH forces upon us. Elucidation of the drivers of ITH could enable development of novel biomarkers whose interrogation might permit quantitative evaluation of the ITH inherent in a tumor in order to predict the poor prognosis risk associated with that tumor. This review proposes centrosome amplification (CA), aided and abetted by centrosome clustering mechanisms, as a critical driver of chromosomal instability (CIN) that makes a key contribution to ITH generation. Herein we also evaluate how a tumor?s inherent mitotic propensity, which reflects the cell cycling kinetics within the tumor?s proliferative cells, functions as the indispensable engine underpinning CIN, and determines the rate of CIN. We thus expound how the forces of centrosome amplification and mitotic propensity collaborate to sculpt the genetic landscape of a tumor and spawn extensive subclonal diversity. As such, centrosome amplification and mitotic propensity profiles could serve as clinically facile and powerful prognostic biomarkers that would enable more accurate risk segmentation of patients and design of individualized therapies. Twit Text FOAVip Turning the headlights on novel cancer biomarkers: Inspection of mechanics underlying intratumor heterogeneity ????Mol Aspects Med http://www.kidney.de/pget.php?&tw=1&pmid=26024970 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26024970 #FOAvip English Wikipedia <ref>{{Cite pmid|26024970}}</ref> Turning the headlights on novel cancer biomarkers: Inspection of mechanics underlying intratumor heterogeneity #MMPMID26024970 McBride M; Rida PC; Aneja R Mol Aspects Med 2015[Nov]; 45 (ä): 3-13 PMID26024970show ga Although the existence of intratumoral heterogeneity (ITH) in the expression of common biomarkers has been described by pathologists since the late 1890s, we have only recently begun to fathom the staggering extent and near ubiquity of this phenomenon. From the tumor?s perspective, ITH provides a stabilizing diversity that allows for the evolution of aggressive cancer phenotypes. As the weight of the evidence correlating ITH to poor prognosis burgeons, it has become increasingly important to determine the mechanisms by which a tumor acquires ITH, find clinically-adaptable means to quantify ITH and design strategies to deal with the numerous profound clinical ramifications that ITH forces upon us. Elucidation of the drivers of ITH could enable development of novel biomarkers whose interrogation might permit quantitative evaluation of the ITH inherent in a tumor in order to predict the poor prognosis risk associated with that tumor. This review proposes centrosome amplification (CA), aided and abetted by centrosome clustering mechanisms, as a critical driver of chromosomal instability (CIN) that makes a key contribution to ITH generation. Herein we also evaluate how a tumor?s inherent mitotic propensity, which reflects the cell cycling kinetics within the tumor?s proliferative cells, functions as the indispensable engine underpinning CIN, and determines the rate of CIN. We thus expound how the forces of centrosome amplification and mitotic propensity collaborate to sculpt the genetic landscape of a tumor and spawn extensive subclonal diversity. As such, centrosome amplification and mitotic propensity profiles could serve as clinically facile and powerful prognostic biomarkers that would enable more accurate risk segmentation of patients and design of individualized therapies. äTurning the headlights on novel cancer biomarkers: Inspection of mecha(epmc).pdf DeepDyve Pubget Overpricing