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10.1002/1878-0261.12084 http://scihub22266oqcxt.onion/10.1002/1878-0261.12084 C5496493!5496493!28548388     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 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+Oncol 2017 ; 11 (7): 739-54 Nephropedia Template TP {{tp|p=28548388|t=2017. Epithelial/mesenchymal plasticity: how have quantitative mathematical models helped improve our understanding?|pdf=|usr=}}{{28548388}} gab.com Text Epithelial/mesenchymal plasticity: how have quantitative mathematical models helped improve our understanding JO: Mol Oncol http://www.kidney.de/pget.php?&tw=1&pmid=28548388 #FOAvip Phenotypic plasticity, the ability of cells to reversibly alter their phenotypes in response to signals, presents a significant clinical challenge to treating solid tumors. Tumor cells utilize phenotypic plasticity to evade therapies, metastasize, and colonize distant organs. As a result, phenotypic plasticity can accelerate tumor progression. A well?studied example of phenotypic plasticity is the bidirectional conversions among epithelial, mesenchymal, and hybrid epithelial/mesenchymal (E/M) phenotype(s). These conversions can alter a repertoire of cellular traits associated with multiple hallmarks of cancer, such as metabolism, immune evasion, invasion, and metastasis. To tackle the complexity and heterogeneity of these transitions, mathematical models have been developed that seek to capture the experimentally verified molecular mechanisms and act as ?hypothesis?generating machines?. Here, we discuss how these quantitative mathematical models have helped us explain existing experimental data, guided further experiments, and provided an improved conceptual framework for understanding how multiple intracellular and extracellular signals can drive E/M plasticity at both the single?cell and population levels. We also discuss the implications of this plasticity in driving multiple aggressive facets of tumor progression. Twit Text FOAVip Epithelial/mesenchymal plasticity: how have quantitative mathematical models helped improve our understanding ????Mol Oncol http://www.kidney.de/pget.php?&tw=1&pmid=28548388 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28548388 #FOAvip English Wikipedia <ref>{{Cite pmid|28548388}}</ref> Epithelial/mesenchymal plasticity: how have quantitative mathematical models helped improve our understanding? #MMPMID28548388 Jolly MK; Tripathi SC; Somarelli JA; Hanash SM; Levine H Mol Oncol 2017[Jul]; 11 (7): 739-54 PMID28548388show ga Phenotypic plasticity, the ability of cells to reversibly alter their phenotypes in response to signals, presents a significant clinical challenge to treating solid tumors. Tumor cells utilize phenotypic plasticity to evade therapies, metastasize, and colonize distant organs. As a result, phenotypic plasticity can accelerate tumor progression. A well?studied example of phenotypic plasticity is the bidirectional conversions among epithelial, mesenchymal, and hybrid epithelial/mesenchymal (E/M) phenotype(s). These conversions can alter a repertoire of cellular traits associated with multiple hallmarks of cancer, such as metabolism, immune evasion, invasion, and metastasis. To tackle the complexity and heterogeneity of these transitions, mathematical models have been developed that seek to capture the experimentally verified molecular mechanisms and act as ?hypothesis?generating machines?. Here, we discuss how these quantitative mathematical models have helped us explain existing experimental data, guided further experiments, and provided an improved conceptual framework for understanding how multiple intracellular and extracellular signals can drive E/M plasticity at both the single?cell and population levels. We also discuss the implications of this plasticity in driving multiple aggressive facets of tumor progression. äEpithelial/mesenchymal plasticity: how have quantitative mathematical (epmc).pdf DeepDyve Pubget Overpricing