Epithelial/mesenchymal plasticity: how have quantitative mathematical models helped improve our understanding?

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dc.citation.firstpage739en_US
dc.citation.issueNumber7en_US
dc.citation.journalTitleMolecular Oncologyen_US
dc.citation.lastpage754en_US
dc.citation.volumeNumber11en_US
dc.contributor.authorJolly, Mohit Kumaren_US
dc.contributor.authorTripathi, Satyendra C.en_US
dc.contributor.authorSomarelli, Jason A.en_US
dc.contributor.authorHanash, Samir M.en_US
dc.contributor.authorLevine, Herberten_US
dc.contributor.orgCenter for Theoretical Biological Physicsen_US
dc.date.accessioned2017-08-21T14:34:15Zen_US
dc.date.available2017-08-21T14:34:15Zen_US
dc.date.issued2017en_US
dc.description.abstractPhenotypic 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.en_US
dc.identifier.citationJolly, Mohit Kumar, Tripathi, Satyendra C., Somarelli, Jason A., et al.. "Epithelial/mesenchymal plasticity: how have quantitative mathematical models helped improve our understanding?." <i>Molecular Oncology,</i> 11, no. 7 (2017) Wiley: 739-754. https://doi.org/10.1002/1878-0261.12084.en_US
dc.identifier.digitalEpithelial_mesenchymal_plasticityen_US
dc.identifier.doihttps://doi.org/10.1002/1878-0261.12084en_US
dc.identifier.urihttps://hdl.handle.net/1911/97371en_US
dc.language.isoengen_US
dc.publisherWileyen_US
dc.rightsThis is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.en_US
dc.rights.urihttps://creativecommons.org/licenses/by/4.0/en_US
dc.subject.keywordcirculating tumor cellsen_US
dc.subject.keywordcollective cell migrationen_US
dc.subject.keywordepithelial-mesenchymal transitionen_US
dc.subject.keywordhybrid epithelial/mesenchymalen_US
dc.subject.keywordmathematical modelingen_US
dc.subject.keywordstemnessen_US
dc.titleEpithelial/mesenchymal plasticity: how have quantitative mathematical models helped improve our understanding?en_US
dc.typeJournal articleen_US
dc.type.dcmiTexten_US
dc.type.publicationpublisher versionen_US
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