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dc.contributor.authorPereira, Lloyden
dc.contributor.authorMariadason, John Men
dc.contributor.authorHannan, Ross Den
dc.contributor.authorDhillon, Amardeep Sen
dc.identifier.citationFrontiers in Oncology 2015; 5: 13en
dc.description.abstractColorectal cancer (CRC) is a genetically heterogeneous disease that develops and progresses through several distinct pathways characterized by genomic instability. In recent years, it has emerged that inherent plasticity in some populations of CRC cells can contribute to heterogeneity in differentiation state, metastatic potential, therapeutic response, and disease relapse. Such plasticity is thought to arise through interactions between aberrant signaling events, including persistent activation of the APC/β-catenin and KRAS/BRAF/ERK pathways, and the tumor microenvironment. Here, we highlight key concepts and evidence relating to the role of epithelial-mesenchymal plasticity as a driver of CRC progression and stratification of the disease into distinct molecular and clinicopathological subsets.en
dc.subject.othercancer stem cellen
dc.subject.otherepithelial–mesenchymal transitionen
dc.subject.othertumor progressionen
dc.titleImplications of epithelial-mesenchymal plasticity for heterogeneity in colorectal cancer.en
dc.typeJournal Articleen
dc.identifier.journaltitleFrontiers in oncologyen
dc.identifier.affiliationOlivia Newton-John Cancer Research Institute, Austin Hospital , Melbourne, VIC , Australiaen
dc.identifier.affiliationResearch Division, Peter MacCallum Cancer Centre , Melbourne, VIC , Australiaen
dc.identifier.affiliationSir Peter MacCallum Department of Oncology, The University of Melbourne , Melbourne, VIC , Australiaen
dc.identifier.affiliationDepartment of Pathology, The University of Melbourne , Melbourne, VIC , Australia-
dc.identifier.affiliationDepartment of Biochemistry and Molecular Biology, The University of Melbourne , Melbourne, VIC , Australia-
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