The epigenetics of epithelial-mesenchymal plasticity in cancer

By W. Tam, R. Weinberg. Nature Medicine, 2013

1,077 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/cac15f7474703d72796db82637449318e77f5081

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In Oncology

Citations in the corpus

Cancer epigenetics: Tumor Heterogeneity, Plasticity of Stem-like States, and Drug Resistance (2014, background): “Plasticity of the resultant populations for self-renewing properties may still be present, but the EMT phenotypes involved might be of the more mixed EMT-epithelial types proposed recently in the range of breast cancer cell phenotypes (Tam and Weinberg, 2013).”
Regulation of epithelial-mesenchymal transition through epigenetic and post-translational modifications (2016, background): “On the other hand, histone deacetylases (HDACs) catalyze the removal of the acetyl residues in the chromatin of inactive regions [31, 74, 75].”
Epithelial-mesenchymal transition spectrum quantification and its efficacy in deciphering survival and drug responses of cancer patients (2014, neutral): “In the case of acquired EMT, the process may be triggered by changes in the tumour microenvironment (Valastyan & Weinberg, 2011; Lee & Nelson, 2012; Tam & Weinberg, 2013; Van den Eynden et al , 2013) or the influence of drug treatment or cytotoxic stress (Frisch et al , 2013; Marchini et al ,…”
Implications of the Hybrid Epithelial/Mesenchymal Phenotype in Metastasis (2015, background): “…CTCs in a semi-mesenchymal phenotype, rather than those “frozen” or locked in a full EMT phenotype, have the highest plasticity to switch between proliferative and invasive modes, are capable of completing the invasion-metastasis cascade, and should therefore be regarded as CSCs (120, 147–150).”