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This review collates the current approaches employed in developing therapeutics against cancer\u2010associated <jats:styled-content style=\"fixed-case\">EMT<\/jats:styled-content>, and provides an assessment of their respective strengths and drawbacks. We reflect on the close relationship between <jats:styled-content style=\"fixed-case\">EMT<\/jats:styled-content> and chemoresistance against current targeted therapeutics, with a special focus on the epigenetic mechanisms that link these processes. This prompts the hypothesis that carcinoma\u2010associated <jats:styled-content style=\"fixed-case\">EMT<\/jats:styled-content> shares a common epigenetic pathway to cellular plasticity as somatic cell reprogramming during tissue repair and regeneration. Indeed, their striking resemblance suggests that <jats:styled-content style=\"fixed-case\">EMT<\/jats:styled-content> in carcinoma is a pathological adaptation of an intrinsic program of cellular plasticity that is crucial to tissue homeostasis. We thus propose a revised approach that targets the epigenetic mechanisms underlying pathogenic <jats:styled-content style=\"fixed-case\">EMT<\/jats:styled-content> to arrest cellular plasticity regardless of upstream cancer\u2010driving mutations.<\/jats:p>","DOI":"10.1002\/1878-0261.12082","type":"journal-article","created":{"date-parts":[[2017,5,25]],"date-time":"2017-05-25T16:58:19Z","timestamp":1495731499000},"page":"878-891","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":90,"title":["The <scp>EMT<\/scp> spectrum and therapeutic opportunities"],"prefix":"10.1002","volume":"11","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-2963-9305","authenticated-orcid":false,"given":"Dominic C.","family":"Voon","sequence":"first","affiliation":[{"name":"Institute for Frontier Science Initiative Kanazawa University Ishikawa Japan"},{"name":"Division of Genetics Cancer Research Institute Kanazawa University Ishikawa 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