{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,25]],"date-time":"2026-10-25T12:39:00Z","timestamp":1792931940482,"version":"4.5.0"},"reference-count":156,"publisher":"Portland Press Ltd.","issue":"4","license":[{"start":{"date-parts":[[2022,3,30]],"date-time":"2022-03-30T00:00:00Z","timestamp":1648598400000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["portlandpress.com"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2022,4,29]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:p>Acute myeloid leukaemia (AML) is an aggressive disease of the bone marrow with a poor prognosis. Evidence suggests long established chemotherapeutic regimens used to treat AML are reaching the limits of their efficacy, necessitating the urgent development of novel targeted therapies. Canonical Wnt signalling is an evolutionary conserved cascade heavily implicated in normal developmental and disease processes in humans. For over 15 years its been known that the central mediator of this pathway, \u03b2-catenin, is dysregulated in AML promoting the emergence, maintenance, and drug resistance of leukaemia stem cells. Yet, despite this knowledge, and subsequent studies demonstrating the therapeutic potential of targeting Wnt activity in haematological cancers, \u03b2-catenin inhibitors have not yet reached the clinic. The aim of this review is to summarise the current understanding regarding the role and mechanistic dysregulation of \u03b2-catenin in AML, and assess the therapeutic merit of pharmacologically targeting this molecule, drawing on lessons from other disease contexts.<\/jats:p>","DOI":"10.1042\/bsr20211841","type":"journal-article","created":{"date-parts":[[2022,3,30]],"date-time":"2022-03-30T10:57:46Z","timestamp":1648637866000},"update-policy":"https:\/\/doi.org\/10.1042\/crossmark_policy","source":"Crossref","is-referenced-by-count":25,"title":["Targeting \u03b2-catenin in acute myeloid leukaemia: past, present, and future perspectives"],"prefix":"10.1042","volume":"42","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-9160-8676","authenticated-orcid":false,"given":"Megan","family":"Wagstaff","sequence":"first","affiliation":[{"name":"School of Life Sciences, University of Sussex, Brighton, U.K."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-0847-6885","authenticated-orcid":false,"given":"Brandon","family":"Coke","sequence":"additional","affiliation":[{"name":"School of Biological Sciences, University of Southampton, Southampton, U.K."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Georgia\u00a0R.","family":"Hodgkiss","sequence":"additional","affiliation":[{"name":"School of Life Sciences, University of Sussex, Brighton, U.K."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-0429-6294","authenticated-orcid":false,"given":"Rhys\u00a0G.","family":"Morgan","sequence":"additional","affiliation":[{"name":"School of Life Sciences, University of Sussex, Brighton, U.K."}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"288","published-online":{"date-parts":[[2022,4,21]]},"reference":[{"key":"2022042111255535800_B1","doi-asserted-by":"publisher","first-page":"41","DOI":"10.1038\/s41408-021-00425-3","article-title":"Acute myeloid leukemia: current progress and future directions","volume":"11","author":"Kantarjian","year":"2021","journal-title":"Blood Cancer J."},{"key":"2022042111255535800_B2","doi-asserted-by":"publisher","first-page":"72","DOI":"10.1186\/s13045-020-00908-z","article-title":"The global burden and attributable risk factor analysis of acute myeloid leukemia in 195 countries and territories from 1990 to 2017: estimates based on the global burden of disease study 2017","volume":"13","author":"Yi","year":"2020","journal-title":"J. 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