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Despite AML displaying extensive biological and clinical heterogeneity, LSC with high interleukin-3 receptor (IL3R) levels are a constant yet puzzling feature, as this receptor lacks tyrosine kinase activity. Here, we show that the heterodimeric IL3R\u03b1\/\u03b2c receptor assembles into hexamers and dodecamers through a unique interface in the 3D structure, where high IL3R\u03b1\/\u03b2c ratios bias hexamer formation. Importantly, receptor stoichiometry is clinically relevant as it varies across the individual cells in the AML hierarchy, in which high IL3R\u03b1\/\u03b2c ratios in LSCs drive hexamer-mediated stemness programs and poor patient survival, while low ratios mediate differentiation. Our study establishes a new paradigm in which alternative cytokine receptor stoichiometries differentially regulate cell fate, a signaling mechanism that may be generalizable to other transformed cellular hierarchies and of potential therapeutic significance.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Significance:<\/jats:title>\n                    <jats:p>Stemness is a hallmark of many cancers and is largely responsible for disease emergence, progression, and relapse. Our finding that clinically significant stemness programs in AML are directly regulated by different stoichiometries of cytokine receptors represents a hitherto unexplained mechanism underlying cell-fate decisions in cancer stem cell hierarchies.<\/jats:p>\n                    <jats:p>This article is highlighted in the In This Issue feature, p. 1749<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1158\/2159-8290.cd-22-1396","type":"journal-article","created":{"date-parts":[[2023,5,16]],"date-time":"2023-05-16T09:07:41Z","timestamp":1684228061000},"page":"1922-1947","update-policy":"https:\/\/doi.org\/10.1158\/crossmark_policy","source":"Crossref","is-referenced-by-count":11,"title":["Distinct Assemblies of Heterodimeric Cytokine Receptors Govern Stemness Programs in Leukemia"],"prefix":"10.1158","volume":"13","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-5844-7644","authenticated-orcid":false,"given":"Winnie L.","family":"Kan","sequence":"first","affiliation":[{"name":"1Cytokine Receptor Laboratory, Centre for Cancer Biology, SA Pathology and the University of South Australia, Adelaide, South Australia, Australia."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-5650-5767","authenticated-orcid":false,"given":"Urmi","family":"Dhagat","sequence":"additional","affiliation":[{"name":"2Australian Cancer Research Foundation Rational Drug Discovery Centre, St. Vincent's Institute of Medical Research, Fitzroy, Victoria, Australia."},{"name":"3Department of Biochemistry and Pharmacology and the Australian Cancer Research Foundation Facility for Innovative Cancer Drug Discovery, Bio21 Molecular Science and Biotechnology Institute, University of Melbourne, Parkville, Victoria, Australia."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-5013-6123","authenticated-orcid":false,"given":"Kerstin 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