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This suggests the hypothesis that hypoxia contributes to the chemoresistance of AML\u2010LSCs and may represent a therapeutic target to sensitize AML\u2010LSCs to chemotherapy. Here, we identify HIF<jats:sup>high<\/jats:sup> and HIF<jats:sup>low<\/jats:sup> specific AML subgroups (inv(16)\/<jats:italic>t<\/jats:italic>(8;21) and MLLr, respectively) and provide a comprehensive single\u2010cell expression atlas of 119,000 AML cells and AML\u2010LSCs in paired diagnostic\u2010relapse samples from these molecular subgroups. The HIF\/hypoxia pathway signature is attenuated in AML\u2010LSCs compared with more differentiated AML cells\u00a0but is more expressed than in healthy hematopoietic cells. Importantly, chemical inhibition of HIF cooperates with standard\u2010of\u2010care chemotherapy to impair AML growth and to substantially eliminate AML\u2010LSCs in vitro and in vivo. These findings support the HIF pathway in the stem cell\u2010driven drug resistance of AML and unravel avenues for combinatorial targeted and chemotherapy\u2010based approaches to specifically eliminate AML\u2010LSCs.<\/jats:p>","DOI":"10.1002\/hem3.45","type":"journal-article","created":{"date-parts":[[2024,2,26]],"date-time":"2024-02-26T12:45:07Z","timestamp":1708951507000},"source":"Crossref","is-referenced-by-count":13,"title":["Integrative single\u2010cell expression and functional studies unravels a sensitization to cytarabine\u2010based chemotherapy through HIF pathway inhibition in AML leukemia stem cells"],"prefix":"10.1002","volume":"8","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-2183-7443","authenticated-orcid":false,"given":"Talia","family":"Velasco\u2010Hernandez","sequence":"first","affiliation":[{"name":"Josep Carreras Leukemia Research Institute  Barcelona Spain"},{"name":"Red Espa\u00f1ola de Terapias Avanzadas (TERAV)\u2010Instituto de Salud Carlos III (ISCIII) 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