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The mechanisms contributing to quiescence of\n                    <jats:italic>ETV6::RUNX1<\/jats:italic>\n                    + preleukemic cells still remain elusive. In this study, we identify linker histone H1\u20100 as a critical mediator of the\n                    <jats:italic>ETV6::RUNX1<\/jats:italic>\n                    + preleukemic state by employing human\n                    <jats:styled-content>\u2010<\/jats:styled-content>\n                    induced pluripotent stem cell (hiPSC) models engineered by using CRISPR\/Cas9 gene editing. Global gene expression analysis revealed upregulation of\n                    <jats:italic>H1\u20100<\/jats:italic>\n                    in\n                    <jats:italic>ETV6::RUNX1<\/jats:italic>\n                    + hiPSCs that was preserved upon hematopoietic differentiation. Moreover, whole transcriptome data of 1,727 leukemia patient samples showed significantly elevated\n                    <jats:italic>H1\u20100<\/jats:italic>\n                    levels in\n                    <jats:italic>ETV6::RUNX1<\/jats:italic>\n                    +\u2009BCP\u2010ALL compared to other leukemia entities. Using dual\u2010luciferase promoter assays, we show that ETV6::RUNX1 induces\n                    <jats:italic>H1\u20100<\/jats:italic>\n                    promoter activity. We further demonstrate that depletion of H1\u20100 specifically inhibits ETV6::RUNX1 signature genes, including\n                    <jats:italic>RAG1<\/jats:italic>\n                    and\n                    <jats:italic>EPOR<\/jats:italic>\n                    . Single\u2010cell sequencing showed that\n                    <jats:italic>H1\u20100<\/jats:italic>\n                    is highly expressed in quiescent hematopoietic cells. Importantly, H1\u20100 protein levels correspond to susceptibility of BCP\u2010ALL cells towards histone deacetylase inhibitors (HDACis) and combinatorial treatment using the H1\u20100\u2010inducing HDACi Quisinostat showed promising synergism with established chemotherapeutic drugs. Taken together, our data identify H1\u20100 as a key regulator of the\n                    <jats:italic>ETV6::RUNX1<\/jats:italic>\n                    + transcriptome and indicate that the addition of Quisinostat may be beneficial to target non\u2010responsive or relapsing\n                    <jats:italic>ETV6::RUNX1<\/jats:italic>\n                    +\u2009BCP\u2010ALL.\n                  <\/jats:p>","DOI":"10.1002\/hem3.70116","type":"journal-article","created":{"date-parts":[[2025,4,4]],"date-time":"2025-04-04T05:15:13Z","timestamp":1743743713000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":5,"title":["H1\u20100 is a specific mediator of the repressive ETV6::RUNX1 transcriptional landscape in preleukemia and B cell acute lymphoblastic leukemia"],"prefix":"10.1002","volume":"9","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-4174-7568","authenticated-orcid":false,"given":"Vera 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