{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"institution":[{"name":"bioRxiv"}],"indexed":{"date-parts":[[2026,6,24]],"date-time":"2026-06-24T05:50:40Z","timestamp":1782280240185,"version":"3.54.5"},"posted":{"date-parts":[[2025,3,20]]},"group-title":"Cancer Biology","reference-count":81,"publisher":"openRxiv","license":[{"start":{"date-parts":[[2025,3,20]],"date-time":"2025-03-20T00:00:00Z","timestamp":1742428800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc-nd\/4.0\/"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"accepted":{"date-parts":[[2025,3,20]]},"abstract":"<jats:title>Summary<\/jats:title>\n                <jats:p>\n                  Accumulating evidence links pediatric cancers to prenatal transformation events, yet the influence of the developmental stage on oncogenesis remains elusive. We investigated how hematopoietic stem cell developmental stages affect leukemic transformation, disease progression, and therapy response using a novel, humanized model of NUP98::NSD1-driven pediatric acute myeloid leukemia, that is particularly aggressive with WT1 co-mutations. Fetal-derived hematopoietic stem cells readily transform into leukemia, and\n                  <jats:italic>WT1<\/jats:italic>\n                  mutations further enhance stemness and alter lineage hierarchy. In contrast, stem cells from later developmental stages become progressively resistant to transformation. Single-cell analyses revealed that fetal-origin leukemia stem cells exhibit greater quiescence and reliance on oxidative phosphorylation than their postnatal counterparts. These differences drive distinct therapeutic responses, despite identical oncogenic mutations. In patients, onco-fetal transcriptional programs correlate with worse outcomes. By targeting key vulnerabilities of fetal-origin leukemia cells, we identified combination therapies that significantly reduce aggressiveness, highlighting the critical role of ontogeny in pediatric cancer treatment.\n                <\/jats:p>","DOI":"10.1101\/2025.03.19.643917","type":"posted-content","created":{"date-parts":[[2025,3,23]],"date-time":"2025-03-23T01:22:07Z","timestamp":1742692927000},"source":"Crossref","is-referenced-by-count":0,"title":["Ontogeny Dictates Oncogenic Potential, Lineage Hierarchy, and Therapy Response in Pediatric Leukemia"],"prefix":"10.64898","author":[{"given":"Ke","family":"Wang","sequence":"first","affiliation":[{"name":"Department of Oncological Sciences, Icahn School of Medicine at Mount Sinai, New York, NY, USA"},{"name":"Tisch Cancer Institute, Icahn School of Medicine at Mount Sinai, New York, NY, USA"},{"name":"Black Family Stem Cell Institute, Icahn School of Medicine at Mount Sinai, New York, NY, USA"},{"name":"Center for Advancement of Blood Cancer Therapies, Icahn School of Medicine at Mount Sinai, New York, NY, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shayan","family":"Saniei","sequence":"additional","affiliation":[{"name":"Department of Oncological Sciences, Icahn School of Medicine at Mount Sinai, New York, NY, USA"},{"name":"Tisch Cancer Institute, Icahn School of Medicine at Mount Sinai, New York, NY, USA"},{"name":"Black Family Stem Cell Institute, Icahn School of Medicine at Mount Sinai, New York, NY, USA"},{"name":"Center for Advancement of Blood Cancer Therapies, Icahn School of Medicine at Mount Sinai, New York, NY, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Nikita","family":"Poddar","sequence":"additional","affiliation":[{"name":"Department of Oncological Sciences, Icahn School of Medicine at Mount Sinai, New York, NY, USA"},{"name":"Tisch Cancer Institute, Icahn School of Medicine at Mount Sinai, New York, NY, USA"},{"name":"Black Family Stem Cell 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