{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,11,6]],"date-time":"2026-11-06T10:29:12Z","timestamp":1793960952832,"version":"4.8.0"},"reference-count":46,"publisher":"SAGE Publications","issue":"23-24","license":[{"start":{"date-parts":[[2026,10,19]],"date-time":"2026-10-19T00:00:00Z","timestamp":1792368000000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.sagepub.com\/page\/policies\/text-and-data-mining-license"}],"funder":[{"name":"Canadian Institute of Health Research","award":["FRN 150772"],"award-info":[{"award-number":["FRN 150772"]}],"id":[{"id":"https:\/\/ror.org\/01gavpb45","id-type":"ROR","asserted-by":"crossref"}]}],"content-domain":{"domain":["journals.sagepub.com"],"crossmark-restriction":true},"short-container-title":["Stem Cells and Development"],"published-print":{"date-parts":[[2026,12,1]]},"abstract":"<jats:p>\n                    Patient-derived induced pluripotent stem cells (iPSCs) provide a renewable model for studying acute myeloid leukemia (AML), but whether AML-iPSCs faithfully preserve the functional heterogeneity of genetically distinct AML clones remains unclear. Here, we functionally characterized a genetically defined AML-iPSC resource comprising 34 AML-iPSC lines from 11 AML patients, with complementary assays performed across partially overlapping subsets of lines. AML-iPSC lines were classified as aberration-positive (Ab\n                    <jats:sup>+<\/jats:sup>\n                    ) or aberration-negative (Ab\n                    <jats:sup>\u2212<\/jats:sup>\n                    ) based on retention of the clinically defining patient-specific leukemia-associated genetic abnormalities. Representative Ab\n                    <jats:sup>+<\/jats:sup>\n                    and Ab\n                    <jats:sup>\u2212<\/jats:sup>\n                    AML-iPSC lines derived from donor hematopoietic cells exhibited comparable differentiation capacity across nonhematopoietic lineages, whereas Ab\n                    <jats:sup>+<\/jats:sup>\n                    AML-iPSC lines demonstrated reduced hematopoietic differentiation, as determined by phenotypic analysis and functional colony-forming assays. Across overlapping subsets of AML-iPSC lines, these clone-specific hematopoietic phenotypes were conserved across four independent differentiation platforms, supporting that they reflect stable clone-specific properties rather than methodological artifacts. Residual hematopoietic progenitors derived from Ab\n                    <jats:sup>+<\/jats:sup>\n                    AML-iPSC lines retained leukemic features, including persistence of leukemia-associated genetic abnormalities, immature blast-like morphology, and enhanced serial replating capacity indicative of self-renewal-associated properties. In a representative paired patient model, these progenitors also demonstrated persistent myeloid-skewed hematopoietic output following xenotransplantation. Together, these findings establish a renewable platform for mechanistic studies investigating how clonal heterogeneity contributes to disease evolution and therapeutic resistance in AML following pluripotent reprogramming.\n                  <\/jats:p>","DOI":"10.1177\/15473287261495853","type":"journal-article","created":{"date-parts":[[2026,10,20]],"date-time":"2026-10-20T05:42:16Z","timestamp":1792474936000},"page":"459-477","update-policy":"https:\/\/doi.org\/10.1177\/sage-journals-update-policy","source":"Crossref","is-referenced-by-count":0,"title":["Genetically Defined Acute Myeloid Leukemia Induced Pluripotent Stem Cell Clones Reveal Selective Impairment of Hematopoietic Development"],"prefix":"10.1177","volume":"35","author":[{"given":"Deanna P.","family":"Porras","sequence":"first","affiliation":[{"name":"Department of Biochemistry and Biomedical Sciences, McMaster University, Hamilton, Ontario, Canada."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Amy","family":"Qiao","sequence":"additional","affiliation":[{"name":"Department of Biochemistry and Biomedical Sciences, McMaster University, Hamilton, Ontario, Canada."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Meaghan","family":"Doyle","sequence":"additional","affiliation":[{"name":"Department of Biochemistry and Biomedical Sciences, McMaster University, Hamilton, Ontario, Canada."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hailey","family":"Kadonoff","sequence":"additional","affiliation":[{"name":"Department of Biochemistry and Biomedical Sciences, McMaster University, Hamilton, Ontario, Canada."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kinga","family":"Vojnits","sequence":"additional","affiliation":[{"name":"Department of Biology, Acadia University, Wolfville, Nova Scotia, Canada."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Diana","family":"Golubeva","sequence":"additional","affiliation":[{"name":"Department of Biochemistry and Biomedical Sciences, McMaster University, Hamilton, Ontario, Canada."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Cameron G.","family":"Hollands","sequence":"additional","affiliation":[{"name":"Department of Biochemistry and Biomedical Sciences, McMaster University, Hamilton, Ontario, Canada."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Allison","family":"Boyd","sequence":"additional","affiliation":[{"name":"Department of Biochemistry and Biomedical Sciences, McMaster University, Hamilton, Ontario, Canada."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-9304-5130","authenticated-orcid":false,"given":"Mickie","family":"Bhatia","sequence":"additional","affiliation":[{"name":"Department of Biochemistry and Biomedical Sciences, McMaster University, Hamilton, Ontario, Canada."},{"name":"Michael G. 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