{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,2]],"date-time":"2026-07-02T17:18:26Z","timestamp":1783012706796,"version":"3.54.6"},"reference-count":6,"publisher":"Wiley","issue":"2","license":[{"start":{"date-parts":[[2026,4,27]],"date-time":"2026-04-27T00:00:00Z","timestamp":1777248000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"},{"start":{"date-parts":[[2026,4,27]],"date-time":"2026-04-27T00:00:00Z","timestamp":1777248000000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["European J of Haematology"],"published-print":{"date-parts":[[2026,8]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:p>\n                    BCR::ABL1 acquisition is an emerging but poorly characterized resistance mechanism in\n                    <jats:italic>FLT3<\/jats:italic>\n                    \u2010mutated AML. Using multiomic single\u2010cell DNA sequencing, we characterized clonal evolution in a patient with\n                    <jats:italic>FLT3<\/jats:italic>\n                    \u2010ITD AML who acquired BCR::ABL1 with FLT3 inhibitor resistance. Phylogenetic reconstruction confirmed BCR::ABL1 as a branch event co\u2010occurring with\n                    <jats:italic>FLT3<\/jats:italic>\n                    \u2010ITD and restricted to specific blast populations, supporting BCR::ABL1 acquisition as a resistance mechanism.\n                  <\/jats:p>","DOI":"10.1111\/ejh.70207","type":"journal-article","created":{"date-parts":[[2026,4,28]],"date-time":"2026-04-28T05:21:38Z","timestamp":1777353698000},"page":"501-503","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Multiomic Single\u2010Cell Sequencing Identifies\n                    <i>BCR::ABL1<\/i>\n                    as an Acquired Resistance Mechanism in\n                    <i>FLT3+<\/i>\n                    <scp>AML<\/scp>"],"prefix":"10.1111","volume":"117","author":[{"given":"Vanessa E.","family":"Kennedy","sequence":"first","affiliation":[{"name":"Department of Medicine Stanford University  Stanford California USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Cheryl A. 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