{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,11,13]],"date-time":"2026-11-13T10:44:56Z","timestamp":1794566696110,"version":"4.9.1"},"reference-count":37,"publisher":"American Society of Hematology","issue":"23","content-domain":{"domain":["ashpublications.org"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2025,12,4]]},"abstract":"<jats:sec>\n                    <jats:title>Abstract<\/jats:title>\n                    <jats:p>Genomic profiling in patients with chronic-phase chronic myeloid leukemia (CP-CML) demonstrated somatic variants in blood cancer-related gene variants (CGVs) and rearrangements associated with the formation of the Philadelphia chromosome (Ph-associated rearrangements) at diagnosis, collectively termed additional genetic abnormalities (AGAs). AGAs had a negative impact on failure-free survival (FFS) and molecular response in imatinib-treated patients. We investigated whether treatment with more potent therapies could overcome the negative impact of AGAs at diagnosis. Targeted RNA-based next-generation sequencing was performed on diagnostic samples of 315 patients consecutively enrolled in 4 clinical trials of frontline potent tyrosine kinase inhibitors (TKIs) in CP-CML. AGAs were present in 34% of patients at diagnosis, including 20% harboring CGVs and 18% with Ph-associated rearrangements (4% had both). Although the negative impact of Ph-associated rearrangements was overcome by more potent inhibitors, patients with CGVs continued to experience inferior outcomes. This result was largely attributable to patients with ASXL1 variants, observed in 7% overall. Patients harboring ASXL1 variants also had inferior outcomes compared with those with wild-type ASXL1 in terms of 12-month major molecular response (55% vs 83%; P = .001), 2-year FFS (61% vs 91%; P &amp;lt; .001), and notably, the development of treatment-emergent BCR::ABL1 kinase domain mutations at 2 years (35% vs 1%; P &amp;lt; .001). In multivariable models, both CGVs and ASXL1 variants were predictors of each outcome. Treatment with frontline potent TKIs overcame the negative impact of Ph-associated rearrangements observed with frontline imatinib. However, inferior outcomes were still associated with the presence of CGVs. The acquisition of TKI-resistant BCR::ABL1 mutations was almost exclusively associated with mutated ASXL1 at diagnosis.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1182\/blood.2025030259","type":"journal-article","created":{"date-parts":[[2025,9,2]],"date-time":"2025-09-02T21:00:10Z","timestamp":1756846810000},"page":"2821-2832","update-policy":"https:\/\/doi.org\/10.1182\/blood.2019cm0000","source":"Crossref","is-referenced-by-count":20,"title":["Impact of\n                    <i>ASXL1<\/i>\n                    at diagnosis in patients with CML receiving frontline potent TKIs: high risk of kinase domain mutations"],"prefix":"10.1182","volume":"146","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-5895-8797","authenticated-orcid":false,"given":"Naranie","family":"Shanmuganathan","sequence":"first","affiliation":[{"name":"1Department of Haematology, Royal Adelaide Hospital and SA Pathology, Adelaide, Australia"},{"name":"2Department of Genetics and Molecular Pathology, SA 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Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Carol","family":"Wadham","sequence":"additional","affiliation":[{"name":"2Department of Genetics and Molecular Pathology, SA Pathology, Adelaide, Australia"},{"name":"3Centre for Cancer Biology, SA Pathology and University of South Australia, Adelaide, Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Adelina","family":"Fernandes","sequence":"additional","affiliation":[{"name":"2Department of Genetics and Molecular Pathology, SA Pathology, Adelaide, Australia"},{"name":"5Adelaide Medical School, The University of Adelaide, Adelaide, Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Muneeza","family":"Maqsood","sequence":"additional","affiliation":[{"name":"2Department of Genetics and Molecular Pathology, SA Pathology, Adelaide, Australia"},{"name":"3Centre for Cancer Biology, SA Pathology and University of South Australia, Adelaide, 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SA Pathology and University of South Australia, Adelaide, Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-9205-1934","authenticated-orcid":false,"given":"Dominic","family":"Kaczorowski","sequence":"additional","affiliation":[{"name":"2Department of Genetics and Molecular Pathology, SA Pathology, Adelaide, Australia"},{"name":"3Centre for Cancer Biology, SA Pathology and University of South Australia, Adelaide, Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-7171-2935","authenticated-orcid":false,"given":"David M.","family":"Ross","sequence":"additional","affiliation":[{"name":"1Department of Haematology, Royal Adelaide Hospital and SA Pathology, Adelaide, Australia"},{"name":"3Centre for Cancer Biology, SA Pathology and University of South Australia, Adelaide, Australia"},{"name":"4Precision Cancer Medicine Theme, South Australian Health and Medical Research Institute, Adelaide, Australia"},{"name":"5Adelaide Medical School, The University of Adelaide, Adelaide, Australia"},{"name":"6Australasian Leukemia and Lymphoma Group, Melbourne, Australia"},{"name":"7Department of Haematology, Flinders University and Medical Centre, Adelaide, Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-9452-1533","authenticated-orcid":false,"given":"Agnes S. 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