{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,31]],"date-time":"2026-10-31T02:33:02Z","timestamp":1793413982600,"version":"4.5.0"},"reference-count":71,"publisher":"American Society of Hematology","issue":"21","license":[{"start":{"date-parts":[[2024,2,23]],"date-time":"2024-02-23T00:00:00Z","timestamp":1708646400000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by-nc-nd\/4.0\/"}],"content-domain":{"domain":["ashpublications.org"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2024,5,23]]},"abstract":"<jats:sec>\n                  <jats:title>Abstract<\/jats:title>\n                  <jats:p>Acute lymphoblastic leukemia (ALL) with fusions of ABL-class tyrosine kinase genes other than BCR::ABL1 occurs in \u223c3% of children with ALL. The tyrosine kinase genes involved in this BCR::ABL1-like (Ph-like) subtype include ABL1, PDGFRB, ABL2, and CSF1R, each of which has up to 10 described partner genes. ABL-class ALL resembles BCR::ABL1-positive ALL with a similar gene expression profile, poor response to chemotherapy, and sensitivity to tyrosine kinase inhibitors (TKIs). There is a lack of comprehensive data regarding TKI sensitivity in the heterogeneous group of ABL-class ALL. We observed variability in TKI sensitivity within and among each ABL-class tyrosine kinase gene subgroup. We showed that ALL samples with fusions for any of the 4 tyrosine kinase genes were relatively sensitive to imatinib. In contrast, the PDGFRB-fused ALL samples were less sensitive to dasatinib and bosutinib. Variation in ex\u00a0vivo TKI response within the subset of samples with the same ABL-class tyrosine kinase gene was not associated with the ALL immunophenotype, 5\u2032 fusion partner, presence or absence of Src-homology-2\/3 domains, or deletions of IKZF1, PAX5, or CDKN2A\/B. In conclusion, the tyrosine kinase gene involved in ABL-class ALL is the main determinant of TKI sensitivity and relevant for specific TKI selection.<\/jats:p>\n               <\/jats:sec>","DOI":"10.1182\/blood.2023023120","type":"journal-article","created":{"date-parts":[[2024,2,23]],"date-time":"2024-02-23T21:45:35Z","timestamp":1708724735000},"page":"2178-2189","update-policy":"https:\/\/doi.org\/10.1182\/blood.2019cm0000","source":"Crossref","is-referenced-by-count":27,"title":["Tyrosine kinase inhibitor response of ABL-class acute lymphoblastic leukemia: the role of kinase type and SH3 domain"],"prefix":"10.1182","volume":"143","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-7657-7397","authenticated-orcid":false,"given":"Inge","family":"van Outersterp","sequence":"first","affiliation":[{"name":"1Princess M\u00e1xima Center for Pediatric Oncology, Utrecht, The Netherlands"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-1327-1662","authenticated-orcid":false,"given":"Sarah K.","family":"Tasian","sequence":"additional","affiliation":[{"name":"2Division of Oncology, Children's Hospital of Philadelphia, Philadelphia, PA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Caitlin E. J.","family":"Reichert","sequence":"additional","affiliation":[{"name":"1Princess M\u00e1xima Center for Pediatric Oncology, Utrecht, The Netherlands"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Aur\u00e9lie","family":"Boeree","sequence":"additional","affiliation":[{"name":"1Princess M\u00e1xima Center for Pediatric Oncology, Utrecht, The Netherlands"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hester A.","family":"de Groot-Kruseman","sequence":"additional","affiliation":[{"name":"1Princess M\u00e1xima Center for Pediatric Oncology, Utrecht, The Netherlands"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-2167-3805","authenticated-orcid":false,"given":"Gabriele","family":"Escherich","sequence":"additional","affiliation":[{"name":"3Department of Pediatric Hematology and Oncology, University Medical Center Hamburg Eppendorf, Hamburg, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-4848-7789","authenticated-orcid":false,"given":"Judith M.","family":"Boer","sequence":"additional","affiliation":[{"name":"1Princess M\u00e1xima Center for Pediatric Oncology, Utrecht, The Netherlands"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-5795-2921","authenticated-orcid":false,"given":"Monique L.","family":"den Boer","sequence":"additional","affiliation":[{"name":"1Princess M\u00e1xima Center for Pediatric Oncology, Utrecht, The Netherlands"},{"name":"4Department of Pediatric Oncology and Hematology, Erasmus MC-Sophia Children's Hospital, Rotterdam, The Netherlands"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"234","reference":[{"issue":"9","key":"2024052315213513300_bib1","doi-asserted-by":"crossref","first-page":"1376","DOI":"10.1038\/s41588-022-01159-z","article-title":"The genomic landscape of pediatric 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