{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,14]],"date-time":"2026-09-14T16:19:37Z","timestamp":1789402777442,"version":"build-2803163510"},"reference-count":0,"publisher":"OAE Publishing Inc.","issue":"10","funder":[{"name":"Ares Pharmaceuticals"}],"content-domain":{"domain":["oaepublish.com"],"crossmark-restriction":false},"short-container-title":["Cancer Drug Resist"],"abstract":"<jats:p>Aim: The main goal of this study was to elucidate at the transcript level the tyrosine kinase expression profiles of primary leukemia cells from mixed lineage leukemia 1 gene rearranged (KMT2A\/MLL-R+) acute myeloid leukemia (AML) and acute lymphoblastic leukemia (ALL) patients.  Methods: We evaluated protein tyrosine kinase (PTK) gene expression profiles of primary leukemic cells in KMT2A\/MLL-R+ AML and ALL patients using publicly available archived datasets.  Results: Our studies provided unprecedented evidence that the genetic signatures of KMT2A\/MLL-R+ AML and ALL cells are characterized by transcript-level overexpression of specific PTK. In infants, children and adults with KMT2A\/MLL-R+ ALL, as well as pediatric patients with KMT2A\/MLL-R+ AML, the gene expression levels for FLT3, BTK, SYK, JAK2\/JAK3, as well as several SRC family PTK were differentially amplified. In adults with KMT2A\/MLL-R+ AML, the gene expression levels for SYK, JAK family kinase TYK2, and the SRC family kinases FGR and HCK were differentially amplified.  Conclusion: These results provide new insights regarding the clinical potential of small molecule inhibitors of these PTK, many of which are already FDA\/EMA-approved for other indications, as components of innovative multi-modality treatment platforms against KMT2A\/MLL-R+ acute leukemias.<\/jats:p>","DOI":"10.20517\/cdr.2022.78","type":"journal-article","created":{"date-parts":[[2022,10,9]],"date-time":"2022-10-09T02:19:46Z","timestamp":1665281986000},"page":"902-16","update-policy":"https:\/\/doi.org\/10.20517\/oae.crossmark.policy","source":"Crossref","is-referenced-by-count":12,"title":["Tyrosine kinases in KMT2A\/MLL-rearranged acute leukemias as potential therapeutic targets to overcome cancer drug resistance"],"prefix":"10.20517","volume":"5","author":[{"given":"Fatih M.","family":"Uckun","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sanjive","family":"Qazi","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"8410","published-online":{"date-parts":[[2022]]},"container-title":["Cancer Drug Resistance"],"original-title":[],"deposited":{"date-parts":[[2024,1,18]],"date-time":"2024-01-18T03:46:23Z","timestamp":1705549583000},"score":1,"resource":{"primary":{"URL":"https:\/\/www.oaepublish.com\/articles\/cdr.2022.78"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[2022]]},"references-count":0,"journal-issue":{"issue":"10","published-online":{"date-parts":[[2022]]}},"URL":"https:\/\/doi.org\/10.20517\/cdr.2022.78","relation":{},"ISSN":["2578-532X"],"issn-type":[{"value":"2578-532X","type":"electronic"}],"subject":[],"published":{"date-parts":[[2022]]}}}