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In CML-iPSCs, the phosphorylation of ERK1\/2, AKT, and JNK, which are essential for the maintenance of both BCR-ABL (+) leukemia cells and iPSCs, were unchanged after imatinib treatment, whereas the phosphorylation of signal transducer and activator of transcription (STAT)5 and CRKL was significantly decreased. These results suggest that the signaling for iPSCs maintenance compensates for the inhibition of BCR-ABL. CML-iPSC\u2013derived hematopoietic cells recovered the sensitivity to imatinib although CD34+38\u221290+45+ immature cells were resistant to imatinib, which recapitulated the pathophysiologic feature of the initial CML. CML-iPSCs provide us with a novel platform to investigate CML pathogenesis on the basis of patient-derived samples.<\/jats:p>","DOI":"10.1182\/blood-2011-07-367441","type":"journal-article","created":{"date-parts":[[2012,5,17]],"date-time":"2012-05-17T13:07:13Z","timestamp":1337260033000},"page":"6234-6242","update-policy":"https:\/\/doi.org\/10.1182\/blood.2019cm0000","source":"Crossref","is-referenced-by-count":139,"title":["Generation of induced pluripotent stem cells from primary chronic myelogenous leukemia patient samples"],"prefix":"10.1182","volume":"119","author":[{"given":"Keiki","family":"Kumano","sequence":"first","affiliation":[{"name":"Department of Hematology and Oncology, Graduate School of Medicine, University of Tokyo, Tokyo, Japan;"},{"name":"Core Research for Evolutional Science and Technology, Japan Science and Technology Agency, Tokyo, 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