{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,8]],"date-time":"2026-03-08T19:52:19Z","timestamp":1772999539067,"version":"3.50.1"},"reference-count":38,"publisher":"Wiley","issue":"2","license":[{"start":{"date-parts":[[2009,9,18]],"date-time":"2009-09-18T00:00:00Z","timestamp":1253232000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"},{"start":{"date-parts":[[2009,9,18]],"date-time":"2009-09-18T00:00:00Z","timestamp":1253232000000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Hematological Oncology"],"published-print":{"date-parts":[[2010,6]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>We analysed the dynamic change of imatinib\u2010resistant mutations in BCR\u2010ABL kinase domain focusing on T315I mutation during dasatinib or nilotinib therapy. Fifty\u2010five imatinib\u2010resistant chronic myeloid leukaemia patients (32 patients with imatinib\u2010resistant mutations and 23 patients without mutation) in different disease phases were treated with dasatinib (median 17.3 months) or nilotinib (median 6.8 months). Among the 32 patients with baseline mutation, mutations including M244V, G250E, E255K, M351T, H396R, S417Y, E450K and E459K disappeared in 8 patients and new mutations were detected in 9 patients, all of which were T315I. Among the 23 patients without baseline mutation, 4 patients showed newly developed mutations including T315I, T315I\u2009+\u2009E459K, M244V and F359V. The T315I was the most frequently detected mutation in imatinib therapy (16%, 9 of 55) as well as in dasatinib or nilotinib therapy (24%, 11 of 44). Patients with imatinib resistant baseline mutations had a higher rate of mutation development during dasatinib or nilotinib treatment compared to patients without baseline mutations (28% vs. 17%). Copyright \u00a9 2009 John Wiley &amp; Sons, Ltd.<\/jats:p>","DOI":"10.1002\/hon.918","type":"journal-article","created":{"date-parts":[[2009,9,18]],"date-time":"2009-09-18T09:53:58Z","timestamp":1253267638000},"page":"82-88","source":"Crossref","is-referenced-by-count":11,"title":["Dynamic change of T315I BCR\u2010ABL kinase domain mutation in Korean chronic myeloid leukaemia patients during treatment with Abl tyrosine kinase inhibitors"],"prefix":"10.1002","volume":"28","author":[{"given":"Wan\u2010Seok","family":"Kim","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Dongho","family":"Kim","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Dong\u2010Wook","family":"Kim","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Il\u2010Young","family":"Kweon","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Soo\u2010Hyun","family":"Kim","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Hyun\u2010Gyung","family":"Goh","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Sa\u2010Hee","family":"Park","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Jeong","family":"Lee","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"311","published-online":{"date-parts":[[2009,9,18]]},"reference":[{"key":"e_1_2_1_2_2","doi-asserted-by":"publisher","DOI":"10.1038\/306277a0"},{"key":"e_1_2_1_3_2","doi-asserted-by":"publisher","DOI":"10.1056\/NEJM200104053441401"},{"key":"e_1_2_1_4_2","doi-asserted-by":"publisher","DOI":"10.1056\/NEJMoa011573"},{"key":"e_1_2_1_5_2","doi-asserted-by":"publisher","DOI":"10.1182\/blood-2006-01-0092"},{"key":"e_1_2_1_6_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0140-6736(02)07679-1"},{"key":"e_1_2_1_7_2","doi-asserted-by":"publisher","DOI":"10.1016\/S1535-6108(02)00096-X"},{"key":"e_1_2_1_8_2","doi-asserted-by":"publisher","DOI":"10.1182\/blood.V99.9.3472"},{"key":"e_1_2_1_9_2","doi-asserted-by":"publisher","DOI":"10.1126\/science.1062538"},{"key":"e_1_2_1_10_2","doi-asserted-by":"publisher","DOI":"10.1182\/blood.V95.11.3498"},{"key":"e_1_2_1_11_2","doi-asserted-by":"publisher","DOI":"10.1182\/blood.V96.3.1070"},{"key":"e_1_2_1_12_2","doi-asserted-by":"publisher","DOI":"10.1182\/blood.V95.5.1758.005a41_1758_1766"},{"key":"e_1_2_1_13_2","doi-asserted-by":"crossref","first-page":"160a","DOI":"10.1182\/blood.V104.11.553.553","article-title":"The 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