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Standard\u2010dose imatinib (400 mg\/day in chronic phase, 600 mg\/day in advanced CML) now dominates the management of this disease, producing considerably higher hematologic, cytogenetic, and molecular response rates than seen with previous drug therapies. However, although many patients respond well to standard\u2010dose imatinib initially, some patients do not achieve adequate levels of response or discontinue therapy because of resistance. One approach to improving treatment response with first\u2010line imatinib may be to increase the imatinib dose (800 mg\/day), although recent trial data indicate that overall increases in response rates may be modest. Newer Bcr\u2010Abl tyrosine kinase inhibitors can induce responses in patients with all phases of imatinib\u2010resistant CML, even those with imatinib\u2010resistant mutations in the\n                    <jats:italic>BCR\u2010ABL<\/jats:italic>\n                    gene. Furthermore, in initial studies, first\u2010line dasatinib or nilotinib treatment has produced response rates that compare favorably with historical controls treated with imatinib, although confirmation is required from head\u2010to\u2010head clinical trials. Future clinical approaches may include drug combinations, which may allow quiescent leukemia stem cells to be eradicated. Further improvements in drug treatment for first\u2010line CML are expected during the next few years. Am. J. Hematol. 2009. \u00a9 2009 Wiley\u2010Liss, Inc.\n                  <\/jats:p>","DOI":"10.1002\/ajh.21380","type":"journal-article","created":{"date-parts":[[2009,2,19]],"date-time":"2009-02-19T13:37:28Z","timestamp":1235050648000},"page":"287-293","source":"Crossref","is-referenced-by-count":39,"title":["First\u2010line therapy for chronic myeloid leukemia: Past, present, and future"],"prefix":"10.1002","volume":"84","author":[{"given":"Carolina","family":"Pavlovsky","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hagop","family":"Kantarjian","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jorge E.","family":"Cortes","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2009,3,20]]},"reference":[{"key":"e_1_2_1_2_2","doi-asserted-by":"publisher","DOI":"10.1182\/blood.V96.10.3343"},{"key":"e_1_2_1_3_2","doi-asserted-by":"publisher","DOI":"10.7326\/0003-4819-145-12-200612190-00008"},{"key":"e_1_2_1_4_2","doi-asserted-by":"publisher","DOI":"10.1182\/blood-2008-03-144790"},{"key":"e_1_2_1_5_2","doi-asserted-by":"publisher","DOI":"10.1038\/nrc2147"},{"key":"e_1_2_1_6_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.bbmt.2006.03.012"},{"key":"e_1_2_1_7_2","unstructured":"National Comprehensive Cancer Network (NCCN). 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