{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,13]],"date-time":"2026-10-13T00:04:25Z","timestamp":1791849865405,"version":"4.3.4"},"reference-count":84,"publisher":"Wiley","issue":"5","license":[{"start":{"date-parts":[[2014,4,12]],"date-time":"2014-04-12T00:00:00Z","timestamp":1397260800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American J Hematol"],"published-print":{"date-parts":[[2014,5]]},"abstract":"<jats:p><jats:bold><jats:italic>Disease overview<\/jats:italic><\/jats:bold>: Chronic Myeloid Leukemia (CML) is a myeloproliferative neoplasm with an incidence of 1\u20132 cases per 100,000 adults, and accounts for \u223c15% of newly diagnosed cases of leukemia in adults. <jats:bold><jats:italic>Diagnosis<\/jats:italic><\/jats:bold>: CML is characterized by a balanced genetic translocation, t(9;22)(q34;q11.2), involving a fusion of the Abelson oncogene (ABL) from chromosome 9q34 with the breakpoint cluster region (BCR) gene on chromosome 22q11.2. This rearrangement is known as the Philadelphia chromosome. The molecular consequence of this translocation is the generation of a BCR\u2010ABL fusion oncogene, which in turn translates into a Bcr\u2010Abl oncoprotein. <jats:bold><jats:italic>Frontline therapy<\/jats:italic><\/jats:bold>: Three tyrosine kinase inhibitors (TKIs), imatinib, nilotinib, and dasatinib have been approved by the US Food and Drug Administration for the first\u2010line treatment of patients with newly diagnosed CML in chronic phase (CML\u2010CP). Clinical trials with second generation TKIs reported significantly deeper and faster responses; their impact on long\u2010term survival remains to be determined. <jats:bold><jats:italic>Salvage therapy<\/jats:italic><\/jats:bold>: For patients who fail frontline therapy, second\u2010line options include second and third generation TKIs. Although second and third generation TKIs are potent and specific BCR\u2010ABL TKIs, they exhibit unique pharmacological profiles and response patterns relative to different patient characteristics, such as patients comorbidities, disease stage, and BCR\u2010ABL mutational status. Patients who develop the T315I \u201cgatekeeper\u201d mutation display resistance to all currently available TKIs except ponatinib. Allogeneic transplantation remains an important therapeutic option for CML\u2010CP who have failed at least 2 TKIs, and for all patients in advanced phase disease. Am. J. Hematol. 89:547\u2013556, 2014. \u00a9 2014 Wiley Periodicals, Inc.<\/jats:p>","DOI":"10.1002\/ajh.23691","type":"journal-article","created":{"date-parts":[[2014,4,12]],"date-time":"2014-04-12T07:53:56Z","timestamp":1397289236000},"page":"547-556","source":"Crossref","is-referenced-by-count":156,"title":["Chronic myeloid leukemia: 2014 update on diagnosis, monitoring, and management"],"prefix":"10.1002","volume":"89","author":[{"given":"Elias","family":"Jabbour","sequence":"first","affiliation":[{"name":"Department of Leukemia The University of Texas M. D. Anderson Cancer Center Houston Texas"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hagop","family":"Kantarjian","sequence":"additional","affiliation":[{"name":"Department of Leukemia The University of Texas M. D. 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