{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,22]],"date-time":"2026-10-22T08:24:38Z","timestamp":1792657478347,"version":"4.5.0"},"reference-count":297,"publisher":"Harborside Press, LLC","issue":"1","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2024,2]]},"abstract":"<jats:p>\n                    Chronic myeloid leukemia (CML) is defined by the presence of Philadelphia chromosome resulting from a reciprocal translocation between chromosomes 9 and 22 [t9;22] that gives rise to a\n                    <jats:italic>BCR::ABL1<\/jats:italic>\n                    fusion gene. CML occurs in 3 different phases (chronic, accelerated, and blast phase) and is usually diagnosed in the chronic phase in developed countries. Tyrosine kinase inhibitor (TKI) therapy is a highly effective treatment option for patients with chronic phase\u2013CML. The primary goal of TKI therapy in patients with chronic phase\u2013CML is to prevent disease progression to accelerated phase\u2013CML or blast phase\u2013CML. Discontinuation of TKI therapy with careful monitoring is feasible in selected patients. This manuscript discusses the recommendations outlined in the NCCN Guidelines for the diagnosis and management of patients with chronic phase\u2013CML.\n                  <\/jats:p>","DOI":"10.6004\/jnccn.2024.0007","type":"journal-article","created":{"date-parts":[[2024,2,23]],"date-time":"2024-02-23T15:30:09Z","timestamp":1708702209000},"page":"43-69","source":"Crossref","is-referenced-by-count":137,"title":["Chronic Myeloid Leukemia, Version 2.2024, NCCN Clinical Practice Guidelines in Oncology"],"prefix":"10.6004","volume":"22","author":[{"given":"Neil P.","family":"Shah","sequence":"first","affiliation":[{"name":"UCSF Helen Diller Family Comprehensive Cancer Center"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ravi","family":"Bhatia","sequence":"additional","affiliation":[{"name":"O\u2019Neal Comprehensive Cancer Center at UAB"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jessica K.","family":"Altman","sequence":"additional","affiliation":[{"name":"Robert H. 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Blood 2003;102:276\u2013283."},{"key":"B195","series-title":"J Clin Oncol","first-page":"4100","article-title":"ABL mutations in late chronic phase chronic myeloid leukemia patients with up-front cytogenetic resistance to imatinib are associated with a greater likelihood of progression to blast crisis and shorter survival: a study by the GIMEMA Working Party on Chronic Myeloid Leukemia","volume":"23","author":"Soverini S","year":"2005","unstructured":"Soverini S, Martinelli G, Rosti G,  ABL mutations in late chronic phase chronic myeloid leukemia patients with up-front cytogenetic resistance to imatinib are associated with a greater likelihood of progression to blast crisis and shorter survival: a study by the GIMEMA Working Party on Chronic Myeloid Leukemia. 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Haematologica 2007;92:401\u2013404."},{"key":"B205","series-title":"Blood","first-page":"4839","article-title":"Characteristics and outcome of chronic myeloid leukemia patients with F317L BCR-ABL kinase domain mutation after therapy with tyrosine kinase inhibitors","volume":"112","author":"Jabbour E","year":"2008","unstructured":"Jabbour E, Kantarjian HM, Jones D,  Characteristics and outcome of chronic myeloid leukemia patients with F317L BCR-ABL kinase domain mutation after therapy with tyrosine kinase inhibitors. Blood 2008;112:4839\u20134842."},{"key":"B206","series-title":"Blood","first-page":"4944","article-title":"Dasatinib treatment of chronic-phase chronic myeloid leukemia: analysis of responses according to preexisting BCR-ABL mutations","volume":"114","author":"M\u00fcller MC","year":"2009","unstructured":"M\u00fcller MC, Cortes JE, Kim DW,  Dasatinib treatment of chronic-phase chronic myeloid leukemia: analysis of responses according to preexisting BCR-ABL mutations. 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Cancer Cell 2019;36:431\u2013443.e5."},{"key":"B209","series-title":"Blood","first-page":"489","article-title":"BCR-ABL1 compound mutations in tyrosine kinase inhibitor-resistant CML: frequency and clonal relationships","volume":"121","author":"Khorashad JS","year":"2013","unstructured":"Khorashad JS, Kelley TW, Szankasi P,  BCR-ABL1 compound mutations in tyrosine kinase inhibitor-resistant CML: frequency and clonal relationships. Blood 2013;121:489\u2013498."},{"key":"B210","series-title":"Cancer Cell","first-page":"428","article-title":"BCR-ABL1 compound mutations combining key kinase domain positions confer clinical resistance to ponatinib in Ph chromosome-positive leukemia","volume":"26","author":"Zabriskie MS","year":"2014","unstructured":"Zabriskie MS, Eide CA, Tantravahi SK,  BCR-ABL1 compound mutations combining key kinase domain positions confer clinical resistance to ponatinib in Ph chromosome-positive leukemia. Cancer Cell 2014;26:428\u2013442."},{"key":"B211","series-title":"Blood","first-page":"703","article-title":"Compound mutations in BCR-ABL1 are not major drivers of primary or secondary resistance to ponatinib in CP-CML patients","volume":"127","author":"Deininger MW","year":"2016","unstructured":"Deininger MW, Hodgson JG, Shah NP,  Compound mutations in BCR-ABL1 are not major drivers of primary or secondary resistance to ponatinib in CP-CML patients. Blood 2016;127:703\u2013712."},{"key":"B212","series-title":"J Mol Diagn","first-page":"177","article-title":"An intron-derived insertion\/truncation mutation in the BCR-ABL kinase domain in chronic myeloid leukemia patients undergoing kinase inhibitor therapy","volume":"10","author":"Laudadio J","year":"2008","unstructured":"Laudadio J, Deininger MW, Mauro MJ,  An intron-derived insertion\/truncation mutation in the BCR-ABL kinase domain in chronic myeloid leukemia patients undergoing kinase inhibitor therapy. J Mol Diagn 2008;10:177\u2013180."},{"key":"B213","series-title":"Leuk Res","first-page":"108","article-title":"Resistance to imatinib in patients with chronic myelogenous leukemia and the splice variant BCR-ABL1(35INS)","volume":"49","author":"Berman E","year":"2016","unstructured":"Berman E, Jhanwar S, Hedvat C,  Resistance to imatinib in patients with chronic myelogenous leukemia and the splice variant BCR-ABL1(35INS). Leuk Res 2016;49:108\u2013112."},{"key":"B214","series-title":"Leuk Res","first-page":"10","article-title":"Implications of BCR-ABL1 kinase domain-mediated resistance in chronic myeloid leukemia","volume":"38","author":"Soverini S","year":"2014","unstructured":"Soverini S, Branford S, Nicolini FE,  Implications of BCR-ABL1 kinase domain-mediated resistance in chronic myeloid leukemia. Leuk Res 2014;38:10\u201320."},{"key":"B215","series-title":"Blood","first-page":"2926","article-title":"Real-time quantitative PCR analysis can be used as a primary screen to identify patients with CML treated with imatinib who have BCR-ABL kinase domain mutations","volume":"104","author":"Branford S","year":"2004","unstructured":"Branford S, Rudzki Z, Parkinson I,  Real-time quantitative PCR analysis can be used as a primary screen to identify patients with CML treated with imatinib who have BCR-ABL kinase domain mutations. Blood 2004;104:2926\u20132932."},{"key":"B216","series-title":"Haematologica","first-page":"235","article-title":"The role of serial BCR-ABL transcript monitoring in predicting the emergence of BCR-ABL kinase mutations in imatinib-treated patients with chronic myeloid leukemia","volume":"91","author":"Wang L","year":"2006","unstructured":"Wang L, Knight K, Lucas C,  The role of serial BCR-ABL transcript monitoring in predicting the emergence of BCR-ABL kinase mutations in imatinib-treated patients with chronic myeloid leukemia. Haematologica 2006;91:235\u2013239."},{"key":"B217","series-title":"J Clin Oncol","first-page":"3659","article-title":"Significance of increasing levels of minimal residual disease in patients with Philadelphia chromosome-positive chronic myelogenous leukemia in complete cytogenetic response","volume":"27","author":"Kantarjian HM","year":"2009","unstructured":"Kantarjian HM, Shan J, Jones D,  Significance of increasing levels of minimal residual disease in patients with Philadelphia chromosome-positive chronic myelogenous leukemia in complete cytogenetic response. J Clin Oncol 2009;27:3659\u20133663."},{"key":"B218","series-title":"Br J Haematol","first-page":"373","article-title":"Does a rise in the BCR-ABL1 transcript level identify chronic phase CML patients responding to imatinib who have a high risk of cytogenetic relapse?","volume":"145","author":"Marin D","year":"2009","unstructured":"Marin D, Khorashad JS, Foroni L,  Does a rise in the BCR-ABL1 transcript level identify chronic phase CML patients responding to imatinib who have a high risk of cytogenetic relapse? Br J Haematol 2009;145:373\u2013375."},{"key":"B219","series-title":"Blood","first-page":"2598","article-title":"Determining the rise in BCR-ABL RNA that optimally predicts a kinase domain mutation in patients with chronic myeloid leukemia on imatinib","volume":"114","author":"Press RD","year":"2009","unstructured":"Press RD, Willis SG, Laudadio J,  Determining the rise in BCR-ABL RNA that optimally predicts a kinase domain mutation in patients with chronic myeloid leukemia on imatinib. Blood 2009;114:2598\u20132605."},{"key":"B220","series-title":"Lancet Oncol","first-page":"1029","article-title":"Discontinuation of imatinib in patients with chronic myeloid leukaemia who have maintained complete molecular remission for at least 2 years: the prospective, multicentre Stop Imatinib (STIM) trial","volume":"11","author":"Mahon FX","year":"2010","unstructured":"Mahon FX, R\u00e9a D, Guilhot J,  Discontinuation of imatinib in patients with chronic myeloid leukaemia who have maintained complete molecular remission for at least 2 years: the prospective, multicentre Stop Imatinib (STIM) trial. 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J Clin Oncol 2017;35:298\u2013305."},{"key":"B222","series-title":"Eur J Cancer","first-page":"3242","article-title":"Imatinib discontinuation in chronic phase myeloid leukaemia patients in sustained complete molecular response: a randomised trial of the Dutch-Belgian Cooperative Trial for Haemato-Oncology (HOVON)","volume":"49","author":"Thielen N","year":"2013","unstructured":"Thielen N, van der Holt B, Cornelissen JJ,  Imatinib discontinuation in chronic phase myeloid leukaemia patients in sustained complete molecular response: a randomised trial of the Dutch-Belgian Cooperative Trial for Haemato-Oncology (HOVON). 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