{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,30]],"date-time":"2026-09-30T23:53:48Z","timestamp":1790812428898,"version":"4.1.0"},"reference-count":39,"publisher":"Wiley","issue":"14","license":[{"start":{"date-parts":[[2026,7,15]],"date-time":"2026-07-15T00:00:00Z","timestamp":1784073600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc-nd\/4.0\/"},{"start":{"date-parts":[[2026,7,15]],"date-time":"2026-07-15T00:00:00Z","timestamp":1784073600000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"content-domain":{"domain":["acsjournals.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Cancer"],"published-print":{"date-parts":[[2026,7,15]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>No large, randomized trials have compared three or more tyrosine kinase inhibitors (TKIs) in a single chronic myeloid leukemia (CML) cohort. Most studies are two\u2010arm comparisons versus imatinib, or rely on indirect methods.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>A retrospective cohort study was conducted of 349 patients with chronic\u2010 and accelerated\u2010phase CML treated between 2007 and 2023 at Cleveland Clinic centers in Northeast Ohio. Overall survival (OS), event\u2010free survival (EFS), 12\u2010month therapeutic milestone achievement, and BCR\u2010ABL1 transcript decline velocity across first\u2010, second\u2010, and third\u2010line TKIs were compared. Baseline demographics, comorbidities, cytogenetics, and hematologic parameters were collected. Multivariable regression and time\u2010dependent Cox models were adjusted for confounders and varying therapy initiation times.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      First\u2010line TKIs included imatinib (53%), dasatinib (30%), nilotinib (15%), and bosutinib (2%). Median age ranged from 52 to 60 years, most patients were White, and high\u2010risk cytogenetics were rare. Five\u2010year OS ranged from 78% for dasatinib to 90% for nilotinib, with nilotinib associated with improved OS (hazard ratio [HR], 0.43) and EFS (HR, 0.48) and the fastest BCR\u2010ABL1 decline (\u03b2 = \u22128.3%) versus imatinib. In second\u2010 (\n                      <jats:italic>n<\/jats:italic>\n                      \u00a0=\u00a0181) and third\u2010line therapy (\n                      <jats:italic>n<\/jats:italic>\n                      \u00a0=\u00a091), no significant differences in outcomes were observed. Across all lines, time\u2010dependent modeling showed improved EFS only for nilotinib (HR, 0.61). Unadjusted OS was higher in patients starting treatment in 2007\u20132010 versus later periods but differences disappeared after adjustment.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>Real\u2010world data indicate that imatinib achieves comparable response rates to newer TKIs, with durable survival. Nilotinib consistently shows faster BCR\u2010ABL1 decline and improved EFS overall, consistent with prior network meta\u2010analyses. Lack of improvement in OS over time suggests the need to investigate factors influencing long\u2010term outcomes in CML.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1002\/cncr.70524","type":"journal-article","created":{"date-parts":[[2026,7,15]],"date-time":"2026-07-15T18:07:34Z","timestamp":1784138854000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":1,"title":["Longitudinal analysis of tyrosine kinase inhibitor therapy outcomes and BCR\u2010ABL1 transcript decline velocity in chronic myeloid leukemia: A 16\u2010year real\u2010world study"],"prefix":"10.1002","volume":"132","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-3289-2333","authenticated-orcid":false,"given":"Moaath K.","family":"Mustafa Ali","sequence":"first","affiliation":[{"name":"Department of Hematology and Medical Oncology Cleveland Clinic Taussig Cancer Institute  Cleveland Ohio 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N.","family":"Mohamed","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine Cleveland Clinic  Cleveland Ohio USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Muaz Alsabbagh","family":"Alchirazi","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine Cleveland Clinic  Cleveland Ohio USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Aastha","family":"Dhakal","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine Cleveland Clinic  Cleveland Ohio USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ali","family":"Mushtaq","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine Cleveland Clinic  Cleveland Ohio USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Naveen","family":"Rehman","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine Cleveland Clinic  Cleveland Ohio 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