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dc.contributor.authorVandyke, K.-
dc.contributor.authorFitter, S.-
dc.contributor.authorDrew, J.-
dc.contributor.authorFukumoto, S.-
dc.contributor.authorSchultz, C.-
dc.contributor.authorSims, N.-
dc.contributor.authorYeung, D.-
dc.contributor.authorHughes, T.-
dc.contributor.authorZannettino, A.-
dc.identifier.citationJournal of Clinical Endocrinology and Metabolism, 2013; 98(1):67-76-
dc.description.abstractCONTEXT: Imatinib is a tyrosine kinase inhibitor that has been successfully used to treat Philadelphia chromosome-positive chronic myeloid leukemia (CML) and Kit+ gastrointestinal stromal tumors. We have previously shown that imatinib therapy is associated with an increase in trabecular bone volume. OBJECTIVE: In the present study, we performed a prospective analysis of bone indices in imatinib-treated CML patients to determine the mechanism responsible for this altered bone remodeling. DESIGN, PATIENTS, AND INTERVENTION: This study assessed the effects of high-dose (600 mg/d) imatinib on bone parameters in newly diagnosed chronic-phase Philadelphia chromosome-positive CML patients (n = 11) enrolled in the TIDEL II study. At baseline and after 6, 12, and 24 months of treatment, serum markers of bone remodeling were quantitated, dual-energy x-ray absorptiometry analysis of bone mineral density (BMD) was carried out, and a bone biopsy was collected for histological and micro-computed tomography analysis. RESULTS: Our studies show that the increase in trabecular bone volume and trabecular thickness after imatinib treatment was associated with a significant decrease in osteoclast numbers, accompanied by a significant decrease in serum levels of a marker of osteoclast activity. In contrast, osteoblast numbers were not altered by up to 24 months of imatinib treatment. Notably, we also found that imatinib caused a site-specific decrease in BMD at the femoral neck. CONCLUSIONS: These data suggest that imatinib therapy dysregulates bone remodeling, causing a generalized decrease in osteoclast number and activity that is not counterbalanced by a decrease in osteoblast activity, leading to increased trabecular bone volume. Further long-term investigations are required to determine the causes and consequences of the site-specific decrease in BMD at the femoral neck.-
dc.description.statementofresponsibilityKate Vandyke, Stephen Fitter, Jenny Drew, Seiji Fukumoto, Christopher G. Schultz, Natalie A. Sims, David T. Yeung, Timothy P. Hughes, and Andrew C. W. Zannettino-
dc.publisherEndocrine Society-
dc.rightsCopyright © 2013 by The Endocrine Society-
dc.subjectBone and Bones-
dc.subjectFemur Neck-
dc.subjectLumbar Vertebrae-
dc.subjectAntineoplastic Agents-
dc.subjectProtein Kinase Inhibitors-
dc.subjectAbsorptiometry, Photon-
dc.subjectBone Remodeling-
dc.subjectOrgan Specificity-
dc.subjectBone Density-
dc.subjectMiddle Aged-
dc.subjectLeukemia, Myelogenous, Chronic, BCR-ABL Positive-
dc.subjectImatinib Mesylate-
dc.titleProspective histomorphometric and DXA evaluation of bone remodeling in imatinib-treated CML patients: Evidence for site-specific skeletal effects-
dc.typeJournal article-
dc.identifier.orcidVandyke, K. [0000-0002-1033-849X]-
dc.identifier.orcidFitter, S. [0000-0003-1663-6807]-
dc.identifier.orcidYeung, D. [0000-0002-7558-9927]-
dc.identifier.orcidHughes, T. [0000-0002-0910-3730] [0000-0002-7990-4509]-
dc.identifier.orcidZannettino, A. [0000-0002-6646-6167]-
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