{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,2,21]],"date-time":"2026-02-21T12:37:40Z","timestamp":1771677460008,"version":"3.50.1"},"reference-count":63,"publisher":"The Endocrine Society","issue":"1","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2013,1,1]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:sec><jats:title>Context:<\/jats:title><jats:p>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.<\/jats:p><\/jats:sec><jats:sec><jats:title>Objective:<\/jats:title><jats:p>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.<\/jats:p><\/jats:sec><jats:sec><jats:title>Design, Patients, and Intervention:<\/jats:title><jats:p>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.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results:<\/jats:title><jats:p>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.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions:<\/jats:title><jats:p>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.<\/jats:p><\/jats:sec>","DOI":"10.1210\/jc.2012-2426","type":"journal-article","created":{"date-parts":[[2012,11,9]],"date-time":"2012-11-09T04:05:28Z","timestamp":1352433928000},"page":"67-76","source":"Crossref","is-referenced-by-count":24,"title":["Prospective Histomorphometric and DXA Evaluation of Bone Remodeling in Imatinib-Treated CML Patients: Evidence for Site-Specific Skeletal Effects"],"prefix":"10.1210","volume":"98","author":[{"given":"Kate","family":"Vandyke","sequence":"first","affiliation":[{"name":"Myeloma Research Laboratory (K.V., S.F., J.D., A.C.W.Z.), Division of Hematology, Centre for Cancer Biology, SA Pathology, Adelaide, South Australia 5000, Australia"},{"name":"School of Medicine (K.V., T.P.H., A.C.W.Z.), University of Adelaide, Adelaide, South Australia 5005, Australia"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Stephen","family":"Fitter","sequence":"additional","affiliation":[{"name":"Myeloma Research Laboratory (K.V., S.F., J.D., A.C.W.Z.), Division of Hematology, Centre for Cancer Biology, SA Pathology, Adelaide, South Australia 5000, Australia"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Jenny","family":"Drew","sequence":"additional","affiliation":[{"name":"Myeloma Research Laboratory (K.V., S.F., J.D., A.C.W.Z.), Division of Hematology, Centre for Cancer Biology, SA Pathology, Adelaide, South Australia 5000, Australia"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Seiji","family":"Fukumoto","sequence":"additional","affiliation":[{"name":"Division of Nephrology and Endocrinology (S.F.), Department of Medicine, University of Tokyo Hospital, Tokyo 113-8655, Japan;"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Christopher G.","family":"Schultz","sequence":"additional","affiliation":[{"name":"Department of Nuclear Medicine (C.G.S.), Royal Adelaide Hospital, Adelaide, South Australia 5000, Australia"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Natalie A.","family":"Sims","sequence":"additional","affiliation":[{"name":"Bone Cell Biology and Disease Unit (N.A.S.), St. Vincent's Institute, Fitzroy, Melbourne, Victoria 3065, Australia"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"David T.","family":"Yeung","sequence":"additional","affiliation":[{"name":"Division of Hematology (D.T.Y., T.P.H.), Centre for Cancer Biology, SA Pathology, Adelaide, South Australia 5000, Australia"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Timothy P.","family":"Hughes","sequence":"additional","affiliation":[{"name":"School of Medicine (K.V., T.P.H., A.C.W.Z.), University of Adelaide, Adelaide, South Australia 5005, Australia"},{"name":"Division of Hematology (D.T.Y., T.P.H.), Centre for Cancer Biology, SA Pathology, Adelaide, South Australia 5000, Australia"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Andrew C. 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