Abstract
Background: The tyrosine kinase (TK) inhibitor imatinib (IMA) has dramatically improved the treatment results of chronic myeloid leukemia (CML) via blockade of the constitutively activated TK bcr-abl. However, IMA also inhibits other TKs like PDGFR-alpha and -beta and c-FMS, thus exerting a negative impact on the differentiation and proliferation of osteoclasts and osteoblasts. As a net result, disturbances of bone metabolism and remodeling have been described in animal models and in adult patients (pts) in vivo.
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