| Literature DB >> 17910634 |
Babatunde O Oyajobi1, I Ross Garrett, Anjana Gupta, Alda Flores, Javier Esparza, Steve Muñoz, Ming Zhao, Gregory R Mundy.
Abstract
Impaired bone formation contributes to the lack of bone healing in multiple myeloma and there is a need for agents with bone anabolic properties to reverse the bone deficit in patients. Bortezomib, a proteasome inhibitor with antitumour efficacy in myeloma patients, enhanced new bone formation in mouse calvarial cultures; this effect was blocked by dickkopf 1(Dkk1), an antagonist of Wnt signalling implicated in myeloma bone disease. Bortezomib inhibited Dkk1 expression in calvariae and bone marrow-derived stromal cells, suggesting a novel mechanism by which bortezomib exerts its effects in bone. Clinical trials in patients with myeloma bone disease are needed to validate these results.Entities:
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Year: 2007 PMID: 17910634 PMCID: PMC4482356 DOI: 10.1111/j.1365-2141.2007.06829.x
Source DB: PubMed Journal: Br J Haematol ISSN: 0007-1048 Impact factor: 6.998