Abstract
Abstract Background: Thalidomide inhibits angiogenesis and growth of multiple myeloma. Liposomal doxorubicin is mainly absorbed and degraded by monocyte-macrophage lineage in vivo, implicating a possible targeting effect. Given that osteoclasts (OCs) are derived from precursors of monocyte-macrophage lineage, we hypothesized that thalidomide, liposomal doxorubicin and their combination may affect osteoclastogenesis. Materials and Methods: We isolated CD14+ monocytes from peripheral blood mononuclear cells of healthy subjects and generated OCs under stimulation with macrophage-colony forming factor and receptor activator of NK-κB ligand. Cell viability, surface CD51/61 expression, and tartrate-resistant acid phosphatase (TRAP) activity were assessed by using MTT, flow cytometry and immunohistochemical staining, respectively. Bone resorption activity of OCs was examined. Results: The combination of thalidomide (purchased from TTY Biopharm, Taiwan) and liposomal doxorubicin (purchased from TTY Biopharm, Taiwan) profoundly inhibited the amount of harvested viable OCs. The expression of osteoclast-specific surface antigen CD51/61 was markedly inhibited by each drug and their combination. Specifically, the amount of multinucleated TRAP-positive cells characteristics of OCs and bone resorption activity of OCs were suppressed by each drug and, the mostly, their combination. Conclusion: Thalidomide, liposomal doxorubicin and their combination, beyond currently clinical indications, might be effective regimen to inhibit human osteoclastogenesis. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 2148. doi:10.1158/1538-7445.AM2011-2148
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