My research focuses on the mechanisms by which osteocytes contribute to generate a microenvironment that is conducive to tumor progression, bone destruction and muscle weakness in multiple myeloma disease. Current projects investigate the effects of genetic and pharmacological inhibition of osteocyte-derived factors (i.e Sclerostin, Rankl) in tumor growth and multiple myeloma-induced bone fragility and muscle weakness; the role of bidirectional Notch signaling between MM cells and osteocytes in multiple myeloma disease; and the effects of Aplidin (a novel anti-tumor drug that targets eEF1A2), alone or in combination with other anti-tumor drugs, on bone cells and tumor progression. I also collaborate in studies examining the role of osteocytes in multiple myeloma-induced bone pain; the regulation of the skeletal actions of parathyroid hormone; and the deleterious effects that glucocorticoids have in the skeleton.
My research focuses on understanding the mechanisms by which myeloma cells alter the biology of other cells in the tumor/bone marrow microenvironment with the final goal of identifying targetable factors for the treatment of multiple myeloma.
