My research focuses on the translation of the benchwork into new therapeutic approaches/strategies for multiple myeloma. One of my research goals is to study the mechanism underlying the pathogenesis of myeloma and find out new targets for myeloma therapy. I have been investigating the interaction of myeloma cells with bone marrow microenvironment under obese condition, including marrow adipocytes and related signaling pathways, and investigating the impact of such interaction on myeloma therapeutic response and bone metastasis and lesions, which are the major problems in myeloma patients.

Another focus of my research is on the pathogenesis of bone destruction chemotherapy resistance in multiple myeloma, and myeloma-associated bone disease. We also investigate the active role of bone marrow-derived macrophages in myeloma drug resistance. In addition, we have demonstrated the contribution of p38 MAPK signaling in myeloma cells to osteolytic bone lesions by activating osteoclastogenesis and inhibiting osteoblastogenesis. Our studies are emphasis on translating these results into providing better therapeutic targets. One of our most compelling findings is developing monoclonal antibodies specific for human beta2 microglobulin and underlying that the antibodies remarkably induce myeloma cell apoptosis. Our results strong suggest the antibodies as a potential, novel therapeutic agent for the treatment of myeloma