Multiple Myeloma (MM) is a malignancy of terminally differentiated plasma cells, characterized by the clonal expansion of myeloma cells in the bone marrow. Glucocorticoids are at the mainstay in the treatment of MM, owing to their ability to induce apoptosis in lymphoid cells. However, despite treatment improvements over the past years, patients eventually relapse. These relapses can be partly accounted to the emergence of therapy resistance. The tumor microenvironment, the bone marrow, also plays central role in the pathogenesis and drug resistance in MM. We have recently identified CCR1, together with its ligand CCL3, to have a pivotal role in the sensitivity of MM cells to glucocorticoid induced apoptosis. We show that a combination of glucocorticoids together with CCR1 inhibitors, leads to enhanced cell killing effects in myeloma cells. This opens up the road for CCR1 to be exploited as a new therapeutic target in MM treatment. In addition, we also show CCR1 to be one of the drivers of the emergence of glucocorticoid resistance
Bert Luyckx (Sat,) studied this question.