Upregulation of AXL and β-catenin in chronic lymphocytic leukemia cells cultured with bone marrow stroma cells is associated with enhanced drug resistance

Despite the advent of even more effective therapies, Chronic Lymphocytic Leukemia (CLL) is still incurable and patients often develop drug resistance. We and others have found that bone marrow stromal cells (BMSCs) are excellent models for assessing the mechanism(s) by which stroma cells nurture CLL B-cells and we have shown that BMSC protects leukemic B-cells from spontaneous and drug-induced apoptosis 1 . The leukemic B-cell derives survival signals from stromal cells and the bone marrow site is able to harbor residual leukemic B-cells protected from chemotherapy. Prior evidence indicates that the facilitation of residual disease burden may be a key pathway to clonal evolution and ultimate clinical relapses difficult to treat in CLL 2 .