Taken together, our data shed new light on the molecular mechanism of CAM-DR in MM, and targeting ARF1 may be a novel therapeutic approach for improving the effectiveness of chemotherapy in MM.
Taken together, our data shed new light on the molecular mechanism of CAM-DR in MM, and targeting PKM2 may be a novel therapeutic approach for improving the effectiveness of chemotherapy in MM.
Taken together, our findings support the hypotheses that CD44 and CAM-DR contribute to lenalidomide resistance in multiple myeloma, that CD44 should be evaluated as a putative biomarker of sensitivity to lenalidomide, and that ATRA or other approaches that target CD44 may overcome clinical lenalidomide resistance.
Previous investigations have suggested cell adhesion-mediated drug resistance (CAM-DR) in multiple myeloma (MM) is a primary factor for minimal residual disease (MRD) leading to relapse after chemotherapy.
In this report, we extend the CAM-DR phenotype to primary specimens from patients with myeloma, providing further evidence that CAM-DR is a viable clinical form of drug resistance.
In transfection studies, however, transcriptional activity of the N-CAM promoter was observed in N-CAM-negative cells, leading us to conclude that the up-regulation of N-CAM in MMcannot be explained by a simple transcriptional gene activation.