Abstract
Receptor activator of NFκB ligand (RANKL) is mainly known for its role in bone metabolism, constituting a target for therapeutic interventions. Increasing evidence suggests that RANKL is also involved in oncogenesis and tumor progression, including a prominent role in host-tumor interaction. Our data suggest that targeting RANKL may reinforce natural killer (NK) cell-mediated antitumor responses in patients affected by hematological malignancies.
Disclosure of Potential Conflicts of Interest
The authors were supported by grants from Deutsche Forschungsgemeinschaft (SA1360/7-1) and Deutsche Krebshilfe (109620).