Inhibition of p38-MAPK Signaling Pathway Attenuates Breast Cancer Induced Bone Pain and Disease Progression in a Murine Model of Cancer-Induced Bone Pain

Abstract

Blockade of non-evoked pain behaviors but not hypersensitivity suggests differences in the underlying mechanisms of specific components of the pain syndrome and a possibility to individualize aspects of pain management. While it is not known whether the role of p38 MAPK signaling can be expanded to other cancers, the data suggest a need for understanding molecular mechanisms and cellular events that initiate and maintain cancer-induced bone pain for effective management for both ongoing pain as well as breakthrough pain.