Our findings describe a novel bone cancer pain mechanism and provide a new insight into the physiological and pathological functions of GM-CSF.<b>SIGNIFICANCE STATEMENT</b> It has been reported that granulocyte-macrophage colony-stimulating factor (GM-CSF) plays a key role in bone cancer pain, yet the underlying mechanisms involved in the GM-CSF-mediated signaling pathway in nociceptors is not fully understood.
Granulocyte-macrophage colony-stimulating factor (GM-CSF) is well described in inflammation-induced pain, and early-phase clinical trials evaluating its antagonism have exemplified its importance as a peripheral pain target.
Compared to ANNA1 alone, CRMP5 neuropathy has a higher prevalence of pain (79% vs 46%, <i>p</i> = 0.008), asymmetric polyradiculoneuropathy (54% vs 12%, <i>p</i> < 0.001), and inflammatory spinal fluids (elevated CSF protein or nucleated cell count 92% vs 60%, <i>p</i> = 0.022).