The TOLL of inflammation in multiple myeloma.

摘要

In this issue of Cancer Biology & Therapy, Bao et al. report that the Toll-like receptor (TLR) 4 ligand, lipopolysaccharide (LPS), induced increases in proliferation, survival and chemotherapeutic/immune escape in human myeloma cell lines and primary multiple myeloma cells. TLR activation represents a double-edged sword with one edge initiating and propagating a robust inflammatory response to limit pathogen entry whilst the second edge has the potential to form a sustained, chronic inflammatory environment that feeds and accentuates a disease state. With the rapid development of TLR-based agonists and antagonists targeted for therapeutic application, examining TLR signaling within different cancer models may reveal how best to apply these new therapeutic tools.