Chronic inflammation is frequently at the route of multiple cancers, particularly in colorectal cancers where ulcerative colitis increases the risk of developing colon cancer 20-fold.
Patients with ulcerative colitis are often treated with NSAIDs to reduce inflammation, which can reduce their cancer risk by 50%. Molecules that drive inflammation may be attractive therapeutic targets to prevent and treat inflammation-driven cancers.
Chemokine receptors are one of the primary classes of molecules that regulate inflammation and many cancers express molecules that activate these receptors. Researchers at the University of Glasgow in Glasgow, Scotland recently demonstrated that the chemokine receptor CXCR2 is a critical mediator of inflammation-driven tumorigenesis.
In this issue of the Journal of Clinical Investigation, Thomas Jamieson and colleagues show that mice lacking CXCR2 or mice that are treated with CXCR2 inhibitors are less susceptible to inflammation-driven colon and skin cancer.
These studies indicate that CXCR2 inhibitors may have potential as a therapy to treat or prevent inflammation-driven cancers.
TITLE:Inhibition of CXCR2 profoundly suppresses inflammation-driven and spontaneous tumorigenesis