New research shows that inflammatory macrophages can be redirected and induced to deplete fibrosis characteristic of pancreatic ductal adenocarcinoma tumors.
Pancreatic ductal adenocarcinoma (PDAC) is the fourth most common cause of cancer death, because of its tendency to cause symptoms only at a late and advanced stage. Despite our advancing knowledge of PDAC, the prognosis remains strikingly poor owing to resistance to standard therapies. The tumor stroma comprises abundant extracellular matrix (ECM) and extensive collagen, which often contribute to formation of a dense fibrosis. In addition, the tumor microenvironment is typically marked by a robust infiltrate of immunosuppressive macrophages. Together, these hallmark characteristics form a major barrier to drug delivery. Thus, strategies targeting this tumor microenvironment are necessary to improve the prognosis of PDAC patients.
