About the Cover
Tumor survival depends on a nurturing environment and a tumor's ability to “stay below the radar” of the immune surveillance network. In this month's issue, Pickup et al. have identified a key molecule produced by pancreatic ductal carcinomas, G-CSF (granulocyte colony-stimulating factor), which induced developing granulocytes to differentiate into myeloid suppressor cells and promoted a protumor microenvironment. Removing G-CSF while subjecting mice with aggressive pancreatic ductal tumors to treatment with gemcitabine (a DNA synthesis inhibitor) had therapeutic benefit. A subset of patients have mutations that abrogate TGFβ signaling (similar to the mouse models used), so targeting G-CSF in these patients could potentially enhance their responses to treatment. Read more starting on page 718. Micrograph from Fig. 4C. Artwork by Lewis Long.