Journal
CANCER CELL
Volume 21, Issue 6, Pages 822-835Publisher
CELL PRESS
DOI: 10.1016/j.ccr.2012.04.025
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Funding
- Abramson Family Cancer Research Institute
- Cancer Research Institute
- National Institutes of Health [K12 CA076931, K08 088945]
- Gabrielle's Angel Foundation for Cancer Research
- American Gastroenterological Association
- Pennsylvania Department of Health
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Cancer-associated inflammation is thought to be a barrier to immune surveillance, particularly in pancreatic ductal adenocarcinoma (PDA). Gr-1(+) CD11b(+) cells are a key feature of cancer inflammation in PDA, but remain poorly understood. Using a genetically engineered mouse model of PDA, we show that tumor-derived granulocyte-macrophage colony-stimulating factor (GM-CSF) is necessary and sufficient to drive the development of Gr-1(+) CD11b(+) cells that suppressed antigen-specific T cells. In vivo, abrogation of tumor-derived GM-CSF inhibited the recruitment of Gr-1(+) CD11b(+) cells to the tumor microenvironment and blocked tumor development a finding that was dependent on CD8(+) T cells. In humans, PDA tumor cells prominently expressed GM-CSF in vivo. Thus, tumor-derived GM-CSF is an important regulator of inflammation and immune suppression within the tumor microenvironment.
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