期刊
CANCER CELL
卷 21, 期 6, 页码 836-847出版社
CELL PRESS
DOI: 10.1016/j.ccr.2012.04.024
关键词
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资金
- National Institutes of Health [5 P30CA016087-31, CA055360]
- AACR-PanCAN [08-60-25-BARS]
- Irvington Institute of the Cancer Research Institute
Stromal responses elicited by early stage neoplastic lesions can promote tumor growth. However, the molecular mechanisms that underlie the early recruitment of stromal cells to sites of neoplasia remain poorly understood. Here, we demonstrate an oncogenic Kras(G12D)-dependent upregulation of GM-CSF in mouse pancreatic ductal epithelial cells (PDECs). An enhanced GM-CSF production is also observed in human PanIN lesions. Kras(G12D)-dependent production of GM-CSF in vivo is required for the recruitment of Gr1(+)CD11b(+) myeloid cells. The suppression of GM-CSF production inhibits the in vivo growth of Kras(G12D)-PDECs, and, consistent with the role of GM-CSF in Gr1(+)CD11b(+) mobilization, this effect is mediated by CD8(+)T cells. These results identify a pathway that links oncogenic activation to the evasion of antitumor immunity.
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