Journal
CANCER CELL
Volume 37, Issue 3, Pages 289-+Publisher
CELL PRESS
DOI: 10.1016/j.ccell.2020.02.008
Keywords
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Funding
- NCI [F99CA223043, R01CA181745, P50CA196510, R01CA177670, R01CA203890, P30CA09184215, P30CA91842]
- BJC Cancer Frontier Fund
- ICTS/CTSA from the NCRR [UL1RR024992]
- ICTS/CTSA from the NIH [UL1RR024992]
- NIDDK [P30DK052574]
- Foundation for Barnes-Jewish Hospital
- [1DP5OD026427]
- [CDI-CORE2015-505]
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Here, we utilized spontaneous models of pancreatic and lung cancer to examine how neoantigenicity shapes tumor immunity and progression. As expected, neoantigen expression during lung adenocarcinoma development leads to T cell-mediated immunity and disease restraint. By contrast, neoantigen expression in pancreatic ductal adenocarcinoma (PDAC) results in exacerbation of a fibro-inflammatory microenvironment that drives disease progression and metastasis. Pathogenic T(H)17 responses are responsible for this neoantigen-induced tumor progression in PDAC. Underlying these divergent T cell responses in pancreas and lung cancer are differences in infiltrating conventional dendritic cells (cDCs). Overcoming cDC deficiency in early-stage PDAC leads to disease restraint, while restoration of cDC function in advanced PDAC restores tumorrestraining immunity and enhances responsiveness to radiation therapy.
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