Journal
CANCER CELL
Volume 31, Issue 3, Pages 311-325Publisher
CELL PRESS
DOI: 10.1016/j.ccell.2017.02.008
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Funding
- Chromosome Metabolism and Cancer Training Grant Program [T32 2T32CA009657-26A1]
- Solid Tumor Translational Research Award
- Irvington Institute Fellowship Program of the Cancer Research Institute
- Jack and Sylvia Paul Estate Fund to Support Collaborative Immunotherapy Research
- NIH National Cancer Institute [CA018029, CA033084]
- Pancreatic Cancer Action Network [16-65-GREE]
- Juno, Therapeutics
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T cell dysfunction in solid tumors results from multiple mechanisms. Altered signaling pathways in tumor cells help produce a suppressive tumor microenvironment enriched for inhibitory cells, posing a major obstacle for cancer immunity. Metabolic constraints to cell function and survival shape tumor progression and immune cell function. In the face of persistent antigen, chronic T cell receptor signaling drives T lymphocytes to a functionally exhausted state. Here we discuss how the tumor and its microenvironment influences T cell trafficking and function with a focus on melanoma, and pancreatic and ovarian cancer, and discuss how scientific advances may help overcome these hurdles.
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