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Imatinib potentiates antitumor T cell responses in gastrointestinal stromal tumor through the inhibition of Ido
Open accessAbstract
Imatinib mesylate targets mutated KIT oncoproteins in gastrointestinal stromal tumor (GIST) and produces a clinical response in 80% of patients. The mechanism is believed to depend predominantly on the inhibition of KIT-driven signals for tumor-cell survival and proliferation. Using a mouse model of spontaneous GIST, we found that the immune system contributes substantially to the antitumor effects of imatinib. Imatinib therapy activated CD8+ T cells and induced regulatory T cell (Treg cell) apoptosis within the tumor by reducing tumor-cell expression of the immunosuppressive enzyme indoleamine 2,3-dioxygenase (Ido). Concurrent immunotherapy augmented the efficacy of imatinib in mouse GIST. In freshly obtained human GIST specimens, the T cell profile correlated with imatinib sensitivity and IDO expression. Thus, T cells are crucial to the antitumor effects of imatinib in GIST, and concomitant immunotherapy may further improve outcomes in human cancers treated with targeted agents.
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Metadata
- Authors
- Balachandran, V. P., Cavnar, M. J., Zeng, S., Bamboat, Z. M., Ocuin, L. M., Obaid, H., Sorenson, E. C., Popow, R., Ariyan, C., Rossi, F., Besmer, P., Guo, T., Antonescu, C. R., Taguchi, T., Yuan, J., Wolchok, J. D., Allison, J. P., & DeMatteo, R. P.
- Venue
- Nature Medicine
- Published
- 2011-08-28
- Volume
- 17
- Issue
- 9
- Pages
- 1094-1100
- ISSN
- 1078-8956 (ISSN-L)
- 1546-170X
- OpenAlex
- W2106631163
- Cited by
- 521
- References
- 58
- FWCI
- 39.05
- Type
- journal article
- Language
- en
- Open access
- green
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