Imatinib potentiates antitumor T cell responses in gastrointestinal stromal tumor through the inhibition of Ido View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2011-09

AUTHORS

Vinod P Balachandran, Michael J Cavnar, Shan Zeng, Zubin M Bamboat, Lee M Ocuin, Hebroon Obaid, Eric C Sorenson, Rachel Popow, Charlotte Ariyan, Ferdinand Rossi, Peter Besmer, Tianhua Guo, Cristina R Antonescu, Takahiro Taguchi, Jianda Yuan, Jedd D Wolchok, James P Allison, Ronald P DeMatteo

ABSTRACT

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 (T(reg) 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. More... »

PAGES

1094

References to SciGraph publications

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/nm.2438

DOI

http://dx.doi.org/10.1038/nm.2438

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1005333082

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/21873989


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