ArticleNature medicine2011
Imatinib potentiates antitumor T cell responses in gastrointestinal stromal tumor through the inhibition of Ido.
Article in Nature medicine, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 309 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
309 citing papers in PubMed, 518 citations in OpenAlex.
- Augmentation of IFN-γ+ CD8+ T cell responses correlates with survival of HCC patients on sorafenib therapy.JCI insight · 2019Trial
- Serum metabolomic profiling of prostate cancer risk in the prostate, lung, colorectal, and ovarian cancer screening trial.British journal of cancer · 2016Trial
- Precision therapeutic strategies for advanced gastrointestinal stromal tumors.Cancer metastasis reviews · 2026Review
- Estrogen-related receptor alpha (ERRα) promotes gastrointestinal stromal tumor progression and epithelial-mesenchymal transition through Wnt/β-catenin.Research square · 2026Article
- Effector Vδ1 γδ T cells mediate anti-tumor immunity and are reprogrammed by imatinib in human gastrointestinal stromal tumor.Research square · 2026Article
- Targeting tumor dormancy: the next frontier in gastrointestinal stromal tumor therapy.Neoplasia (New York, N.Y.) · 2026Review
- Innovative immunotherapy approaches: harnessing synergy of dual checkpoint blockade in oncology.Naunyn-Schmiedeberg's archives of pharmacology · 2026Review
- Regulatory T Cells and Nanomaterials: Dual Perspectives in Therapeutics and Immunomodulation.Small science · 2026Review
- Enhanced formation of tertiary lymphoid structures shapes the anti-tumor microenvironment in gastrointestinal stromal tumors after imatinib targeted therapy.Theranostics · 2026Article
- Article
- Review
- The aryl hydrocarbon receptor: a rehabilitated target for therapeutic immune modulation.Nature reviews. Drug discovery · 2025Review
- Immunotherapy in gastrointestinal stromal tumors: Current landscape and future horizons.World journal of clinical oncology · 2025Article
- Drug-induced tolerant persisters in tumor: mechanism, vulnerability and perspective implication for clinical treatment.Molecular cancer · 2025Review
- Cancer-associated fibroblasts as therapeutic targets for cancer: advances, challenges, and future prospects.Journal of biomedical science · 2025Review
- Efficacy of Wee1 G2 Checkpoint Kinase and Mouse Double Minute 2 Homolog Inhibitors in Gastrointestinal Stromal Tumors Determined by p53 Status.Oncology research · 2025Article
- Mechanisms and signaling pathways of tyrosine kinase inhibitor resistance in chronic myeloid leukemia: A comprehensive review.Leukemia research reports · 2025Review
- A machine learning-derived immune-related prognostic model identifiesFrontiers in immunology · 2025Article
- Genomic and transcriptomic landscape of human gastrointestinal stromal tumors.Nature communications · 2024Article
- Gastrointestinal Stromal Tumor of the Rectum: Report of a Case With Long-Term Imatinib Treatment.Cureus · 2024Article
249 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
18 authors at 4 institutions in 2 countries.
Funding
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.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.