ArticleCancer research2009
Heat shock protein 90 inhibitor 17-dimethylaminoethylamino-17-demethoxygeldanamycin enhances EphA2+ tumor cell recognition by specific CD8+ T cells.
Article in Cancer research, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 1 of them a synthesis that pooled it.
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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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
25 citing papers in PubMed, 1 synthesis or guideline pooled it, 38 citations in OpenAlex.
- Causal effects of blood cells on breast cancer: Evidence from bidirectional Mendelian randomization combined with meta-analysis.Medicine · 2025Pooled it
- Hsp90Pharmaceuticals (Basel, Switzerland) · 2025Review
- HSP90 inhibitor AUY922 suppresses tumor growth and modulates immune response through YAP1-TEAD pathway inhibition in gastric cancer.Cancer letters · 2025Article
- A clinically compatible drug-screening platform based on organotypic cultures identifies vulnerabilities to prevent and treat brain metastasis.EMBO molecular medicine · 2022Article
- Targeting HSP90 Inhibits Proliferation and Induces Apoptosis Through AKT1/ERK Pathway in Lung Cancer.Frontiers in pharmacology · 2021Article
- Antibody Targeting of Eph Receptors in Cancer.Pharmaceuticals (Basel, Switzerland) · 2020Review
- Priming of Anti-tumor Immune Mechanisms by Radiotherapy Is Augmented by Inhibition of Heat Shock Protein 90.Frontiers in oncology · 2020Article
- Combination of Anti-Cancer Drugs with Molecular Chaperone Inhibitors.International journal of molecular sciences · 2019Review
- Transposable element dysregulation in systemic lupus erythematosus and regulation by histone conformation and Hsp90.Clinical immunology (Orlando, Fla.) · 2018Article
- Harness the synergy between targeted therapy and immunotherapy: what have we learned and where are we headed?Oncotarget · 2017Review
- HSP90 inhibition enhances cancer immunotherapy by upregulating interferon response genes.Nature communications · 2017Article
- Update on immune checkpoint inhibitors in gynecological cancers.Journal of gynecologic oncology · 2017Review
- Hsp90: A New Player in DNA Repair?Biomolecules · 2015Review
- Tumor-intrinsic and tumor-extrinsic factors impacting hsp90- targeted therapy.Current molecular medicine · 2012Review
- Combination therapy with HSP90 inhibitor 17-DMAG reconditions the tumor microenvironment to improve recruitment of therapeutic T cells.Cancer research · 2012Article
- Combining immunotherapy and targeted therapies in cancer treatment.Nature reviews. Cancer · 2012Review
- The receptor tyrosine kinase EphA2 is a direct target gene of hypermethylated in cancer 1 (HIC1).The Journal of biological chemistry · 2012Article
- Hsp90 inhibitors are efficacious against Kaposi Sarcoma by enhancing the degradation of the essential viral gene LANA, of the viral co-receptor EphA2 as well as other client proteins.PLoS pathogens · 2012Article
- Hsp90 molecular chaperone inhibitors: are we there yet?Clinical cancer research : an official journal of the American Association for Cancer Research · 2012Review
- The immune response to tumors as a tool toward immunotherapy.Clinical & developmental immunology · 2011Review
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
EphA2, a member of the receptor tyrosine kinase family, is commonly expressed by a broad range of cancer types, where its level of (over)expression correlates with poor clinical outcome. Because tumor cell expressed EphA2 is a nonmutated "self" protein, specific CD8(+) T cells are subject to self-tolerance mechanisms and typically exhibit only moderate-to-low functional avidity, rendering them marginally competent to recognize EphA2(+) tumor cells in vitro or in vivo. We have recently reported that the ability of specific CD8(+) T cells to recognize EphA2(+) tumor cells can be augmented after the cancer cells are pretreated with EphA2 agonists that promote proteasomal degradation and up-regulated expression of EphA2/class I complexes on the tumor cell membrane. In the current study, we show that treatment of EphA2(+) tumor cells with the irreversible heat shock protein 90 inhibitor, 17-dimethylaminoethylamino-17-demethoxygeldanamycin (17-DMAG), similarly enhances their recognition by EphA2-specific CD8(+) T-cell lines and clones in vitro via a mechanism that is dependent on proteasome and transporter-associated protein function as well as the retrotranslocation of EphA2 into the tumor cytoplasm. When 17-DMAG and agonist anti-EphA2 monoclonal antibodies are coapplied, T-cell recognition of tumor cells is further increased over that observed for either agent alone. These studies suggest that EphA2 represents a novel heat shock protein 90 client protein and that the treatment of cancer patients with 17-DMAG-based "pulse" therapy may improve the antitumor efficacy of CD8(+) T effector cells reactive against EphA2-derived epitopes.
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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.