ArticleClinical cancer research : an official journal of the American Association for Cancer Research2017
Entinostat Neutralizes Myeloid-Derived Suppressor Cells and Enhances the Antitumor Effect of PD-1 Inhibition in Murine Models of Lung and Renal Cell Carcinoma.
Article in Clinical cancer research : an official journal of the American Association for Cancer Research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT06930118 (An Exploratory Study Investigating the Combination of Chidamide, Regorafenib, Plus Iparomlimab and Tuvonralimab for the Treatment of Drug-esistant and Efractory Dvanced Colorectal Cancer), which is not on this map. Cited by 259 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.
An Exploratory Study Investigating the Combination of Chidamide, Regorafenib, Plus Iparomlimab and Tuvonralimab for the Treatment of Drug-esistant and Efractory Dvanced Colorectal Cancer
Who cites it
259 citing papers in PubMed, 1 synthesis or guideline pooled it.
- The soldiers needed to be awakened: Tumor-infiltrating immune cells.Frontiers in genetics · 2022Pooled it
- First-line treatment with HDACis plus tislelizumab combined with chemotherapy in advanced NSCLC: a single-arm phase II study.The oncologist · 2025Trial
- Entinostat in combination with nivolumab in metastatic pancreatic ductal adenocarcinoma: a phase 2 clinical trial.Nature communications · 2024Trial
- The PEMDAC phase 2 study of pembrolizumab and entinostat in patients with metastatic uveal melanoma.Nature communications · 2021Trial
- Entinostat plus Pembrolizumab in Patients with Metastatic NSCLC Previously Treated with Anti-PD-(L)1 Therapy.Clinical cancer research : an official journal of the American Association for Cancer Research · 2021Trial
- Myeloid-derived suppressor cells in cancer: biology, regulatory networks and theranostic prospects.Signal transduction and targeted therapy · 2026Review
- Immune Circuit Rewiring by HDAC Inhibition Enables Response to Dual Checkpoint Blockade in Metastatic Breast Cancer.Cancer research · 2026Article
- Metabolic-epigenetic crosstalk in innate immune cell plasticity within the tumor microenvironment.Experimental & molecular medicine · 2026Review
- Single-cell profiling of natural killer/T-cell lymphoma reveals stratified immune features and potential therapeutic implications.Nature communications · 2026Article
- Stepwise Enhancement of HPV16 E6/E7 mRNA Vaccine Efficacy Using HSV-1 gD Epitope Incorporation and Immune-Modulating Agents.Research square · 2026Article
- Cancer stem cell plasticity: mechanisms, immune microenvironment crosstalk, and therapeutic implications.Journal of hematology & oncology · 2026Review
- Entinostat Enhances Antigen-Specific CD8 T-Cell Response to Immunotherapies in Lung Cancer Models.Pharmaceuticals (Basel, Switzerland) · 2026Article
- A Multi-Omics Framework Reveals Tumor Heterogeneity and Predicts Therapeutic Targets in Renal Cell Carcinoma.International journal of molecular sciences · 2026Article
- Overcoming MDSC-Mediated Immunosuppression in Hepatocellular Carcinoma: From Mechanisms to Novel Immunotherapeutic Approaches.Cancers · 2026Review
- HDAC inhibitor GCJ-490A modulates tumor microenvironment and synergizes with PD-1 antibody against breast and lung cancers in syngeneic murine models.Acta pharmacologica Sinica · 2026Article
- Immunotherapy for patients with EGFR-TKI-resistant non-small-cell lung cancer: Potential mechanisms, efficacy predictors, and therapeutic integration.Chinese medical journal pulmonary and critical care medicine · 2026Review
- Targeting metabolic-epigenetic-immune axis in cancer: molecular mechanisms and therapeutic implications.Signal transduction and targeted therapy · 2026Review
- Synergistic Potential of Immune Checkpoint Inhibitor Combined with Neutrophil-Targeted Therapy in Cancer Immunotherapy.Research (Washington, D.C.) · 2026Review
- Targeting innate immunity in cancer: mechanistic foundations, therapeutic vaccination, and clinical translation.Frontiers in immunology · 2026Review
- Myeloid derived suppressor cells in neuroblastoma: mechanisms of immune evasion and therapeutic opportunities.Frontiers in immunology · 2026Review
199 more citing papers are in PubMed but not listed here.
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Authors and funding
12 authors.
Funding
Abstract
purposeRecent advances in immunotherapy highlight the antitumor effects of immune checkpoint inhibition despite a relatively limited subset of patients receiving clinical benefit. The selective class I histone deacetylase inhibitor entinostat has been reported to have immunomodulatory activity including targeting of immune suppressor cells in the tumor microenvironment. Thus, we decided to assess whether entinostat could enhance anti-PD-1 treatment and investigate those alterations in the immunosuppressive tumor microenvironment that contribute to the combined antitumor activity. EXPERIMENTAL
designWe utilized syngeneic mouse models of lung (LLC) and renal cell (RENCA) carcinoma and assessed immune correlates, tumor growth, and survival following treatment with entinostat (5 or 10 mg/kg, p.o.) and a PD-1 inhibitor (10 and 20 mg/kg, s.c.).
resultsEntinostat enhanced the antitumor effect of PD-1 inhibition in two syngeneic mouse tumor models by reducing tumor growth and increasing survival. Entinostat inhibited the immunosuppressive function of both polymorphonuclear (PMN)- and monocytic-myeloid derived suppressor cell (M-MDSC) populations. Analysis of MDSC response to entinostat revealed significantly reduced arginase-1, iNOS, and COX-2 levels, suggesting potential mechanisms for the altered function. We also observed significant alterations in cytokine/chemokine release in vivo with a shift toward a tumor-suppressive microenvironment.
conclusionsOur results demonstrate that entinostat enhances the antitumor effect of PD-1 targeting through functional inhibition of MDSCs and a transition away from an immune-suppressive tumor microenvironment. These data provide a mechanistic rationale for the clinical testing and potential markers of response of this novel combination in solid tumor patients.
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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.