ArticleCancer immunology research2022
Entinostat Decreases Immune Suppression to Promote Antitumor Responses in a HER2+ Breast Tumor Microenvironment.
Article in Cancer immunology research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers, 1 of them a synthesis that pooled it.
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Who cites it
45 citing papers in PubMed, 1 synthesis or guideline pooled it, 59 citations in OpenAlex.
- PD-1/PD-L1 immune checkpoint blockade in breast cancer: research insights and sensitization strategies.Molecular cancer · 2024Pooled it
- Entinostat in combination with nivolumab in metastatic pancreatic ductal adenocarcinoma: a phase 2 clinical trial.Nature communications · 2024Trial
- Next-generation oncolytic virotherapy for lung cancer: bridging innovative vector engineering with clinical immunotherapy.Translational lung cancer research · 2026Review
- Immune Circuit Rewiring by HDAC Inhibition Enables Response to Dual Checkpoint Blockade in Metastatic Breast Cancer.Cancer research · 2026Article
- A Roadmap to Transform Lung Cancer Outcomes: Priorities in Biology, Therapeutic Innovation, Early Detection, Prevention, and Interception.Cancer discovery · 2026Review
- Breast Cancer Milieu Maneuvers Cancer-Associated Macrophages to Synergize Neoplastic Repertoires.Cancers · 2026Review
- TMEM70 drives breast cancer progression via mitochondrial oxidative phosphorylation and microenvironment remodeling.Cancer cell international · 2026Article
- Inference of marker genes of subtle cell state changes via iLR: iterative logistic regression.Bioinformatics (Oxford, England) · 2026Article
- Host-derived interleukin-1α drives tumor immunosuppression by reprogramming tumor-associated myeloid cells.NPJ breast cancer · 2026Article
- MDSCs in Breast Cancer: Metastasis, Lipid Metabolism, and Therapeutics.Molecular cancer research : MCR · 2025Review
- Histone Deacetylase Inhibitors orchestrate epigenetic signalling and alter the nucleoporins and nuclear envelope in cervical cancer.Translational oncology · 2025Article
- Beyond RECIST: mathematical modeling and Bayesian inference reveal the importance of immune parameters in metastatic breast cancer.bioRxiv : the preprint server for biology · 2025Article
- Cancer systems immunology reveals myeloid-T cell interactions and B cell activation mediate response to checkpoint inhibition in metastatic breast cancer.bioRxiv : the preprint server for biology · 2025Article
- Sequencing analysis reveals evidence of immune activation in advanced HER2 negative breast cancer responders treated with entinostat + nivolumab + ipilimumab.Research square · 2025Article
- Age-Dependent Regulation of Hippocampal Inflammation by the Mitochondrial Translocator Protein in Mice.Aging cell · 2025Article
- Review
- NK cell immunopotentiators-loaded nanoliposomes enhance ADCC effect for targeted therapy against HER2-positive breast cancer.Cell communication and signaling : CCS · 2025Article
- Deciphering the role of CNIH4 in pan-cancer landscapes and its significance in breast cancer progression.Frontiers in genetics · 2025Article
- Targeting tumor-associated macrophages: Novel insights into immunotherapy of skin cancer.Journal of advanced research · 2025Review
- The function of CD164 in breast cancer and its possibility as a molecular biomarker: bioinformatics analysis and experimental validation.Frontiers in immunology · 2025Article
Corrections and comments
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Authors and funding
26 authors at 6 institutions in 2 countries.
Funding
Abstract
Therapeutic combinations to alter immunosuppressive, solid tumor microenvironments (TME), such as in breast cancer, are essential to improve responses to immune checkpoint inhibitors (ICI). Entinostat, an oral histone deacetylase inhibitor, has been shown to improve responses to ICIs in various tumor models with immunosuppressive TMEs. The precise and comprehensive alterations to the TME induced by entinostat remain unknown. Here, we employed single-cell RNA sequencing on HER2-overexpressing breast tumors from mice treated with entinostat and ICIs to fully characterize changes across multiple cell types within the TME. This analysis demonstrates that treatment with entinostat induced a shift from a protumor to an antitumor TME signature, characterized predominantly by changes in myeloid cells. We confirmed myeloid-derived suppressor cells (MDSC) within entinostat-treated tumors associated with a less suppressive granulocytic (G)-MDSC phenotype and exhibited altered suppressive signaling that involved the NFκB and STAT3 pathways. In addition to MDSCs, tumor-associated macrophages were epigenetically reprogrammed from a protumor M2-like phenotype toward an antitumor M1-like phenotype, which may be contributing to a more sensitized TME. Overall, our in-depth analysis suggests that entinostat-induced changes on multiple myeloid cell types reduce immunosuppression and increase antitumor responses, which, in turn, improve sensitivity to ICIs. Sensitization of the TME by entinostat could ultimately broaden the population of patients with breast cancer who could benefit from ICIs.
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