ArticleNature communications2022
Combinatorial immunotherapies overcome MYC-driven immune evasion in triple negative breast cancer.
Article in Nature communications, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 50 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
50 citing papers in PubMed, 69 citations in OpenAlex.
- Molecular evaluation of residual disease following neoadjuvant chemotherapy in triple-negative breast cancer CALGB 40603 (Alliance).The Journal of clinical investigation · 2026Trial
- The activity and immune dynamics of PD-1 inhibition on high-risk pulmonary ground glass opacity lesions: insights from a single-arm, phase II trial.Signal transduction and targeted therapy · 2024Trial
- Decoding drug-responsive cell subpopulations in triple-negative breast cancer using single-cell multiomics.iScience · 2026Article
- c-Myc regulated long noncoding RNA TRD-AS1 to affect the progression of oral squamous cell carcinoma.Genes & genomics · 2026Article
- KRAS and MYC synergistic inhibition: a powerful strategy targeting KRAS-mutant cancers.Molecular cancer · 2026Review
- Genomic and Immune Landscape of Recurrent and/or Metastatic Squamous Cell Carcinoma of the Head and Neck Progressing on Anti-PD-1 Treatment.Cancer immunology research · 2026Article
- Single-Cell Profiling Reveals a Treg-Rich, NK Cell-Depleted Immune Microenvironment in Triple-Negative Breast Cancer with High-Glucocorticoid Receptor Expression.Breast cancer (Dove Medical Press) · 2026Article
- Preclinical Nanoparticle Approaches Targeting Tumor-Associated Macrophages in Breast Cancer: From Mechanisms to Therapeutic Strategies.International journal of nanomedicine · 2026Review
- The role of pluripotency regulators in triple-negative breast cancer immune response.Frontiers in genetics · 2026Review
- Tractable mouse TNBC models capture the heterogeneous tumor immune microenvironment and adaptation to PD-L1 blockade.NPJ breast cancer · 2025Article
- Updated efficacy and predictive biomarkers of QL1706, a bifunctional PD-1/CTLA-4 dual blocker in advanced solid tumors-A phase 1/1b study.Cell reports. Medicine · 2025Article
- Targeting c-Myc enhances immunotherapy efficacy in combination with Ras inhibitor in triple-negative breast cancer.Clinical and translational medicine · 2025Article
- Age-related and postmenopausal breast cancer progression and treatment management: The significance of pro-inflammatory cytokines and CXC chemokines.Genes & diseases · 2025Review
- MYC as a Target for Cancer Treatment: from Undruggable to Druggable?Targeted oncology · 2025Review
- Tryptophan Metabolite Indole-3-Aldehyde Induces AhR and c-MYC Degradation to Promote Tumor Immunogenicity.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Reprogramming the tumor microenvironment with c-MYC-based gene circuit platform to enhance specific cancer immunotherapy.Nature communications · 2025Article
- Tumor cell-adipocyte gap junctions activate lipolysis and contribute to breast tumorigenesis.Nature communications · 2025Article
- Article
- Cytokine Networks in Triple-Negative Breast Cancer: Mechanisms, Therapeutic Targets, and Emerging Strategies.Biomedicines · 2025Review
- TME-responsive nanocomposite hydrogel with targeted capacity for enhanced synergistic chemoimmunotherapy of MYC-amplified osteosarcoma.Bioactive materials · 2025Article
Corrections and comments
- Erratum issued
Authors and funding
23 authors at 6 institutions in 5 countries.
Funding
Abstract
Few patients with triple negative breast cancer (TNBC) benefit from immune checkpoint inhibitors with complete and durable remissions being quite rare. Oncogenes can regulate tumor immune infiltration, however whether oncogenes dictate diminished response to immunotherapy and whether these effects are reversible remains poorly understood. Here, we report that TNBCs with elevated MYC expression are resistant to immune checkpoint inhibitor therapy. Using mouse models and patient data, we show that MYC signaling is associated with low tumor cell PD-L1, low overall immune cell infiltration, and low tumor cell MHC-I expression. Restoring interferon signaling in the tumor increases MHC-I expression. By combining a TLR9 agonist and an agonistic antibody against OX40 with anti-PD-L1, mice experience tumor regression and are protected from new TNBC tumor outgrowth. Our findings demonstrate that MYC-dependent immune evasion is reversible and druggable, and when strategically targeted, may improve outcomes for patients treated with immune checkpoint inhibitors.
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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.