ArticleCancer discovery2024
NKG2A Is a Therapeutic Vulnerability in Immunotherapy Resistant MHC-I Heterogeneous Triple-Negative Breast Cancer.
Article in Cancer discovery, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.
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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
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Who cites it
49 citing papers in PubMed.
- NKG2A-HLA-E axis contributes to an immunosuppressive checkpoint network in hepatocellular carcinoma.Journal for immunotherapy of cancer · 2026Article
- Construction and validation of a β-hydroxybutyrylation-related molecular model for predicting prognosis of papillary thyroid carcinoma.Translational cancer research · 2026Article
- PGE2-mediated NK cell reprogramming drives acquired immunotherapy resistance in lung adenocarcinoma.Journal for immunotherapy of cancer · 2026Article
- Triple-Negative Breast Cancer Cells Utilize IL8 and CXCL1 to Suppress NK Cells' Function and Facilitate Cancer Metastasis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Spatial organization of the TNBC tumor microenvironment: multicellular niches, T-cell bottlenecks, and therapeutic opportunities.Journal of translational medicine · 2026Review
- Advances in Mechanism of Action and Efficacy of CBP/p300 Inhibitors in Different Subtypes of Breast Cancer.Molecules (Basel, Switzerland) · 2026Review
- Interactions Between Circulating Tumor Cells and the Immune System in Colorectal Cancer: Friends or Foes?Cancers · 2026Review
- CXCL16-driven CD4Journal for immunotherapy of cancer · 2026Article
- Peripheral blood transcriptional profiling predicts tumor subtype and neoadjuvant chemoimmunotherapy outcomes in human breast cancer.Science translational medicine · 2026Article
- Reinforced immunotherapy of M1 macrophage-derived exosomes with CEL on TNBC via regulating macrophage functions.Journal of advanced research · 2026Article
- NK Cell Activation by Platinum Boosts Immunotherapy in HRAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Logic-Gated HSV-TK/GCV Suicide Gene Circuit for Triple-Negative Breast Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- JAK/STAT-mediated regulation of PD-L1 expression in breast cancer: Molecular mechanisms and implications for immunotherapy.iScience · 2026Review
- The CD94/NKG2A-HLA-E Axis as a Target in Cancer Immunotherapy: A Critical Perspective.Clinical cancer research : an official journal of the American Association for Cancer Research · 2026Review
- The "Cold Tumor" to "Hot Tumor" transformation strategy for triple-negative breast cancer: from mechanism to clinical translation.Molecular and cellular biochemistry · 2026Review
- Targeting glucocorticoid receptor to enhance immunotherapy response in triple negative breast cancer.Breast cancer research : BCR · 2026Article
- AI-driven multi-omics integration in breast cancer: clinical applications, immunotherapy prediction, and translational challenges.Frontiers in molecular biosciences · 2026Review
- Protective NK Cell Reservoir Based on DNA Supramolecular Hydrogel for Enhanced Triple-Negative Breast Cancer Therapy.Research (Washington, D.C.) · 2026Article
- C1orf112 promotes breast cancer growth by modulating the cell cycle.Frontiers in bioengineering and biotechnology · 2026Article
- Single-cell transcriptomic analysis reveals the immunosuppressive status of NK cell subpopulations in TNBC.PloS one · 2026Article
Corrections and comments
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Authors and funding
20 authors.
Funding
Abstract
Despite the success of immune checkpoint inhibition (ICI) in treating cancer, patients with triple-negative breast cancer (TNBC) often develop resistance to therapy, and the underlying mechanisms are unclear. MHC-I expression is essential for antigen presentation and T-cell-directed immunotherapy responses. This study demonstrates that TNBC patients display intratumor heterogeneity in regional MHC-I expression. In murine models, loss of MHC-I negates antitumor immunity and ICI response, whereas intratumor MHC-I heterogeneity leads to increased infiltration of natural killer (NK) cells in an IFNγ-dependent manner. Using spatial technologies, MHC-I heterogeneity is associated with clinical resistance to anti-programmed death (PD) L1 therapy and increased NK:T-cell ratios in human breast tumors. MHC-I heterogeneous tumors require NKG2A to suppress NK-cell function. Combining anti-NKG2A and anti-PD-L1 therapies restores complete response in heterogeneous MHC-I murine models, dependent on the presence of activated, tumor-infiltrating NK and CD8+ T cells. These results suggest that similar strategies may enhance patient benefit in clinical trials. SIGNIFICANCE: Clinical resistance to immunotherapy is common in breast cancer, and many patients will likely require combination therapy to maximize immunotherapeutic benefit. This study demonstrates that heterogeneous MHC-I expression drives resistance to anti-PD-L1 therapy and exposes NKG2A on NK cells as a target to overcome resistance. This article is featured in Selected Articles from This Issue, p. 201.
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Registered trials
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