ArticleThe Journal of clinical investigation2020
CBFB-MYH11 fusion neoantigen enables T cell recognition and killing of acute myeloid leukemia.
Article in The Journal of clinical investigation, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT06499025 (A Clinical Study to Evaluate the Safety and Initial Efficacy of Targeted AML1-ETO Neoantigen Cytotoxic T Cells), which is not on this map. Cited by 59 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.
A Clinical Study to Evaluate the Safety and Initial Efficacy of Targeted AML1-ETO Neoantigen Cytotoxic T Cells (CTL) in the Treatment of Relapsed or Refractory t(8; 21) AML
Who cites it
59 citing papers in PubMed, 108 citations in OpenAlex.
- Minor histocompatibility antigen TCR-T.Blood advances · 2026Review
- Disrupting the CBFβ-SMMHC-RUNX1 oncogenic protein-protein interaction in inv(16) AML: from fusion biology to targeted therapy.Discover oncology · 2026Review
- Neoantigen Targeting as a Novel Approach for Therapy-Resistant Tumors.Molecular diagnosis & therapy · 2026Review
- The GF-NEO discovery platform unveils a [KQE][DG] sequence motif within fusion neoantigens in pediatric cancer.iScience · 2026Article
- Article
- mRNA vaccines in cancer immunotherapy: current progress and perspectives in solid tumors and hematologic malignancies.MedScience · 2026Review
- Targeting the roots of myeloid malignancies with T cell receptors.Nature reviews. Cancer · 2025Review
- Alternative splicing: from tumorigenesis to neoantigen-mediated cancer immunotherapy.Biomarker research · 2025Review
- Identification of specific T-cell response and T-cell receptor targeting shared neoantigen for acute myeloid leukemia.Blood cancer journal · 2025Article
- Endogenous T cell responses to fusion-derived neoantigens in pediatric acute leukemias.Leukemia · 2025Article
- Neoantigen-driven personalized tumor therapy: An update from discovery to clinical application.Chinese medical journal · 2025Review
- SF3B1K700E Neoantigen Is a CD8+ T-cell Target Shared across Human Myeloid Neoplasms.Cancer immunology research · 2025Article
- Characterization of Tumor Antigens from Multi-omics Data: Computational Approaches and Resources.Genomics, proteomics & bioinformatics · 2025Review
- Computation strategies and clinical applications in neoantigen discovery towards precision cancer immunotherapy.Biomarker research · 2025Review
- Current developments in T-cell receptor therapy for acute myeloid leukemia.Blood advances · 2025Review
- Detecting known neoepitopes, gene fusions, transposable elements, and circular RNAs in cell-free RNA.Bioinformatics (Oxford, England) · 2025Article
- Navigating established and emerging biomarkers for immune checkpoint inhibitor therapy.Cancer cell · 2025Review
- A 5-lncRNA signature predicts clinical prognosis and demonstrates a different mRNA expression in adult soft tissue sarcoma.Translational cancer research · 2025Article
- Review
- MutatedFrontiers in immunology · 2025Article
Corrections and comments
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Authors and funding
15 authors at 2 institutions in 1 country.
Funding
Abstract
Proteins created from recurrent fusion genes like CBFB-MYH11 are prevalent in acute myeloid leukemia (AML), often necessary for leukemogenesis, persistent throughout the disease course, and highly leukemia specific, making them attractive neoantigen targets for immunotherapy. A nonameric peptide derived from a prevalent CBFB-MYH11 fusion protein was found to be immunogenic in HLA-B*40:01+ donors. High-avidity CD8+ T cell clones isolated from healthy donors killed CBFB-MYH11+ HLA-B*40:01+ AML cell lines and primary human AML samples in vitro. CBFB-MYH11-specific T cells also controlled CBFB-MYH11+ HLA-B*40:01+ AML in vivo in a patient-derived murine xenograft model. High-avidity CBFB-MYH11 epitope-specific T cell receptors (TCRs) transduced into CD8+ T cells conferred antileukemic activity in vitro. Our data indicate that the CBFB-MYH11 fusion neoantigen is naturally presented on AML blasts and enables T cell recognition and killing of AML. We provide proof of principle for immunologically targeting AML-initiating fusions and demonstrate that targeting neoantigens has clinical relevance even in low-mutational frequency cancers like fusion-driven AML. This work also represents a first critical step toward the development of TCR T cell immunotherapy targeting fusion gene-driven AML.
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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.