ArticleCancers2021
An HLA-A*11:01-Binding Neoantigen from Mutated NPM1 as Target for TCR Gene Therapy in AML.
Article in Cancers, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 13 citations in OpenAlex.
- Minor histocompatibility antigen TCR-T.Blood advances · 2026Review
- Neoantigen Targeting as a Novel Approach for Therapy-Resistant Tumors.Molecular diagnosis & therapy · 2026Review
- Article
- SF3B1K700E Neoantigen Is a CD8+ T-cell Target Shared across Human Myeloid Neoplasms.Cancer immunology research · 2025Article
- Current developments in T-cell receptor therapy for acute myeloid leukemia.Blood advances · 2025Review
- MutatedFrontiers in immunology · 2025Article
- Protective effects for HLA-B*40:01 and C*03:04 in NPM1-mutated AML: result of a large HLA association study.Frontiers in immunology · 2025Article
- Identification of shared neoantigens derived from frameshift mutations in theFrontiers in immunology · 2025Article
- CAR'TCR-T cells co-expressing CD33-CAR and dNPM1-TCR as superior dual-targeting approach for AML treatment.Molecular therapy. Oncology · 2024Article
- Hotspot DNA Methyltransferase 3A (Biomedicines · 2024Article
- Review
Corrections and comments
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Authors and funding
20 authors at 1 institution in 1 country.
Funding
Abstract
Acute myeloid leukemia (AML) is a hematological malignancy caused by clonal expansion of myeloid progenitor cells. Most patients with AML respond to chemotherapy, but relapses often occur and infer a very poor prognosis. Thirty to thirty-five percent of AMLs carry a four base pair insertion in the nucleophosmin 1 gene (NPM1) with a C-terminal alternative reading frame of 11 amino acids. We previously identified various neopeptides from the alternative reading frame of mutant NPM1 (dNPM1) on primary AML and isolated an HLA-A*02:01-restricted T-cell receptor (TCR) that enables human T-cells to kill AML cells upon retroviral gene transfer. Here, we isolated T-cells recognizing the dNPM1 peptide AVEEVSLRK presented in HLA-A*11:01. The TCR cloned from a T-cell clone recognizing HLA-A*11:01+ primary AML cells conferred in vitro recognition and lysis of AML upon transfer to CD8 cells, but failed to induce an anti-tumor effect in immunodeficient NSG mice engrafted with dNPM1 OCI-AML3 cells. In conclusion, our data show that AVEEVSLRK is a dNPM1 neoantigen on HLA-A*11:01+ primary AMLs. CD8 cells transduced with an HLA-A*11:01-restricted TCR for dNPM1 were reactive against AML in vitro. The absence of reactivity in a preclinical mouse model requires further preclinical testing to predict the potential efficacy of this TCR in clinical development.
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Registered trials
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