17 DHC 2025
22 - 24 January 2025
Immunology Abstracts (4)
Abstract
1246: T cell receptor gene therapy targeting mutant NPM1 on acute myeloid leukemia
23 January
11:45 12:00
Paper

T cell receptor gene therapy targeting mutant NPM1 on acute myeloid leukemia

Eva M. Argiro (1), Nadine E. Struckman (1), E. Onur Karakaslar (2,3,4), Georgia Koutsoumpli (1), Ian C.D. Johnston (5), Erik B. van den Akker (2,3,4), J.H. Frederik Falkenburg (1), Mirjam H.M. Heemskerk (1), Rosa de Groot (1), Constantijn J.M. Halkes (1), Marieke Griffioen (1)
(1) Leiden University Medical Center, Department of Hematology, Leiden, (2) Leiden University Medical Center, Department of Biomedical Data Sciences, Leiden, (3) Delft University of Technology, Pattern Recognition & Bioinformatics, Delft, (4) Leiden University Medical Center, Leiden Center for Computational Oncology, Leiden, (5) Miltenyi Biotec B.V., Bergisch Gladbach
Potential conflict(s) of interest: details
  • Other support (specified) The phase I/II clinical trial is sponsored by Miltenyi.
Introduction

Acute myeloid leukemia (AML) is a life-threatening malignancy that requires further therapeutic improvement. One of the most common AML sub-entities is AML with mutant NPM1 (dNPM1-AML), in which a 4 base pair frameshift insertion occurs in the NPM1 gene. We previously reported on a T cell receptor (TCR) which, upon transfer to CD8 T cells, is able to target AML cells carrying this mutation by recognizing CLAVEEVSL, a 9-mer dNPM1-derived neoantigen presented by HLA-A*02:01. Since dNPM1-AML is a highly heterogeneous disease, highlighted by the recent identification of distinct dNPM1-AML subtypes by bulk transcriptomics, we here investigated the inter- and intra-patient heterogeneity in more detail and assessed the in vitro susceptibility of AML cells with different phenotypes to lysis by dNPM1-A2 TCR-engineered T cells. 

Methods

A 28-color spectral flow cytometry-based antibody panel was used to phenotype dNPM1-AML cells and to assess lysis of different leukemic cell subsets in co-culture with dNPM1-A2 TCR-T cells.

Results

Different dNPM1-AML cells were identified, with early hematopoietic stem cell- or progenitor-like phenotypes or more mature monocyte- or dendritic cell-like phenotypes. Upon coculture with dNPM1-A2 TCR-engineered T cells, all subpopulations were efficiently lysed, albeit with different kinetics. 

Conclusion

The results emphasize the potential of dNPM1-A2 TCR-T cells as a therapeutic strategy to treat patients with dNPM1-AML. This strategy is currently being evaluated in a first-in-human phase I/II clinical trial at the Leiden University Medical Center. 

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