Language

English

Publication Date

1-1-2025

Journal

PLoS One

DOI

10.1371/journal.pone.0324443

PMID

40526635

PMCID

PMC12173385

PubMedCentral® Posted Date

6-17-2025

PubMedCentral® Full Text Version

Post-print

Abstract

Novel agents targeting upregulated signaling pathways are needed to improve outcomes in T-cell acute lymphoblastic leukemia (T-ALL), since conventional cytotoxic chemotherapy regimens have reached the limits of tolerability. We identified upregulated, targetable signaling pathways common to both human T-ALL samples and a KrasLSL-G12D/+.Mb1Cre/+ murine model of T-ALL. We found the NAMPT inhibitor FK866 had the greatest cytotoxicity of a panel of small molecule inhibitors tested in human and mouse T-ALL cell lines, and in patient derived xenograft (PDX)-expanded T-ALL patient samples. We subsequently tested FK866 in vivo in PDX mouse models of T-ALL, and found that it significantly reduced the peripheral blood disease burden and prolonged the survival of leukemic mice (median survival of 60.5 vs 21 days, p = 0.0007). This screen for targetable pathways in T-ALL generated in vitro and in vivo preclinical data supporting NAMPT inhibition as a promising strategy for the treatment of T-ALL.

Keywords

Nicotinamide Phosphoribosyltransferase, Animals, Humans, Mice, Precursor T-Cell Lymphoblastic Leukemia-Lymphoma, Piperidines, Cytokines, Acrylamides, Cell Line, Tumor, Xenograft Model Antitumor Assays, Signal Transduction

Published Open-Access

yes

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