Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Sphingosine-1-phosphate receptor modulators resensitize FLT3-ITD acute myeloid leukemia cells with NRAS mutations to FLT3 inhibitors.

Leukemia - 1 Aug 2026

Chatterjee Aditi, Mustafa Ali Moaath K, Bailey Christopher M, Liu Yuchen, Small Donald, Smith Catherine C, Traer Elie, Wang Yin, Silvestri Giovannino, Baer Maria R

Abstract excerpt

FLT3 inhibitor efficacy in AML with FLT3-ITD is short-lived, frequently due to new mutations, most commonly in NRAS. Sphingosine kinase 1 (SPHK1), which phosphorylates sphingosine to generate sphingosine-1-phosphate (S1P), is upregulated and localized to the plasma membrane in RAS-mutated cells. We studied S1P and FLT3 co-targeting to overcome FLT3 inhibitor resistance in NRAS-mutated FLT3-ITD AML cells....

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Apoptosis
Share to Cell Line, Tumor

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Drug Resistance, Neoplasm

Share to fms-Like Tyrosine Kinase 3

Share to GTP Phosphohydrolases

Share to Leukemia, Myeloid, Acute

Share to Protein Kinase Inhibitors

Share to Xenograft Model Antitumor Assays

Source

Identifiers

PMID: 42230959
DOI: 10.1038/s41375-026-02982-7

Genes

FLT3
NRAS
SPHK1
BAD

Variants

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Sphingosine-1-phosphate receptor modulators resensitize FLT3-ITD acute myeloid leukemia cells with NRAS mutations to FLT3 inhibitors.PMID 42230959Read ↗

Sphingosine-1-phosphate receptor modulators resensitize FLT3-ITD acute myeloid leukemia cells with <i>NRAS</i> mutations to FLT3 inhibitorsSemantic proximity Read ↗

Expression of myeloid Src-family kinases is associated with poor prognosis in AML and influences Flt3-ITD kinase inhibitor acquired resistanceSemantic proximity Read ↗

Using combination therapy to override stromal-mediated chemoresistance in mutant FLT3-positive AML: synergism between FLT3 inhibitors, dasatinib/multi-targeted inhibitors and JAK inhibitors.Semantic proximity Read ↗

A structure-based modelling approach identifies effective drug combinations for RAS-mutant acute myeloid leukemiaSemantic proximity Read ↗

A Novel Function of Sphingolipid Signaling via S1PR3 in Hematopoietic and Leukemic Stem CellsSemantic proximity Read ↗

A critical role for PLCG1 in RAS activation by BCR-ABL1 and FLT3-ITDSemantic proximity Read ↗

Narazaciclib, a novel multi-kinase inhibitor with potent activity against CSF1R, FLT3 and CDK6, shows strong anti-AML activity in defined preclinical models.Semantic proximity Read ↗

Functional Characterization of FLT3 Receptor Signaling Deregulation in Acute Myeloid Leukemia by Single Cell Network Profiling (SCNP)Semantic proximity Read ↗

Enhancing Therapeutic Efficacy of FLT3 Inhibitors with Combination Therapy for Treatment of Acute Myeloid Leukemia.Semantic proximity Read ↗

Inhibitors of the tyrosine kinases FMS-like tyrosine kinase-3 and WEE1 induce apoptosis and DNA damage synergistically in acute myeloid leukemia cellsSemantic proximity Read ↗

Inhibition of Flt3-activating mutations does not prevent constitutive activation of ERK/Akt/STAT pathways in some AML cells: a possible cause for the limited effectiveness of monotherapy with small-molecule inhibitors.Semantic proximity Read ↗

Quantitative phosphoproteomics uncovers synergy between DNA-PK and FLT3 inhibitors in acute myeloid leukaemiaSemantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.