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Article

Targeting MCL-1 and MAPK overcomes venetoclax resistance in FLT3-ITD-positive AML cells harbouring activating PTPN11 (SHP-2) mutations.

British journal of haematology - 1 Mar 2026

Fleischmann Maximilian, Hansen Ole, Voigtländer Diana, Bechwar Julia, Schwietzer Lenny-Joseph, Bahr Sanja, Schnetzke Ulf, Fischer Mike, Heidel Florian H, Schnöder Tina M, Müller Jörg P, Hochhaus Andreas, Scholl Sebastian

Abstract excerpt

Venetoclax (VEN)-based therapies have improved the treatment of acute myeloid leukaemia (AML); however, the emergence of resistance remains a major limitation. Mutations in protein tyrosine phosphatase (PTP) non-receptor type 11 (PTPN11) and FMS like tyrosine kinase 3 with internal tandem duplication (FLT3-ITD) are common in resistant patients and are linked to activation of mitogen-activated protein kinase...

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Share to Bridged Bicyclo Compounds, Heterocyclic
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Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

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Share to Myeloid Cell Leukemia Sequence 1 Protein

Share to Protein Tyrosine Phosphatase, Non-Receptor Type 11

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Source

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Identifiers

PMID: 41608989
DOI: 10.1111/bjh.70344
PMCID: PMC12995534

Genes

PTPN11
FLT3
TRA
F3

Variants

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 6 Sept 2026.

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