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Article

Inhibition of the proteasome and proteaphagy enhances apoptosis in FLT3-ITD-driven acute myeloid leukemia.

FEBS open bio - 1 Jan 2021

Lopez-Reyes Rosa G, Quinet Grégoire, Gonzalez-Santamarta Maria, Larrue Clément, Sarry Jean-Emmanuel, Rodriguez Manuel S

Abstract excerpt

Acute myeloid leukaemia (AML) is a clonal disorder that affects hematopoietic stem cells or myeloid progenitors. One of the most common mutations that results in AML occurs in the gene encoding fms-like tyrosine kinase 3 (FLT3). Previous studies have demonstrated that AML cells expressing FLT3-internal tandem duplication (ITD) are more sensitive to the proteasome inhibitor bortezomib (Bz) than FLT3 wild-type...

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Source

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Identifiers

PMID: 33410599
DOI: 10.1002/2211-5463.12950
PMCID: PMC7780102

Genes

FLT3

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 6 Sept 2026. Manifest publication-graph-cohort-2026-09-06.1.

Source receipt: pubmed, retrieved 6 Sept 2026.

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Inhibition of the proteasome and proteaphagy enhances apoptosis in FLT3-ITD-driven acute myeloid leukemia.PMID 33410599Read ↗

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