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Article

Sorafenib induces paradoxical phosphorylation of the extracellular signal-regulated kinase pathway in acute myeloid leukemia cells lacking FLT3-ITD mutation.

Leukemia & lymphoma - 1 Jan 2015

Fouladi Fariba, Jehn Lutz B, Metzelder Stephan K, Hub Florian, Henkenius Katharina, Burchert Andreas, Brendel Cornelia, Stiewe Thorsten, Neubauer Andreas

Abstract excerpt

Gain-of-function mutations in the RAS and FLT3 genes are frequently found in cells of acute myeloid leukemia (AML), leading to constitutive activation of signaling pathways that regulate fundamental cellular processes, and are therefore attractive targets for AML therapy. The multi-targeted kinase inhibitor sorafenib is efficacious in AML with FLT3-internal tandem duplication (ITD), but resistance to therapy is...

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Identifiers

PMID: 25665465
DOI: 10.3109/10428194.2014.1003055
PMCID: PMC4732463

Genes

FLT3

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

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