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

Sorafenib is a potent inhibitor of FIP1L1-PDGFRalpha and the imatinib-resistant FIP1L1-PDGFRalpha T674I mutant.

Blood - 15 Aug 2006

Lierman Els, Folens Cedric, Stover Elizabeth H, Mentens Nicole, Van Miegroet Helen, Scheers Werner, Boogaerts Marc, Vandenberghe Peter, Marynen Peter, Cools Jan

Abstract excerpt

The FIP1L1-PDGFRA oncogene is a common cause of chronic eosinophilic leukemia (CEL), and encodes an activated tyrosine kinase that is inhibited by imatinib. FIP1L1-PDGFRA-positive patients with CEL respond to low-dose imatinib therapy, but resistance due to acquired T674I mutation has been observed. We report here the identification of sorafenib as a potent inhibitor of the FIP1 like 1-platelet-derived growth...

Read the complete abstract on PubMed

Topics

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

Share to Benzenesulfonates
Share to Hypereosinophilic Syndrome

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to K562 Cells

Share to mRNA Cleavage and Polyadenylation Factors

Share to Niacinamide

Share to Phenylurea Compounds

Share to Receptor, Platelet-Derived Growth Factor alpha

Share to Sorafenib

Source

Open in PubMed Open full text

Identifiers

PMID: 16645167
DOI: 10.1182/blood-2006-02-004457
PMCID: PMC1895882

Genes

CEL
PDGFRA

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 1 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Sorafenib is a potent inhibitor of FIP1L1-PDGFRalpha and the imatinib-resistant FIP1L1-PDGFRalpha T674I mutant.PMID 16645167Read ↗

FIP1L1-PDGFRalpha D842V, a novel panresistant mutant, emerging after treatment of FIP1L1-PDGFRalpha T674I eosinophilic leukemia with single agent sorafenib.Semantic proximity Read ↗

The low frequency of clinical resistance to PDGFR inhibitors in myeloid neoplasms with abnormalities of PDGFRA might be related to the limited repertoire of possible PDGFRA kinase domain mutations in vitro.Semantic proximity Read ↗

Limited clinical activity of nilotinib and sorafenib in FIP1L1-PDGFRA positive chronic eosinophilic leukemia with imatinib-resistant T674I mutationSemantic proximity Read ↗

A novel FIP1L1-PDGFRA mutant destabilizing the inactive conformation of the kinase domain in chronic eosinophilic leukemia/hypereosinophilic syndrome.Semantic proximity Read ↗

Antitumor activity of S116836, a novel tyrosine kinase inhibitor, against imatinib-resistant FIP1L1-PDGFRα-expressing cells.Semantic proximity Read ↗

The ability of sorafenib to inhibit oncogenic PDGFRbeta and FLT3 mutants and overcome resistance to other small molecule inhibitors.Semantic proximity Read ↗

The FIP1L1-PDGFRα fusion tyrosine kinase in hypereosinophilic syndrome and chronic eosinophilic leukemia: implications for diagnosis, classification, and managementSemantic proximity Read ↗

The conformational control inhibitor of tyrosine kinases DCC-2036 is effective for imatinib-resistant cells expressing T674I FIP1L1-PDGFRα.Semantic proximity Read ↗

PKC412 overcomes resistance to imatinib in a murine model of FIP1L1-PDGFRα-induced myeloproliferative disease.Semantic proximity Read ↗

Crenolanib inhibits the drug-resistant PDGFRA D842V mutation associated with imatinib-resistant gastrointestinal stromal tumors.Semantic proximity Read ↗

Atypical Phenotype and Treatment Response Pattern in a Patient with FIP1L1-PDGFRα Mutation.Semantic proximity Read ↗

Preliminary in vitro and in vivo investigation of a potent platelet derived growth factor receptor (PDGFR) family kinase inhibitor.Semantic proximity Read ↗

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