(Q39640407)

English

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

scientific article published on 25 October 2010

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scholarly article

1 reference

Europe PubMed Central

PubMed publication ID

13 September 2017

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 (English)

1 reference

Europe PubMed Central

PubMed publication ID

13 September 2017

author name string

N von Bubnoff

1

1 reference

Europe PubMed Central

PubMed publication ID

13 September 2017

S P Gorantla

2

1 reference

Europe PubMed Central

PubMed publication ID

13 September 2017

R A Engh

3

1 reference

Europe PubMed Central

PubMed publication ID

13 September 2017

T M Oliveira

4

1 reference

Europe PubMed Central

PubMed publication ID

13 September 2017

S Thöne

5

1 reference

Europe PubMed Central

PubMed publication ID

13 September 2017

E Aberg

6

1 reference

Europe PubMed Central

PubMed publication ID

13 September 2017

C Peschel

7

1 reference

Europe PubMed Central

PubMed publication ID

13 September 2017

J Duyster

8

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Europe PubMed Central

PubMed publication ID

13 September 2017

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publication date

25 October 2010

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Europe PubMed Central

PubMed publication ID

13 September 2017

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Europe PubMed Central

PubMed publication ID

13 September 2017

30

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Europe PubMed Central

PubMed publication ID

13 September 2017

8

1 reference

Europe PubMed Central

PubMed publication ID

13 September 2017

933-943

1 reference

Europe PubMed Central

PubMed publication ID

13 September 2017

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Comparative analysis of two clinically active BCR-ABL kinase inhibitors reveals the role of conformation-specific binding in resistance

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The hypereosinophilic syndrome: analysis of fourteen cases with review of the literature

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A tyrosine kinase created by fusion of the PDGFRA and FIP1L1 genes as a therapeutic target of imatinib in idiopathic hypereosinophilic syndrome

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

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Activity of dasatinib, a dual SRC/ABL kinase inhibitor, and IPI-504, a heat shock protein 90 inhibitor, against gastrointestinal stromal tumor-associated PDGFRAD842V mutation.

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Clinical resistance to the kinase inhibitor PKC412 in acute myeloid leukemia by mutation of Asn-676 in the FLT3 tyrosine kinase domain

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Molecular correlates of imatinib resistance in gastrointestinal stromal tumors.

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Gain-of-function mutations of platelet-derived growth factor receptor alpha gene in gastrointestinal stromal tumors.

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Impact of baseline BCR-ABL mutations on response to nilotinib in patients with chronic myeloid leukemia in chronic phase

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Nilotinib in imatinib-resistant CML and Philadelphia chromosome-positive ALL

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Identification of a novel activating mutation (Y842C) within the activation loop of FLT3 in patients with acute myeloid leukemia (AML).

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Response and resistance in 300 patients with BCR-ABL-positive leukemias treated with imatinib in a single center: a 4.5-year follow-up

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

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

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The c-KIT mutation causing human mastocytosis is resistant to STI571 and other KIT kinase inhibitors; kinases with enzymatic site mutations show different inhibitor sensitivity profiles than wild-type kinases and those with regulatory-type mutations

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Identification of a point mutation in the catalytic domain of the protooncogene c-kit in peripheral blood mononuclear cells of patients who have mastocytosis with an associated hematologic disorder

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Pharmacokinetics and pharmacodynamics of imatinib in a phase I trial with chronic myeloid leukemia patients

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Activity of bosutinib, dasatinib, and nilotinib against 18 imatinib-resistant BCR/ABL mutants

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Detection and molecular monitoring of FIP1L1-PDGFRA-positive disease by analysis of patient-specific genomic DNA fusion junctions

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Primary resistance to imatinib in Fip1-like 1-platelet-derived growth factor receptor alpha-positive eosinophilic leukemia

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The small molecule tyrosine kinase inhibitor AMN107 inhibits TEL-PDGFRbeta and FIP1L1-PDGFRalpha in vitro and in vivo

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Phase I clinical and pharmacokinetic study of the Novel Raf kinase and vascular endothelial growth factor receptor inhibitor BAY 43-9006 in patients with advanced refractory solid tumors.

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Classification and diagnosis of myeloproliferative neoplasms: the 2008 World Health Organization criteria and point-of-care diagnostic algorithms

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FMS-like tyrosine kinase 3-internal tandem duplication tyrosine kinase inhibitors display a nonoverlapping profile of resistance mutations in vitro

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The FIP1L1-PDGFRA T674I mutation can be inhibited by the tyrosine kinase inhibitor AMN107 (nilotinib).

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Myeloid blast crisis evolving during imatinib treatment of an FIP1L1-PDGFR alpha-positive chronic myeloproliferative disease with prominent eosinophilia

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Sorafenib inhibits imatinib-resistant KIT and platelet-derived growth factor receptor beta gatekeeper mutants

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Sorafenib Inhibits the Imatinib-Resistant KITT670I Gatekeeper Mutation in Gastrointestinal Stromal Tumor

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BCR-ABL mutant kinetics in CML patients treated with dasatinib

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Bcr-Abl resistance screening predicts a limited spectrum of point mutations to be associated with clinical resistance to the Abl kinase inhibitor nilotinib (AMN107)

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10.1038/ONC.2010.476

1 reference

Europe PubMed Central

PubMed publication ID

13 September 2017

PubMed publication ID

1 reference

Europe PubMed Central

PubMed publication ID

13 September 2017

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