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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Summary
The acquisition of a T674I resistance mutation at the time of relapse demonstrates that FIP1L1-PDGFRalpha is the target of imatinib, and data indicate that the deletion of genetic material may result in gain-of-function fusion proteins.
- Type
- article
- Published
- 2003-03-27
- Cited by
- 1,751
- References
- 28
- Access
- Open access
- OpenAlex
- https://openalex.org/W2012952884
- Semantic Scholar
- https://api.semanticscholar.org/CorpusID:185159
Keywords
Imatinib, Hypereosinophilic syndrome, Medicine, PDGFRA, Fusion gene
References
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- CGP 57148, a tyrosine kinase inhibitor, inhibits the growth of cells expressing BCR-ABL, TEL-ABL, and TEL-PDGFR fusion proteins.
- Fusion of a novel gene, BTL, to ETV6 in acute myeloid leukemias with a t(4;12)(q11-q12;p13).
- Inhibition of the Abl protein-tyrosine kinase in vitro and in vivo by a 2-phenylaminopyrimidine derivative.
- Treatment of hypereosinophilic syndrome with imatinib mesilate.
- Clinical Resistance to STI-571 Cancer Therapy Caused by BCR-ABL Gene Mutation or Amplification
- THE HYPEREOSINOPHILIC SYNDROME: Analysis of Fourteen Cases With Review of The Literature
- Efficacy and safety of imatinib mesylate in advanced gastrointestinal stromal tumors.
- Multiple BCR-ABL kinase domain mutations confer polyclonal resistance to the tyrosine kinase inhibitor imatinib (STI571) in chronic phase and blast crisis chronic myeloid leukemia.
- Fusion of PDGF receptor beta to a novel ets-like gene, tel, in chronic myelomonocytic leukemia with t(5;12) chromosomal translocation.
- A cellular oncogene is translocated to the Philadelphia chromosome in chronic myelocytic leukaemia
- Successful use of the same slide for consecutive fluorescence in situ hybridization experiments
- Response to imatinib mesylate in patients with chronic myeloproliferative diseases with rearrangements of the platelet-derived growth factor receptor beta.
- Evidence for position effects as a variant ETV6-mediated leukemogenic mechanism in myeloid leukemias with a t(4;12)(q11-q12;p13) or t(5;12)(q31;p13).
- Clinical resistance to the kinase inhibitor STI-571 in chronic myeloid leukemia by mutation of Tyr-253 in the Abl kinase domain P-loop
- STI571 inactivation of the gastrointestinal stromal tumor c-KIT oncoprotein: biological and clinical implications
- The FIP1 gene encodes a component of a yeast pre-mRNA polyadenylation factor that directly interacts with poly(A) polymerase.
- Structure, organization, and transcription units of the human alpha-platelet-derived growth factor receptor gene, PDGFRA.
- H4(D10S170), a gene frequently rearranged in papillary thyroid carcinoma, is fused to the platelet-derived growth factor receptor beta gene in atypical chronic myeloid leukemia with t(5;10)(q33;q22).
- Abl protein-tyrosine kinase inhibitor STI571 inhibits in vitro signal transduction mediated by c-kit and platelet-derived growth factor receptors.
Cited by
- Genetics of papillary thyroid cancer initiation: implications for therapy.
- JAK2V617F-positive Myeloproliferative Neoplasms : KI mouse models, Interferon-α therapy and clonal architecture
- Myeloproliferative syndromes: diagnosis and therapeutic options.
- [Hypereosinophilic dermatitis. An overlooked diagnosis?].
- The eosinophilias, including the idiopathic hypereosinophilic syndrome
- Imatinib therapy for hypereosinophilic syndrome and eosinophilia-associated myeloproliferative disorders.
- A new modality for immunosuppression: targeting the JAK/STAT pathway
- Hypereosinophilia with systemic thrombophlebitis.
- Tyrosine kinases as targets for cancer therapy.
- Oncogenes in Myeloproliferative Disorders
- Idiopathic hypereosinophilic syndrome presenting acute abdomen.
- Lymphocytic variant hypereosinophilic syndromes.
- Where lies the blame for resistance—tumor or host?
- Hypereosinophilic syndrome: another face of janus?
- Pathogenetic insight and prognostic information from standard and molecular cytogenetic studies in the BCR-ABL-negative myeloproliferative neoplasms (MPNs)
- Decreased bone turnover despite persistent secondary hyperparathyroidism during prolonged treatment with imatinib.
- Inflammatorische fibroide Polypen sind echte Neoplasien mit PDGFRA-Mutationen
- A curious case of a 'burned-out' hypereosinophilic syndrome.
- R-loop-mediated genome instability in mRNA cleavage and polyadenylation mutants.
- Loeffler Endocarditis in a Pediatric Patient
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