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Efficacy and safety of a specific inhibitor of the BCR-ABL tyrosine kinase in chronic myeloid leukemia.
STI571 is well tolerated and has significant antileukemic activity in patients with CML in whom treatment with interferon alfa had failed and demonstrates the potential for the development of anticancer drugs based on the specific molecular abnormality present in a human cancer.
Acute myeloid leukemia.
- F. Giles, A. Keating, A. Goldstone, I. Avivi, C. Willman, H. Kantarjian
- BiologyHematology. American Society of Hematology…
Recent advances in understanding of the pathophysiology of acute myeloid leukemia (AML) and allied conditions are reviewed, including the advanced myelodysplastic syndromes (MDS), while Drs.
Revised international prognostic scoring system for myelodysplastic syndromes.
This revised IPSS-R comprehensively integrated the numerous known clinical features into a method analyzing MDS patient prognosis more precisely than the initial IPSS and should prove beneficial for predicting the clinical outcomes of untreated MDS patients and aiding design and analysis of clinical trials in this disease.
Imatinib compared with interferon and low-dose cytarabine for newly diagnosed chronic-phase chronic myeloid leukemia.
Imatinib was superior to interferon alfa plus low-dose cytarabine as first-line therapy in newly diagnosed chronic-phase CML and was better tolerated than combination therapy.
Five-year follow-up of patients receiving imatinib for chronic myeloid leukemia.
After 5 years of follow-up, continuous treatment of chronic-phase CML with imatinib as initial therapy was found to induce durable responses in a high proportion of patients.
European LeukemiaNet recommendations for the management of chronic myeloid leukemia: 2013.
Optimal responders to chronic myeloid leukemia treatment should continue therapy indefinitely, with careful surveillance, or they can be enrolled in controlled studies of treatment discontinuation once a deeper molecular response is achieved.
Clinical effect of point mutations in myelodysplastic syndromes.
Mutations in TP53, EZH2, ETV6, RUNX1, and ASXL1 are predictors of poor overall survival in patients with myelodysplastic syndromes, independently of established risk factors.
Activity of a specific inhibitor of the BCR-ABL tyrosine kinase in the blast crisis of chronic myeloid leukemia and acute lymphoblastic leukemia with the Philadelphia chromosome.
The BCR-ABL tyrosine kinase inhibitor STI571 is well tolerated and has substantial activity in the blast crises of CML and in Ph-positive ALL.
A tyrosine kinase created by fusion of the PDGFRA and FIP1L1 genes as a therapeutic target of imatinib in idiopathic hypereosinophilic syndrome.
- J. Cools, D. DeAngelo, D. Gilliland
- Medicine, BiologyThe New England journal of medicine
- 27 March 2003
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.
Decitabine improves patient outcomes in myelodysplastic syndromes
Aberrant DNA methylation, which results in leukemogenesis, is frequent in patients with myelodysplastic syndromes (MDS) and is a potential target for pharmacologic therapy. Decitabine indirectly…