Dasatinib in imatinib-resistant Philadelphia chromosome-positive leukemias.
By M. Talpaz, N. Shah, H. Kantarjian, N. Donato, J. Nicoll, R. Paquette, J. Cortes, S. O'brien, C. Nicaise, E. Bleickardt and 6 more. New England Journal of Medicine, 2006
1,710 citations recorded by the source corpus.
Subfields: Genetics, Hematology, Rheumatology
View Paper: https://www.semanticscholar.org/paper/b5bb7903d6fd61a538d1d2fa78dcf282fb541572
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In Genetics
In Hematology
- Brian J. Druker
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- C. Ashby
- Levi A. Garraway
- Andreas Hochhaus
- Nathanael S. Gray
- Zhesheng Chen
In Rheumatology
Citations in the corpus
- Molecular mechanisms of cardiotoxicity of tyrosine kinase inhibition (2007, background): “Both dasatinib and nilotinib are active against some imatinib-resistant BCR–ABL mutants, and dasatinib was recently approved by the FDA for treatment of imatinib-refractory CML and Ph + AL”
- Role of JAK2 in the pathogenesis and therapy of myeloproliferative disorders (2007, methodology): “This strategy has been used to design second-generation ABL inhibitors for the treatment of imatinib refractory CM”
- Src kinases as therapeutic targets for cancer (2009, background): “A phase I study of dasatinib treatment in patients with Philadelphia-chromosome-positive CML who did not respond or were intolerant to imatinib has been reported”
- BCR-ABL tyrosine kinase inhibitors in the treatment of Philadelphia chromosome positive chronic myeloid leukemia: a review. (2010, background): “However, a onger follow-up of the data from the phase I trial of dasatinib ndicated that the once-a-day treatment group experienced sigificantly fewer adverse effects compared to those treated twice aily [69].”
- A Phase 2 Trial of Ponatinib in Philadelphia Chromosome–Positive Leukemias (2013, neutral): “Fatigue 51 (19) 4 (1) 17 (20) 1 (1) 7 (11) 2 (3) 3 (9) 0”
- Roles of the Raf/MEK/ERK pathway in cell growth, malignant transformation and drug resistance. (2007, background): “Thus a side effect of Src family kinase inhibitors such as Dasatinib, which is being used to treat certain Imatinib resistant chronic myeloid leukemia (CML) patients and other cancer patients who overexpresses mutant c-Kit [15,16] would be suppression of Raf-1/MEK/ERK signaling in certain cells.”
- Second generation inhibitors of BCR-ABL for the treatment of imatinib-resistant chronic myeloid leukaemia (2007, background): “Based on positive data in phase I and phase II trial”