An amino-acid switch in the BCR-ABL kinase domain modifies sensitivity to imatinib mesylate
Author:
Publisher
Springer Science and Business Media LLC
Subject
Oncology,Cancer Research,Hematology
Link
http://www.nature.com/articles/2403831.pdf
Reference8 articles.
1. Hochhaus A, Kreil S, Corbin AS, La Rosee P, Muller MC, Lahaye T et al. Molecular and chromosomal mechanisms of resistance to imatinib (STI571) therapy. Leukemia 2002; 16: 2190–2196.
2. Azam M, Latek RR, Daley GQ . Mechanisms of autoinhibition and STI-571/Imatinib resistance revealed by mutagenesis of BCR–ABL. Cell 2003; 112: 831–843.
3. Hantschel O, Superti-Furga G . Regulation of the c-Abl and bcr–abl tyrosine kinases. Nat Rev Mol Cell Biol 2004; 5: 33–45.
4. Goldman JM . Chronic myeloid leukemia-still a few questions. Exp Hematol 2004; 32: 2–10.
5. Branford S, Rudzki Z, Walsh S, Parkinson I, Grigg A, Szer J et al. Detection of BCR-ABL mutations in patients with CML treated with imatinib is virtually always accompanied by clinical resistance, and mutations in the ATP phosphate-binding loop (P-loop) are associated with a poor prognosis. Blood 2003; 102: 276–283.
Cited by 2 articles. 订阅此论文施引文献 订阅此论文施引文献,注册后可以免费订阅5篇论文的施引文献,订阅后可以查看论文全部施引文献
1. Mapping the conformational energy landscape of Abl kinase using ClyA nanopore tweezers;Nature Communications;2022-06-20
2. Part I: Mechanisms of resistance to imatinib in chronic myeloid leukaemia;The Lancet Oncology;2007-11
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