Novel mutations in the kinase domain of BCR-ABL gene causing imatinib resistance in chronic myeloid leukemia patients
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Publisher
Springer Science and Business Media LLC
Subject
Multidisciplinary
Link
http://www.nature.com/articles/s41598-019-38672-x.pdf
Reference43 articles.
1. Ben-Neriah, Y. et al. The chronic myelogenous leukemia- specific P210 protein is the product of the bcr/abl hybrid gene. Science. 233, 212–214 (1986).
2. Elias, M. H. et al. BCR-ABL kinase domain mutations, including 2 novel mutations in imatinib resistant Malaysian chronic myeloid leukemia patients-Frequency and clinical outcome. Leuk Res. 38, 454–459 (2014).
3. Branford, S. et al. High frequency of point mutations clustered within the adenosine triphosphate-binding region of BCR/ABL in patients with chronic myeloid leukemia or Ph-positive acute lymphoblastic leukemia who develop imatinib (STI571) resistance. Blood. 99, 3472–3475 (2002).
4. Branford, S. 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. 102, 276–283 (2003).
5. Jackson, P. & Baltimore, D. N-terminal mutations activate the leukemogenic potential of the myristoylated form of c-abl. EMBO J. 8, 449–456 (1989).
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