References
Gorre ME, Mohammed M, Ellwood K, Hsu N, Paquette R, Rao PN et al. Clinical resistance to STI-571 cancer therapy caused by BCR-ABL gene mutation or amplification. Science 2001; 293: 876–880.
Warmuth M, Simon N, Mitina O, Mathes R, Fabbro D, Manley PW et al. Dual-specific Src and Abl kinase inhibitors, PP1 and CGP76030, inhibit growth and survival of cells expressing Imatinib mesylate-resistant Bcr-Abl kinases. Blood 2003; 101: 664–672.
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.
Al-Ali HK, Heinrich MC, Lange T, Krahl R, Mueller M, Muller C et al. High incidence of BCR-ABL kinase domain mutations and absence of mutations of the PDGFR and KIT activation loops in CML patients with secondary resistance to Imatinib. Hematol J 2004; 5: 55–60.
Gambacorti-Passerini CB, Gunby RH, Piazza R, Galietta A, Rostagno R, Scapozza L . Molecular mechanisms of resistance to Imatinib in Philadelphia-chromosome-positive leukaemias. Lancet Oncol 2003; 4: 75–85.
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.
Gambacorti-Passerini C, Zucchetti M, Russo D, Frapolli R, Verga M, Bungaro S et al. Alpha1 acid glycoprotein binds to imatinib (STI571) and substantially alters its pharmacokinetics in chronic myeloid leukemia patients. Clin Cancer Res 2003; 9: 625–632.
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.
Author information
Authors and Affiliations
Corresponding author
Rights and permissions
About this article
Cite this article
Piazza, R., Magistroni, V., Gasser, M. et al. Evidence for D276G and L364I Bcr-Abl mutations in Ph+ leukaemic cells obtained from patients resistant to Imatinib. Leukemia 19, 132–134 (2005). https://doi.org/10.1038/sj.leu.2403453
Received:
Accepted:
Published:
Issue Date:
DOI: https://doi.org/10.1038/sj.leu.2403453
- Springer Nature Limited
This article is cited by
-
Anticipating Clinical Resistance to Target-Directed Agents
Molecular Diagnosis & Therapy (2006)
-
Occurrence of de novo ABL kinase domain mutations in primary bone marrow cells after BCR-ABL gene transfer and Imatinib mesylate selection
Leukemia (2005)
-
Imatinib dose increase up to 1200 mg daily can induce new durable complete cytogenetic remissions in relapsed Ph+ chronic myeloid leukemia patients
Leukemia (2005)
-
D276G mutation is associated with a poor prognosis in imatinib mesylate-resistant chronic myeloid leukemia patients
Leukemia (2005)
-
Response to ‘D276G mutation is associated with a poor prognosis in imatinib mesylate-resistant chronic myeloid leukemia patients’ by Leguay et al
Leukemia (2005)