Secondary imatinib resistance associated with an aberrant bcr-abl fusion gene (original) (raw)
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- Published: 11 March 2004
Leukemia volume 18, pages 1020–1021 (2004)Cite this article
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TO THE EDITOR
Imatinib (Glivec®) induces major cytogenetic responses in the vast majority of newly diagnosed CML patients. Most of these responses are durable, but a minority of patients progress to accelerated phase and eventually to blast crisis. Mechanisms causing this secondary resistance have been described and include mutations in the ATP binding site of Abl and amplification of genomic Bcr-Abl.1 Here, we describe a CML patient who showed a remarkable clinical course on imatinib, developing blast crisis after having been in a complete cytogenetic response for more than 2 years. The bcr-abl transcript was aberrant, showing an insert of a ‘kringle’ domain of the Kremen-1 gene, which, to the best of our knowledge, has not been reported before.
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References
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Authors and Affiliations
- Department of Hematology, VU University Medical Center, de Boelelaan 1117, Amsterdam, 1081 HV, The Netherlands
J J W M Janssen, J W van Oostveen, Q Waisfisz, G J Schuurhuis & G J Ossenkoppele - III. Medizinische Universitätsklinik, Fakultät für Klinische Medizin Mannheim der Universität Heidelberg, Germany
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Janssen, J., Hochhaus, A., van Oostveen, J. et al. Secondary imatinib resistance associated with an aberrant bcr-abl fusion gene.Leukemia 18, 1020–1021 (2004). https://doi.org/10.1038/sj.leu.2403338
- Received: 21 January 2004
- Accepted: 06 February 2004
- Published: 11 March 2004
- Issue Date: 01 May 2004
- DOI: https://doi.org/10.1038/sj.leu.2403338