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.
Martinelli G, Soverini S, Rosti G, Cilloni D, Baccarani M . New tyrosine kinase inhibitors in chronic myeloid leukemia. Haematologica 2005; 90: 534–541.
Shah NP, Nicoll JM, Nagar B, Gorre ME, Paquette RL, Kuriyan J et al. Multiple BCR-ABL kinase domain mutations confer polyclonal resistance to the tyrosine kinase inhibitor imatinib (STI571) in chronic phase and blast crisis chronic myeloid leukemia. Cancer Cell 2002; 2: 117–125.
Gabert J, Beillard E, van der Velden VH, Bi W, Grimwade D, Pallisgaard N et al. Standardization and quality control studies of ‘real-time’ quantitative reverse transcriptase polymerase chain reaction of fusion gene transcripts for residual disease detection in leukemia – a Europe Against Cancer program. Leukemia 2003; 17: 2318–2357.
Gruber FX, Lamark T, Anonli A, Sovershaev MA, Olsen M, Gedde-Dahl T et al. Selecting and deselecting imatinib-resistant clones: observations made by longitudinal, quantitative monitoring of mutated BCR-ABL. Leukemia 2005; 19: 2159–2165.
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.
Nalla VK, Rogan PK . Automated splicing mutation analysis by information theory. Hum Mutat 2005; 25: 334–342.
Schindler T, Bornmann W, Pellicena P, Miller WT, Clarkson B, Kuriyan J et al. Structural mechanism for STI-571 inhibition of abelson tyrosine kinase. Science 2000; 289: 1938–1942.
Acknowledgements
We thank Per Arne Standal for providing patient samples and Mikhail Sovershaev for support in graphical design. This study was supported by a grant given by the Northern Norwegian Health Authorities (SFP 54-06).
Author information
Authors and Affiliations
Rights and permissions
About this article
Cite this article
Gruber, F., Hjorth-Hansen, H., Mikkola, I. et al. A novel Bcr-Abl splice isoform is associated with the L248V mutation in CML patients with acquired resistance to imatinib. Leukemia 20, 2057–2060 (2006). https://doi.org/10.1038/sj.leu.2404400
Published:
Issue Date:
DOI: https://doi.org/10.1038/sj.leu.2404400
- Springer Nature Limited
This article is cited by
-
A case report of a truncated ABL1 mutation in 2 cases with Philadelphia chromosome-positive B cell precursor acute lymphoblastic leukemia
International Journal of Hematology (2024)
-
Predicting resistance of clinical Abl mutations to targeted kinase inhibitors using alchemical free-energy calculations
Communications Biology (2018)
-
BCR-ABL isoforms associated with intrinsic or acquired resistance to imatinib: more heterogeneous than just ABL kinase domain point mutations?
Medical Oncology (2012)
-
Imatinib resistance and blast transformation of chronic myeloid leukemia associated with a novel tri-nucleotide insertion mutation of BCR-ABL kinase domain at position K294
Annals of Hematology (2012)
-
Characterization of ABL exon 7 deletion by molecular genetic and bioinformatic methods reveals no association with imatinib resistance in chronic myeloid leukemia
Medical Oncology (2012)