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- Christophe Barthe, Marie-Josée Gharbi, Valérie Lagarde, Claudine Chollet, Pascale Cony-Makhoul, Josy Reiffers, John M Goldman, Junia V Melo, and François Xavier Mahon.
- Laboratoire de Greffe de Moelle et Laboratoire d'hématologie, Université Victor Segalen and Service des Maladies du Sang, CHU de Bordeaux, Bordeaux, France.
- Br. J. Haematol. 2002 Oct 1; 119 (1): 109-11.
AbstractThe Abl kinase inhibitor STI571 (imatinib mesylate) induces haematological remissions in many patients with chronic myeloid leukaemia (CML) but advanced stage CML usually becomes resistant to STI571. We describe a patient in whom progressive resistance to STI571 correlated with the appearance of a mutation in the Bcr-Abl kinase domain. This was a G to A transition that resulted in a glutamic acid to lysine substitution at position 255 (E255K) in the Abl type 1a protein. We suggest that the acquisition of point-mutations in the tyrosine kinase domain of Bcr-Abl may cause progressive clinical resistance to STI571.
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