Mutation in the ATP-binding site of BCR-ABL in a patient with chronic myeloid leukaemia with increasing resistance to STI571.

Abstract:

:The 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.

journal_name

Br J Haematol

authors

Barthe C,Gharbi MJ,Lagarde V,Chollet C,Cony-Makhoul P,Reiffers J,Goldman JM,Melo JV,Mahon FX

doi

10.1046/j.1365-2141.2002.03708.x

subject

Has Abstract

pub_date

2002-10-01 00:00:00

pages

109-11

issue

1

eissn

0007-1048

issn

1365-2141

pii

3708

journal_volume

119

pub_type

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