Molecular and chromosomal mechanisms of resistance to imatinib (STI571) therapy

By A. Hochhaus, S. Kreil, A. Corbin, P. L. Rosée, M. Müller, T. Lahaye, Benjamin Hanfstein, C. Schoch, N. Cross, U. Berger and 3 more. Leukemia, 2002

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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. (2003, background): “mg because of 100% Ph positive (19), acquired”
Bcr-Abl kinase domain mutations, drug resistance, and the road to a cure for chronic myeloid leukemia. (2007, background): “F311L(23)) may be ‘propped up’ by mechanisms such as increased Bcr-Abl expression or drug efflux.(24)”
Characterization of AMN107, a selective inhibitor of native and mutant Bcr-Abl. (2005, background): “Relapse is often associated with point mutations in Bcr-Abl that reduce the binding affinity of imatinib, or occasionally with amplification of the BCR-ABL gene (Gorre et al., 2001; Cowan-Jacob et al., 2004; le Coutre et al., 2000; Weisberg and Griffin, 2000; Mahon et al., 2000; Campbell et al., 200”
Dasatinib induces notable hematologic and cytogenetic responses in chronic-phase chronic myeloid leukemia after failure of imatinib therapy. (2007, neutral): “Median age, y (range) 59 (24-79) 59 (24-79) 59 (24-79)”
BCR-ABL tyrosine kinase inhibitors in the treatment of Philadelphia chromosome positive chronic myeloid leukemia: a review. (2010, background): “It has been shown that both mechanism produces an increase in BCR-ABL protein levels, and this restores oncogenic signaling in presence of a given drug concentration [96].”