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ATYPICAL BCR-ABL BREAKPOINTS DISPLAY SELECTIVE RESPONSIVENESS TO TYROSINE KINASE INHIBITORS
Vol 32, Issue 4S1, 2018
Abstract
The BCR-ABL oncoprotein is the culprit of CML as it transforms the hematopoietic stem cell by alteringits survival and proliferation properties. The efficacy of Tyrosine Kinase Inhibitors (TKIs) of the canonicalBCR-ABL variants e1a2 (p190), e13a2 or e14a2 (p210) has been well established. Alternative breakpointsinvolving different BCR and/or ABL exons have been previously described but yet to be characterized.We analyzed 50 CML patients, not presenting the canonical isoforms, finding three atypical BCR-ABLbreakpoints in five subjects: one e12a2ins/del, three 13a3 and one e14a3 transcripts. These atypical isoforms(with the addition of two further deletion mutants lacking the BCR DC2 domain or the ABL SH3 domain)were investigated for their catalytic activity, transforming potential and TKI responsiveness.
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Medical Genetics, University of Torino Medical School, Italy
Department of Biomedical, Surgical and Dental Sciences, University of Milan, Italy