BCR-ABL gene amplification and overexpression in a patient with chronic myeloid leukemia treated with imatinib
D Gadzicki, N von Neuhoff, D Steinemann… - Cancer genetics and …, 2005 - Elsevier
Imatinib mesylate was designed as an inhibitor targeting the BCR-ABL tyrosine kinase, the
molecular counterpart of the Philadelphia translocation t (9; 22)(q34; q11). We report on a
patient with chronic myeloid leukemia (CML) undergoing acceleration during imatinib
treatment. Cytogenetic analysis revealed four different cell populations: 46, XX, t (9; 22)(q34;
q11), der (18) t (2; 18)(p11; p11)[1]/47, idem, i (17)(q10),− der (18) t (2; 18),+ der (22) t (9;
22)[1]/46, idem,− t (9; 22), der (9) t (9; 22), ider (22) t (9; 22)[12]/47, idem,− t (9; 22), der (9) t …
molecular counterpart of the Philadelphia translocation t (9; 22)(q34; q11). We report on a
patient with chronic myeloid leukemia (CML) undergoing acceleration during imatinib
treatment. Cytogenetic analysis revealed four different cell populations: 46, XX, t (9; 22)(q34;
q11), der (18) t (2; 18)(p11; p11)[1]/47, idem, i (17)(q10),− der (18) t (2; 18),+ der (22) t (9;
22)[1]/46, idem,− t (9; 22), der (9) t (9; 22), ider (22) t (9; 22)[12]/47, idem,− t (9; 22), der (9) t …