Chronic myelogenous leukemia (CML) is characterized by Philadelphia (Ph) chromosome with a chimeric gene BCR-ABL created by reciprocal t(9:22) (q34;q11) translocation. Variant Ph chromosome translocations involving chromosomes other than 9 and 22 are found in 5-10% of CML cases. We here report a CML patient who carries a four-way Ph chromosome translocation, t(9;22;15;19) (q34;q11;q15;q13). The patient was diagnosed in 1997 and initially treated with hydroxyurea. In 2002, treatment with imatinib, a selective BCR-ABL tyrosine kinase inhibitor (TKI), was started but Ph-positive chromosomes remained at the levels of 42-65%, indicating imatinib failure. In 2006, the point mutations of F359I and L387M were detected in BCR/ABL gene, which may be related to imatinib failure. Treatment with nilotinib, a TKI with high target specificity, was then started which resulted in durable major molecular response. Administration of nilotinib offered an effective treatment in a CML patient with variant Ph chromosome translocations and BCR-ABL point mutations after imatinib failure.
Chronic myelogenous leukemia ( CML ) is characterized by Philadelphia ( Ph ) chromosome with a chimeric gene BCR - ABL created by reciprocal t(9:22 ) ( q34;q11 ) translocation . Variant Ph chromosome translocations involving chromosomes other than 9 and 22 are found in 5 - 10 % of CML cases . We here report a CML patient who carries a four - way Ph chromosome translocation , t(9;22;15;19 ) ( q34;q11;q15;q13 ) . The patient was diagnosed in 1997 and initially treated with hydroxyurea . In 2002 , treatment with imatinib , a selective BCR - ABL tyrosine kinase inhibitor ( TKI ) , was started but Ph - positive chromosomes remained at the levels of 42 - 65 % , indicating imatinib failure . In 2006 , the point mutations of F359I and L387 M were detected in BCR / ABL gene , which may be related to imatinib failure . Treatment with nilotinib , a TKI with high target specificity , was then started which resulted in durable major molecular response . Administration of nilotinib offered an effective treatment in a CML patient with variant Ph chromosome translocations and BCR - ABL point mutations after imatinib failure .
What tyrosine kinase, involved in a Philadelphia- chromosome positive chronic myelogenous leukemia, is the target of Imatinib (Gleevec)?
What tyrosine kinase , involved in a Philadelphia- chromosome positive chronic myelogenous leukemia , is the target of Imatinib ( Gleevec ) ?
BCR-ABL
BCR-ABL