The disease burden in chronic myeloid leukemia (CML) is linked to the activity of its chimeric oncoprotein, the BCR-ABL1 tyrosine kinase. A recent analysis of the IRIS study showed that imatinib, the first tyrosine kinase inhibitors (TKI), resulted in impressive survival and freedom from disease progression in chronic phase patients. However, 20–30% of these patients eventually develop resistance; due largely to mutations at the ABL1 kinase domain.
Anthony A. Oyekunle, Fausto Castagnetti, Gabriele Gugliotta, Simona Soverini, Michele Baccarani, Gianantonio Rosti (2011). F317L BCR-ABL1 kinase domain mutation associated with a sustained major molecular response in a CML patient on dasatinib. LEUKEMIA RESEARCH, 35, e118-e120 [10.1016/j.leukres.2011.03.021].
F317L BCR-ABL1 kinase domain mutation associated with a sustained major molecular response in a CML patient on dasatinib
CASTAGNETTI, FAUSTO;GUGLIOTTA, GABRIELE;SOVERINI, SIMONA;BACCARANI, MICHELE;ROSTI, GIANANTONIO
2011
Abstract
The disease burden in chronic myeloid leukemia (CML) is linked to the activity of its chimeric oncoprotein, the BCR-ABL1 tyrosine kinase. A recent analysis of the IRIS study showed that imatinib, the first tyrosine kinase inhibitors (TKI), resulted in impressive survival and freedom from disease progression in chronic phase patients. However, 20–30% of these patients eventually develop resistance; due largely to mutations at the ABL1 kinase domain.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.
