BCR-ABL Mutation (T315I, Y253F, Y253H, E255K, E255V, M351T)

The specific clinical function of BCR-ABL inhibitors resulted in improvements in prognosis, response rate, overall survival, and patient outcomes in Chronic Myloid Leukemia (CML) patients compared to previous treatment regimens. However, complete eradication in CML patients receiving Gleevek limited the occurrence of mutations that were mostly due to mutations in the ABL kinase position 315 (T315I) domain. The second generation BCR-ABL TKIs nilotinib (Tasigna) and dasatinib (Sprycel), showed significant activity in clinical trials of patients intolerant or resistant to Gleecek therapy, except in patients with the T315i BCR-ABL mutation.