ABL001 – a new BCR-ABL inhibitor for chronic myeloid leukemia (CML) treatment
Defining Suboptimal Response to BCR-ABL TKI Therapy in CML
Gleevecs mechanism of Action
Second-generation tyrosine kinase inhibitors for chronic myeloid leukemia
Managing BCR-ABL Inhibitor Associated Skin Rash
Bcr-Abl tyrosine-kinase inhibitors (TKI) are the first-line therapy for most patients with chronic myelogenous leukemia (CML). More than 90% of CML cases are caused by a chromosomal abnormality that results in the formation of a so-called Philadelphia chromosome. This abnormality was discovered by Peter Nowell in 1960 and is a consequence of fusion between the Abelson (Abl) tyrosine kinase gene at chromosome 9 and the break point cluster (Bcr) gene at chromosome 22, resulting in a chimeric oncogene (Bcr-Abl) and a constitutively active Bcr-Abl tyrosine kinase that has been implicated in the pathogenesis of CML. Compounds have been developed to selectively inhibit the tyrosine kinase.
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