Sentences with phrase «by imatinib»
This knowledge laid the foundation for the targeted cancer treatment revolution inaugurated by imatinib (Gleevec ®), which has made another blood cancer, chronic myelogenous leukemia, a controllable, chronic disease for many patients.
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[12] It was marketed in 2001 by Novartis as imatinib mesylate (Gleevec in the US, Glivec in Europe).
In the late 1990s, STI - 571 (imatinib, Gleevec / Glivec) was identified by the pharmaceutical company Novartis (then known as Ciba Geigy) in high - throughput screens for tyrosine kinase inhibitors.
In 2001 imatinib was approved for the treatment of chronic myeloid leukemia, a disease that is almost universally caused by a single genetic mutation, known as the Philadelphia chromosome, and its resulting mutant protein.
It has been shown in imatinib - resistant CML that drug resistance conferred by mutations does not necessarily correlate with proliferative advantage and increased kinase activity.34 Other, non-activating mutations or drug - resistance mechanisms, might be acquired by tumor cells.
These mutant kinases are attractive therapeutic targets, as demonstrated by the efficacy of imatinib in BCR - ABL — positive chronic myelogenous leukemia (CML), 5 as well as in MPD associated with activating alleles involving PDGFRA or PDGFRB.2, 6,7 In addition, activating mutations in the FLT3 receptor tyrosine kinase are the most common genetic event in acute myeloid leukemia (AML), and specific inhibitors of the FMS - like tyrosine kinase 3 (FLT3) have entered late - stage clinical trials.8 Although mutations in tyrosine kinases and in other genes have been identified in a subset of MPD and AML, in many cases the genetic events that contribute to the molecular pathogenesis of these diseases remain unknown.
This work, and that of colleagues Brian Druker and Novartis, led to the development of the kinase inhibitor imatinib (Gleevec) as primary therapy for chronic myelogenous leukemia (CML), and the discovery that imatinib resistance is caused by BCR - ABL kinase domain mutations.