Among patients with advanced non-small cell lung cancer without a mutation of a certain gene (EGFR), conventional chemotherapy, compared with treatment using epidermal growth factor
receptor tyrosine kinase inhibitors, was associated with improvement in survival without progression of the cancer, but not with overall survival, according to a study in the April 9 issue of JAMA.
Multi-center, placebo - controlled, double - blind, randomized study of oral toceranib phosphate (SU11654),
a receptor tyrosine kinase inhibitor, for the treatment of dogs with recurrent (either local or distant) mast cell tumor following surgical excision.
Not exact matches
Epidermal growth factor
receptor (EGFR)
tyrosine kinase inhibitors (TKIs) are the preferred treatment option for patients with advanced non-small cell lung cancer (NSCLC) who have mutations in the EGFR gene.
Approximately 10 - 15 % of Caucasian and 30 - 35 % of Asian patients with NSCLC have a mutation in the epidermal growth factor
receptor (EGFR), which can be successfully targeted with EGFR
inhibitors called
tyrosine kinase inhibitors (TKI), such as erlotinib, gefitinib and afatinib.
The researchers, including scientists from pharmaceutical company AstraZeneca, report in an advanced online publication in Nature Medicine on May 4, that their findings indicate «an underappreciated genomic heterogeneity» in mechanisms of resistance to
tyrosine kinase inhibitor (TKI) drugs that target the Epidermal Growth Factor
Receptor (EGFR) mutation that drive some cases of non-small cell lung cancer (NSCLC).
In 2005, Cagan's team created a general fly model of a human thyroid tumor caused by mutations in the Ret
receptor tyrosine kinase gene, then screened a panel of drugs including a
kinase inhibitor called vandetanib that suppressed the tumor (Cancer Res, 65:3538 - 41, 2005).
Scanning electron micrograph of the coronary microvasculature of a mouse that has been treated with a small molecule
tyrosine kinase inhibitor of platelet - derived growth factor
receptor beta.
The researchers also screened more than 100 anticancer compounds to see whether they killed lab - grown cancer cells from the devils and found that both strains responded to
inhibitors of proteins known as
receptor tyrosine kinases.
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.
«In the near future, we'll likely see more medications specifically targeting
receptors on cells involved in allergic reactions, such as
tyrosine kinase inhibitors (mast cells), for dermatologic use.»
Investigated TAM family
receptor tyrosine kinase gene expression in response to small molecule
inhibitors in glioblastoma multiforme