«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.»
Not exact matches
For example, epidermal growth factor (EGFR) mutations may result in sensitivity to drugs that are EGFR
tyrosine kinase inhibitors (TKIs), such
as erlotinib or gefitinib, whereas individuals with the EGFR T790M mutation are more resistant to these drugs.
(Moussa is listed
as an inventor on a patent application that Georgetown University filed related to nilotinib and the use of other
tyrosine kinase inhibitors for the treatment of neurodegenerative diseases.)
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.
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.
The statement also makes recommendations for clinical guidance and research priorities, such
as optimal choice of EGFR
tyrosine kinase inhibitors (TKIs), management of brain metastasis, role of re-biopsies, and use of circulating free DNA (cfDNA) for molecular studies.
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.
However,
as proposed for the T790M mutation in the EGFR, 31 the significant gain - of - function property conferred by the mutations that we describe here may favor their initial presence before drug selection, and rapid selection during
tyrosine kinase inhibitor - based therapy.
Inform and educate clinicians
as to updates and revisions of their Molecular testing Guideline for the Selection of Lung cancer Patients for Treatment with Targeted
Tyrosine Kinase Inhibitors.
More recently, the chemotherapy agent melphalan has been described
as having efficacy and the newer
tyrosine kinase inhibitors (e.g. Palladia) may prove beneficial.