Today, it is estimated that about a third of pharmaceutical research and development effort goes into
targeting tyrosine kinase receptors and their signaling pathways for cancer therapies.
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.
Not exact matches
The
target for ibrutinib, an enzyme called Bruton's
tyrosine kinase (BTK), is a key component of B - cell receptor signaling.
These receptors, called receptor
tyrosine kinases (RTKs), transmit instructions through the cell wall and down through a cascade of reactions to a
target gene in the nucleus.
Based on the current study results, the team believes a particular enzyme, «dual specificity
tyrosine - regulated
kinase - 1a (DYRK1A),» is the likely
target of harmine.
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.
During the early years of my PhD studies, I was very fascinated by the exciting discoveries in the field of signal transduction, in particular how receptor
tyrosine kinases are activated to transmit their signals and how protein complexes are formed through defined protein folds (domains) interacting with specific cellular
targets.
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).
These therapies, the first an antibody and the second of a class called
tyrosine kinase inhibitors (TKIs), reduce the ability of a
target gene to manufacture the protein it encodes.
D'Oro, U., Vacchio, M.S., Weissman, A.M. & Ashwell, J.D. Activation of the Lck
tyrosine kinase targets cell surface T cell antigen receptors for lysosomal degradation.
In addition to being integral to cell biology,
tyrosine kinases also present
targets for new anticancer therapies: One of the most highly touted, rationally designed anticancer compounds, Gleevec, inhibits an oncogenic
tyrosine kinase whose aberrant activity fuels the rampant growth of cells in patients with chronic myeloid leukemia.
Azoospermia in mice with
targeted disruption of the Brek / Lmtk2 (brain - enriched
kinase / lemur
tyrosine kinase 2) gene.
Targeting of the c - Abl
tyrosine kinase to mitochondria in endoplasmic reticulum stress - induced apoptosis.
Patients receiving
tyrosine kinase inhibitors (TKIs)
targeting EGFR mutations had a longer overall survival (OS) than those who did not receive TKIs, demonstrating the effectiveness of TKIs for LM therapy.
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.
CONCLUSION / INTERPRETATION: These results indicate that R (+) alpha - lipoic acid directly activates lipid,
tyrosine and serine / threonine
kinases in
target cells, which could lead to the stimulation of glucose uptake induced by this natural cofactor.
Engagement of the Insulin - sensitive Pathway in the Stimulation of Glucose Transport by Alpha - lipoic Acid in 3T3 - L1 Adipocytes Diabetologia 2000 (Mar); 43 (3): 294 — 303 These results indicate that R (+) alpha - lipoic acid directly activates lipid,
tyrosine and serine / threonine
kinases in
target cells, which could lead to the stimulation of glucose uptake induced by this natural cofactor.
«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.»