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 events occur when specific extracellular molecules bind to receptor proteins in the plasma membrane known
as receptor tyrosine kinases and heterotrimeric G - protein - coupled receptors.
Not exact matches
PDGFRα is a cell surface
tyrosine kinase receptor involved in organ development and tumor progression, it is present in multiple cell types such
as mesenchymal cells, neurons, astrocytes, megakaryocytes and oligodendrocyte progenitor.
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.
We review progress with the
receptor tyrosine kinases (growth factor
receptors EGFR, VEGFR, and FGFR) and nonreceptor
tyrosine kinases (Bcr - Abl), where advances have been made with cancer therapeutic agents such
as Herceptin and Gleevec.
Sina Koch (Ehninger, TUD)-- «Aberrant subcellular localization
as a potential mechanism contributing to the abnormal signaling of the mutant Flt3 - ITd
receptor tyrosine kinase in acute myeloid leukemia» (2007)
Further, we identified a role for ABL
kinases in promoting the expression of multiple pro — bone metastasis genes such
as AXL (which encodes a
receptor tyrosine kinase), IL6 (which encodes interleukin - 6), MMP1 (which encodes matrix metalloproteinase 1), and TNC (which encodes tenascin - C) through TAZ - and signal transducer and activator of transcription 5 (STAT5)-- mediated signaling.
Also, genes that code for
receptor tyrosine kinases, a family of
receptors on the surface of cells, may rearrange to form multiple distinct gene fusion partners,
as evidenced in an article by Kulkarni, et al, on a translational study involving a patient who developed a BRAF fusion following treatment with a BRAF inhibitor1.
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 2005, the identification of an activating mutation in JAK2 (the V617F mutation)
as a STAT5 - activating and disease - causing genetic alteration in a significant proportion of patients with myeloproliferative neoplasms (MPNs) has emphasized the oncogenic role of the JAK
tyrosine kinases in hematologic malignancies.2 — 5 JAK2 is a member of the Janus
tyrosine kinase family comprising three other mammalian non-receptor
tyrosine kinases (JAK1, JAK3 and TYK2) that associate with cytokine
receptors lacking intrinsic
kinase activity to mediate cytokine - induced signal transduction and activation of STAT transcription factors.6 All JAKs share a similar protein structure and contain a
tyrosine kinase domain at the C - terminus flanked by a catalytically inactive pseudokinase domain with
kinase - regulatory activity, by an atypical SH2 domain and by a FERM domain that mediates association to the membrane - proximal region of the cytokine
receptors.7, 8 Soon after the discovery of JAK2 V617F, we and others described that activating JAK1 mutations are relatively common in adult patients with T - cell acute lymphoblastic leukemia (ALL) and participate in ALL development allowing for constitutive activation of STAT5.9 — 11 Several STAT5 - activating JAK1 mutations were also reported in AML and breast cancer patients.10
«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.»