Sentences with phrase «tyrosine kinase jak2»

Investigated TAM family receptor tyrosine kinase gene expression in response to small molecule inhibitors in glioblastoma multiforme
More recently, the chemotherapy agent melphalan has been described as having efficacy and the newer tyrosine kinase inhibitors (e.g. Palladia) may prove beneficial.
«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.»
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.
PALLADIA belongs to the tyrosine kinase inhibitor (TKI) class of compounds.
Western blot analysis of of extracts from cells expressing different activated tyrosine kinase proteins, using Phospho - PDGF Receptor (Tyr754)(23B2) Rabbit.
[1] DIM was found to have «lung cancer preventive effects» mediated via modulation of the receptor tyrosine kinase / PI3K / Akt - signaling pathway.
Genistein Inhibits Both Estrogen and Growth Factor — stimulated Proliferation of Human Breast Cancer Cells Cell Growth & Differentiation 1996 (Oct); 7 (10): 1345 — 1351 Genistein is a naturally occurring dietary protein tyrosine kinase (PTK) inhibitor that is hypothesized to be responsible for the lower rate of breast cancer observed in Asian women consuming soy.
In addition to causing the functional inactivation of these phosphatases, low concentrations of H2O2 or an oxidative shift in the GSH: GSSH redox status strongly increases the activity of the basic insulin receptor tyrosine kinase in the absence of insulin.
One of soy's primary isoflavones, genistein, has been shown to inhibit the enzyme tyrosine kinase in the brain.
In fact, numerous animal studies show that soy isoflavones interfere with an enzyme called tyrosine kinase in the hippocampus, a brain region involved with learning and memory.
The product of the resulting BCR - ABL fusion oncogene possesses ABL's so - called tyrosine kinase activity — the ability to add phosphate chemical groups to the amino acid tyrosine — but fails to turn off appropriately.
This reagent, an antibody that detects the phosphotryosine product of the tyrosine kinase reaction, proved crucial to Lydon's enzyme - activity measurements in cells.
Erlotinib, an EGFR tyrosine kinase inhibitor, has proven to be an effective agent in patients with mutations in the EGFR gene, but its efficacy in wild - type EGFR patients was unclear.
Howard Hughes Medical Institute researchers have combed through a catalog of all known tyrosine kinase enzymes to identify new gene mutations that occur in a significant fraction of colon cancers...
According to Vogelstein, genetic mutations can produce a tyrosine kinase that is essentially «turned on» in the absence of a normal activation signal, which is called constitutive activation.
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.
Of particular note were decreased mGluR5 and Tyrosine Kinase c - kit and increased IBA1, CD68, ICAM1, VEGF - D, and TLR4 mRNA expression in Tsc1GFAPCKO mice.
His earlier research focused on BCR - ABL tyrosine kinase function in chronic myeloid leukemia.
Gleevec works so well in chronic myeloid leukemia because it turns off a tyrosine kinase that dramatically reverses the cancer process.»
Hunter's breakthrough, which set the story in motion, was a product of basic research on a chicken RNA tumor virus: the 1979 discovery of the first tyrosine kinase paved the way for our understanding of how cells perceive their environment and respond appropriately to growth signals.
The assay identifies both internal tandem duplication (ITD) and tyrosine kinase domain (TKD) mutations, and identifies even large ITD mutations, missed using many current NGS - based assays.
33) Gandhi J, Zhang J, Xie Y, Shigematsu H, Soh J, Zhang W, Yamamoto H, Peyton M, Girard L, Lockwood WW, Lam WL, Garcia M, Minna JD, Gazdar AF (2009) Alterations in genes of the EGFR signaling pathway and their relationship to EGFR tyrosine kinase inhibitor sensitivity in lung cancer cell lines.
The second most common mutation type in the FLT3 gene is a Tyrosine Kinase Domain (TKD) point mutation in the codon for an aspartate (D835) or an isoleucine (I836) residue that is located in the activation loop of the FLT3 protein.
In particular, he is focused on studying therapeutic resistance to lapatinib, a tyrosine kinase inhibitor of HER2, in breast cancer.
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.
244/2: 30 Functional correction of dwarfism in a mouse model of achondroplasia using the tyrosine kinase inhibitor NVP - BGJ398.
32) Kubo T, Yamamoto H, Lockwood WW, Fujii T, Ouchida M, Soh J, Takigawa J, Kiura K, Shimizu K, Date H, Minna JD, Lam WL, Gazdar AF, Toyooka S (2009) MET gene amplification or EGFR mutation activate MET in lung cancers untreated with EGFR tyrosine kinase inhibitors.
External cues act on tyrosine kinase proteins embedded in the cell membrane to induce a cascade of signals with a vital role in regulating cell proliferation.
Acquired resistance to anti-angiogenic tyrosine kinase inhibitors is an important clinical problem in treating various cancers.
RIPK2 inhibitor 2 appears to inhibit 38 % of the activity of SNARK and 27 % of the activity of FGFR2, GSK3 - β, JNK1, CSNK1G2 (casein kinase 1), and MET tyrosine kinase.
One of the main mechanisms of secondary resistance in patients treated with tyrosine kinase inhibitors is acquisition of new inhibitor - resistant mutations.
Similar results were obtained for the protein tyrosine kinase inhibitor regorafenib (data not shown).
Recently, we and others identified a single recurrent somatic activating mutation (JAK2V617F) in the Janus kinase 2 (JAK2) tyrosine kinase in the myeloproliferative disorders (MPDs) polycythemia vera, essential thrombocythemia, and myeloid metaplasia with myelofibrosis.
The protist, Monosiga brevicollis, has a tyrosine kinase signaling network more elaborate and diverse than found in any known metazoan.
In addition, at least some Eph receptors can also signal through non-canonical mechanisms that are independent of ligand binding and kinase activity, for example through interplay with other receptor tyrosine kinase families and with serine / threonine kinases.
Recently, we and others identified a recurrent somatic activating mutation in the JAK2 tyrosine kinase in polycythemia vera (PV), essential thrombocythemia (ET), and myeloid metaplasia with myelofibrosis (MMM).9 - 13 This mutation results in a valine to phenylalanine substitution at codon 617 within the Jak homology domain 2 (JH2) pseudokinase domain of Janus kinase 2 (JAK2).
The tumor suppressor DAPK is reciprocally regulated by tyrosine kinase Src and phosphatase LAR.
Novel drug therapies and novel indications of drug therapy, e.g. tyrosine kinase inhibitors in lung disease other than lung cancer, biological treatments for asthma, COPD, cystic fibrosis and interstitial lung disease.
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.
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.
The FLT3 tyrosine kinase is one of the most commonly mutated genes in AML, occurring in about 30 % of AML patients at diagnosis.
Muller, W. E. & Schacke, H. Characterization of the receptor protein - tyrosine kinase gene from the marine sponge Geodia cydonium.
The major drawback of tyrosine kinase inhibitor therapy is the development of secondary resistance caused by the acquisition of new mutations.
LabPMM, our internationally harmonized network of accredited laboratories, are the only reference laboratories that provide internationally harmonized, regulatory compliant testing for FLT3 internal tandem duplication (ITD), and Tyrosine Kinase Domain (TKD) mutations.
The NTRK fusions involved a gene segment encoding a tyrosine kinase domain.
Druker also led the original clinical development of Gleevec, which inhibits a biological switch called a tyrosine kinase that is abnormally activated in CML.
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.
FLT3 is a tyrosine kinase important for the development of blood and the immune system.
STAT5 is also activated by the oncogenic breakpoint cluster region (BCR)-- ABL tyrosine kinase and contributes to the transformation of leukemia cells (45).
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