Sentences with phrase «tyrosine kinase gene»

Investigated TAM family receptor tyrosine kinase gene expression in response to small molecule inhibitors in glioblastoma multiforme

Muller, W. E. & Schacke, H. Characterization of the receptor protein - tyrosine kinase gene from the marine sponge Geodia cydonium.

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).

Not exact matches

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.

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.

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.

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.

Gene expression in papillary thyroid carcinomas, with special reference to tyrosine kinase receptors and growth factors.

The activity of tyrosine kinases is typically regulated in an auto - inhibitory fashion, but the BCR - Abl fusion gene codes for a protein that is «always on» or continuously activated leading to unregulated cell division (i.e. cancer).

The Abl gene expresses a membrane - associated protein, a tyrosine kinase, and the BCR - Abl transcript is also translated into a tyrosine kinase.

This gene is the ABL1 gene of chromosome 9 juxtaposed onto the BCR gene of chromosome 22, coding for a hybrid protein: a tyrosine kinase signalling protein that is «always on», causing the cell to divide uncontrollably.

We are focusing on a few key molecular pathways including; 1) Polycomb - mediated epigenetic gene silencing in the tumor initiation, maintenance, and invasion, 2) c - Met (receptor tyrosine kinase) signal transduction pathways in stemness and migration of these tumor cells, 3) Novel mitogenic signaling pathways that are specific to GSCs, and 4) Identification of radio - and chemo - sensitizing pathway to maximize therapeutic efficacy.

Azoospermia in mice with targeted disruption of the Brek / Lmtk2 (brain - enriched kinase / lemur tyrosine kinase 2) gene.

Mutations in fms related tyrosine kinase 3 (FLT3) gene are the most common mutations found in acute myeloid leukemia (AML) and are characterized by an aggressive phenotype with a high prevalence of relapse.

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.

The NTRK fusions involved a gene segment encoding a tyrosine kinase domain.

The FLT3 tyrosine kinase is one of the most commonly mutated genes in AML, occurring in about 30 % of AML patients at diagnosis.

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.

Abbreviations: ACVR2A, activin A receptor type IIA; BMP, bone morphogenetic protein; BMPR, BMP receptor, type II; CNS, Central nervous system; DA, dopaminergic; DMEM / F12, Dulbecco's modified Eagle's medium nutrient mixture F - 12; E, embryonic day; GDF, growth differentiation factor; GO, gene ontology; KEGG, Kyoto encylopedia of genes and genomes; MAPK, Mitogen - activated protein kinase; mDA, midbrain dopaminergic; PD, Parkinson's disease; RIPA, radioimmunoprecipitation assay; SN, Substantia nigra; TGF - β, transforming growth factor - β; TH, tyrosine hydroxylase; VM, ventral midbrain / mesencephalon; Zeb2, Zinc finger E-box-binding homoeobox 2

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.

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.

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.

In this first - of - a-kind survey, researchers used a forward - looking approach to screen the genes that produce tyrosine kinases — reasoning that somewhere in this genomic landscape they might encounter novel mutations that spur colon cancer and other types of cancer.

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...

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.