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.
Not exact matches
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.
They found higher levels of JAK1 in resistant tumors, which caused increased expression of epidermal growth
factor receptor (EGFR)-- a
receptor tyrosine kinase that promotes cell proliferation.
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 1995, I began graduate studies on signal transduction by growth
factors and
receptor tyrosine kinases in the laboratory of Graeme Guy at the Institute of Molecular and Cell Biology (IMCB) in Singapore, obtaining my PhD in 2000.
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).
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.
Gene expression in papillary thyroid carcinomas, with special reference to
tyrosine kinase receptors and growth
factors.
Scanning electron micrograph of the coronary microvasculature of a mouse that has been treated with a small molecule
tyrosine kinase inhibitor of platelet - derived growth
factor receptor beta.
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
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