Mutant EGFR is required for maintenance of glioma growth in vivo, and its ablation leads to escape from receptor dependence.
about
Urokinase receptor and resistance to targeted anticancer agentsA kinome-wide RNAi screen in Drosophila Glia reveals that the RIO kinases mediate cell proliferation and survival through TORC2-Akt signaling in glioblastomaNeutralizing the EGF receptor in glioblastoma cells stimulates cell migration by activating uPAR-initiated cell signaling.uPAR induces expression of transforming growth factor β and interleukin-4 in cancer cells to promote tumor-permissive conditioning of macrophages.EGFR soluble isoforms and their transcripts are expressed in meningiomas.Expression of miR-17-92 enhances anti-tumor activity of T-cells transduced with the anti-EGFRvIII chimeric antigen receptor in mice bearing human GBM xenograftsDevelopment of an EGFRvIII specific recombinant antibodyTraumatic Brain Injury Induces Genome-Wide Transcriptomic, Methylomic, and Network Perturbations in Brain and Blood Predicting Neurological Disorders.Distribution of gefitinib to the brain is limited by P-glycoprotein (ABCB1) and breast cancer resistance protein (ABCG2)-mediated active effluxPro-neural miR-128 is a glioma tumor suppressor that targets mitogenic kinases.A urokinase receptor-Bim signaling axis emerges during EGFR inhibitor resistance in mutant EGFR glioblastoma.Gene expression patterns in the hippocampus during the development and aging of Glud1 (Glutamate Dehydrogenase 1) transgenic and wild type miceCrosstalk between the urokinase-type plasminogen activator receptor and EGF receptor variant III supports survival and growth of glioblastoma cells.Development of Resistance to EGFR-Targeted Therapy in Malignant Glioma Can Occur through EGFR-Dependent and -Independent Mechanisms.Soluble Urokinase Receptor Is Released Selectively by Glioblastoma Cells That Express Epidermal Growth Factor Receptor Variant III and Promotes Tumor Cell Migration and Invasion.Rational development and characterization of humanized anti-EGFR variant III chimeric antigen receptor T cells for glioblastomaGlucose-dependent acetylation of Rictor promotes targeted cancer therapy resistance.Therapeutic targeting of epidermal growth factor receptor in human cancer: successes and limitations.Pertussis Toxin Is a Robust and Selective Inhibitor of High Grade Glioma Cell Migration and Invasion.Complex oncogenic signaling networks regulate brain tumor-initiating cells and their progenies: pivotal roles of wild-type EGFR, EGFRvIII mutant and hedgehog cascades and novel multitargeted therapies.Targeting EGFR for treatment of glioblastoma: molecular basis to overcome resistance.NABTT 0502: a phase II and pharmacokinetic study of erlotinib and sorafenib for patients with progressive or recurrent glioblastoma multiforme.EGFR mutation-induced alternative splicing of Max contributes to growth of glycolytic tumors in brain cancer.Delivery of molecularly targeted therapy to malignant glioma, a disease of the whole brain.Immune-checkpoint blockade and active immunotherapy for glioma.Suppression of microRNA-9 by mutant EGFR signaling upregulates FOXP1 to enhance glioblastoma tumorigenicity.The ShcD signaling adaptor facilitates ligand-independent phosphorylation of the EGF receptor.Mechanism of chemoresistance against tyrosine kinase inhibitors in malignant glioma.Chimeric antigen receptor-modified T cells for the treatment of solid tumors: Defining the challenges and next steps.The expression of calcitonin receptor detected in malignant cells of the brain tumour glioblastoma multiforme and functional properties in the cell line A172.Selective coexpression of VEGF receptor 2 in EGFRvIII-positive glioblastoma cells prevents cellular senescence and contributes to their aggressive nature.P14ARF suppresses tumor-induced thrombosis by regulating the tissue factor pathway.Artesunate enhances the therapeutic response of glioma cells to temozolomide by inhibition of homologous recombination and senescence.MiR-145 reduces ADAM17 expression and inhibits in vitro migration and invasion of glioma cells.Differential gene regulation and tumor inhibitory activities of alpha-, delta- and gamma-tocopherols in estrogen-mediated mammary carcinogenesis.The versatile nature of miR-9/9* in human cancer.EGFRvIII-Stat5 Signaling Enhances Glioblastoma Cell Migration and Survival.
P2860
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P2860
Mutant EGFR is required for maintenance of glioma growth in vivo, and its ablation leads to escape from receptor dependence.
description
2010 nî lūn-bûn
@nan
2010 թուականի Յունուարին հրատարակուած գիտական յօդուած
@hyw
2010 թվականի հունվարին հրատարակված գիտական հոդված
@hy
2010年の論文
@ja
2010年論文
@yue
2010年論文
@zh-hant
2010年論文
@zh-hk
2010年論文
@zh-mo
2010年論文
@zh-tw
2010年论文
@wuu
name
Mutant EGFR is required for ma ...... cape from receptor dependence.
@ast
Mutant EGFR is required for ma ...... cape from receptor dependence.
@en
type
label
Mutant EGFR is required for ma ...... cape from receptor dependence.
@ast
Mutant EGFR is required for ma ...... cape from receptor dependence.
@en
prefLabel
Mutant EGFR is required for ma ...... cape from receptor dependence.
@ast
Mutant EGFR is required for ma ...... cape from receptor dependence.
@en
P2093
P2860
P356
P1476
Mutant EGFR is required for ma ...... cape from receptor dependence.
@en
P2093
Akitake Mukasa
Jill Wykosky
Keith L Ligon
Webster K Cavenee
P2860
P304
P356
10.1073/PNAS.0914356107
P407
P577
2010-01-21T00:00:00Z