Quantitative analysis of EGFRvIII cellular signaling networks reveals a combinatorial therapeutic strategy for glioblastoma. - Wikidata - wikimedia - TriplyDB

Quantitative analysis of EGFRvIII cellular signaling networks reveals a combinatorial therapeutic strategy for glioblastoma.

Quantitative analysis of EGFRvIII cellular signaling networks reveals a combinatorial therapeutic strategy for glioblastoma.

http://www.wikidata.org/entity/Q34655394

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Studying Cellular Signal Transduction with OMIC Technologies Feedback circuit among INK4 tumor suppressors constrains human glioblastoma development Recent advances in the molecular understanding of glioblastoma Cancer systems biology: a network modeling perspective Identification of a PTEN-regulated STAT3 brain tumor suppressor pathway Ligand-Independent EGFR Signaling Aptamer for imaging and therapeutic targeting of brain tumor glioblastoma Molecular characterizations of glioblastoma, targeted therapy, and clinical results to date The epidermal growth factor receptor variant III (EGFRvIII): where wild things are altered Specific visualization of glioma cells in living low-grade tumor tissue Current Therapeutic Advances Targeting EGFR and EGFRvIII in Glioblastoma Phosphoproteomics of collagen receptor networks reveals SHP-2 phosphorylation downstream of wild-type DDR2 and its lung cancer mutants Mesenchymal stem cells modified with a single-chain antibody against EGFRvIII successfully inhibit the growth of human xenograft malignant glioma Phosphoproteome of human glioblastoma initiating cells reveals novel signaling regulators encoded by the transcriptome EGFR Activation Leads to Cell Death Independent of PI3K/AKT/mTOR in an AD293 Cell Line Biological robustness: paradigms, mechanisms, and systems principles Dual Targeting of PDGFRα and FGFR1 Displays Synergistic Efficacy in Malignant Rhabdoid Tumors Adaptor proteins intersectin 1 and 2 bind similar proline-rich ligands but are differentially recognized by SH2 domain-containing proteins Guanylate binding protein-1 mediates EGFRvIII and promotes glioblastoma growth in vivo but not in vitro.EGFR-targeted therapy in malignant glioma: novel aspects and mechanisms of drug resistance.Vascular endothelial growth factor (VEGF) and platelet (PF-4) factor 4 inputs modulate human microvascular endothelial signaling in a three-dimensional matrix migration context.CellNOptR: a flexible toolkit to train protein signaling networks to data using multiple logic formalisms.Linking proteomic and transcriptional data through the interactome and epigenome reveals a map of oncogene-induced signaling.Incorporating molecular tools into early-stage clinical trials Integrating proteomic, transcriptional, and interactome data reveals hidden components of signaling and regulatory networks.Cytoprotective effect of the elongation factor-2 kinase-mediated autophagy in breast cancer cells subjected to growth factor inhibition.Slit2 inhibits glioma cell invasion in the brain by suppression of Cdc42 activity.In-depth qualitative and quantitative profiling of tyrosine phosphorylation using a combination of phosphopeptide immunoaffinity purification and stable isotope dimethyl labeling A quantitative study of the recruitment potential of all intracellular tyrosine residues on EGFR, FGFR1 and IGF1R.Identifying differentially regulated subnetworks from phosphoproteomic data.Quantification of beta-catenin signaling components in colon cancer cell lines, tissue sections, and microdissected tumor cells using reaction monitoring mass spectrometry.Mutant EGFR is required for maintenance of glioma growth in vivo, and its ablation leads to escape from receptor dependence.Cyclooxygenase-2 is a novel transcriptional target of the nuclear EGFR-STAT3 and EGFRvIII-STAT3 signaling axes Triepitopic antibody fusions inhibit cetuximab-resistant BRAF and KRAS mutant tumors via EGFR signal repression.Tissue factor regulation by epidermal growth factor receptor and epithelial-to-mesenchymal transitions: effect on tumor initiation and angiogenesis.A U87-EGFRvIII cell-specific aptamer mediates small interfering RNA delivery.Stable-isotope dilution LC–MS for quantitative biomarker analysis.EGFRvIII and c-Met pathway inhibitors synergize against PTEN-null/EGFRvIII+ glioblastoma xenografts.Proteogenomic convergence for understanding cancer pathways and networks.Recurrent high-grade glioma: a diagnostic and therapeutic challenge.

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P2860

Quantitative analysis of EGFRvIII cellular signaling networks reveals a combinatorial therapeutic strategy for glioblastoma.

http://www.wikidata.org/entity/Q34655394

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Quantitative analysis of EGFRv ...... tic strategy for glioblastoma.

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Proceedings of the National Academy of Sciences of the United States of America

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Quantitative analysis of EGFRv ...... tic strategy for glioblastoma.

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Akitake Mukasa

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Rudy Bonavia

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Ryan A Flynn

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Webster K Cavenee

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Zachary E Brewer

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P2860

Molecular determinants of the response of glioblastomas to EGFR kinase inhibitors.

MET amplification leads to gefitinib resistance in lung cancer by activating ERBB3 signaling.

A selective small molecule inhibitor of c-Met kinase inhibits c-Met-dependent phenotypes in vitro and exhibits cytoreductive antitumor activity in vivo

Met, metastasis, motility and more

Time-resolved mass spectrometry of tyrosine phosphorylation sites in the epidermal growth factor receptor signaling network reveals dynamic modules

Agonists of the retinoic acid- and retinoid X-receptors inhibit hepatocyte growth factor secretion and expression in U87 human astrocytoma cells.

A novel small molecule met inhibitor induces apoptosis in cells transformed by the oncogenic TPR-MET tyrosine kinase.

Malignant glioma: genetics and biology of a grave matter.

A mutant epidermal growth factor receptor common in human glioma confers enhanced tumorigenicity.

Multiple reaction monitoring for robust quantitative proteomic analysis of cellular signaling networks

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104

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Forest M. White

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