An EGFR wild type–EGFRvIII–HB-EGF feed-forward loop regulates the activation of EGFRvIII
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S. Kesari | S. Pingle | S. Burma | D. Boothman | J. Raisanen | K. Hatanpaa | B. Mickey | A. Habib | D. Cipher | S. Chakraborty | L. Li | V. Puliyappadamba | Z. Wang | C. Madden | C-R Yang | D. Saha | A. Rehman | A. J. Jiwani | Christopher J Madden | Li Li | Sharmistha Chakraborty | Chin-Rang Yang | Alizeh Rehman | Ameena J. Jiwani | Bruce E. Mickey | Debabrata Saha | Zhixiang Wang | Santosh Kesari | B. E. Mickey
[1] S. Burma,et al. Opposing effect of EGFRWT on EGFRvIII-mediated NF-κB activation with RIP1 as a cell death switch. , 2013, Cell reports.
[2] J. Pollack,et al. EGFRvIII gene rearrangement is an early event in glioblastoma tumorigenesis and expression defines a hierarchy modulated by epigenetic mechanisms , 2013, Oncogene.
[3] S. Hariono,et al. Kinetics of inhibitor cycling underlie therapeutic disparities between EGFR-driven lung and brain cancers. , 2012, Cancer discovery.
[4] Paul S Mischel,et al. Differential sensitivity of glioma- versus lung cancer-specific EGFR mutations to EGFR kinase inhibitors. , 2012, Cancer discovery.
[5] J. Sarkaria,et al. Activation of Rac1 by Src-dependent phosphorylation of Dock180(Y1811) mediates PDGFRα-stimulated glioma tumorigenesis in mice and humans. , 2011, The Journal of clinical investigation.
[6] D. Housman,et al. Chronic activation of wild-type epidermal growth factor receptor and loss of Cdkn2a cause mouse glioblastoma formation. , 2011, Cancer research.
[7] O. Bogler,et al. Cancer Genes and Genomics Forced Dimerization Increases the Activity of D EGFR / EGFRvIII and Enhances Its Oncogenicity , 2011 .
[8] S. Lawler,et al. The role of sphingosine kinase-1 in EGFRvIII-regulated growth and survival of glioblastoma cells , 2011, Journal of Neuro-Oncology.
[9] S. Burma,et al. Epidermal growth factor receptor in glioma: signal transduction, neuropathology, imaging, and radioresistance. , 2010, Neoplasia.
[10] Yoshitaka Narita,et al. Tumor heterogeneity is an active process maintained by a mutant EGFR-induced cytokine circuit in glioblastoma. , 2010, Genes & development.
[11] J. Rak,et al. Oncogenic epidermal growth factor receptor up-regulates multiple elements of the tissue factor signaling pathway in human glioma cells. , 2010, Blood.
[12] Derek Toomre,et al. Spatial control of EGF receptor activation by reversible dimerization on living cells , 2010, Nature.
[13] S. Gabriel,et al. Integrated genomic analysis identifies clinically relevant subtypes of glioblastoma characterized by abnormalities in PDGFRA, IDH1, EGFR, and NF1. , 2010, Cancer cell.
[14] J. Schlessinger,et al. Cell Signaling by Receptor Tyrosine Kinases , 2000, Cell.
[15] Forest M White,et al. Oncogenic EGFR Signaling Networks in Glioma , 2009, Science Signaling.
[16] A. Scott,et al. The plasticity of oncogene addiction: implications for targeted therapies directed to receptor tyrosine kinases. , 2009, Neoplasia.
[17] D. Housman,et al. Oncogenic EGFR signaling cooperates with loss of tumor suppressor gene functions in gliomagenesis , 2009, Proceedings of the National Academy of Sciences.
[18] K. Ferguson,et al. Structure-based view of epidermal growth factor receptor regulation. , 2008, Annual review of biophysics.
[19] P. Wright,et al. RIP1 links inflammatory and growth factor signaling pathways by regulating expression of the EGFR , 2008, Cell Death and Differentiation.
[20] Keith L. Ligon,et al. Coactivation of Receptor Tyrosine Kinases Affects the Response of Tumor Cells to Targeted Therapies , 2007, Science.
[21] Forest M White,et al. Quantitative analysis of EGFRvIII cellular signaling networks reveals a combinatorial therapeutic strategy for glioblastoma , 2007, Proceedings of the National Academy of Sciences.
[22] A. Scott,et al. The Efficacy of Epidermal Growth Factor Receptor–Specific Antibodies against Glioma Xenografts Is Influenced by Receptor Levels, Activation Status, and Heterodimerization , 2007, Clinical Cancer Research.
[23] Patrick Y Wen,et al. Therapeutic advances in the treatment of glioblastoma: rationale and potential role of targeted agents. , 2006, The oncologist.
[24] Kimmo J Hatanpaa,et al. Differential gene expression analysis reveals generation of an autocrine loop by a mutant epidermal growth factor receptor in glioma cells. , 2006, Cancer research.
[25] W. Cavenee,et al. Immunohistochemical analysis of the mutant epidermal growth factor, ΔEGFR, in glioblastoma , 2006, Brain Tumor Pathology.
[26] Koji Yoshimoto,et al. Molecular determinants of the response of glioblastomas to EGFR kinase inhibitors. , 2005, The New England journal of medicine.
[27] Qian Wang,et al. Control of epidermal growth factor receptor endocytosis by receptor dimerization, rather than receptor kinase activation , 2005, EMBO reports.
[28] L. Gunaratnam,et al. Silencing of epidermal growth factor receptor suppresses hypoxia-inducible factor-2-driven VHL-/- renal cancer. , 2005, Cancer research.
[29] A. Scott,et al. The tumor-specific de2–7 epidermal growth factor receptor (EGFR) promotes cells survival and heterodimerizes with the wild-type EGFR , 2004, Oncogene.
[30] P. Kleihues,et al. Predominant Expression of Mutant EGFR (EGFRvIII) is Rare in Primary Glioblastomas , 2004, Brain pathology.
[31] A. Dowlati,et al. Combined inhibition of epidermal growth factor receptor and JAK/STAT pathways results in greater growth inhibition in vitro than single agent therapy. , 2004, Molecular cancer therapeutics.
[32] R. Jove,et al. Spontaneous activation and signaling by overexpressed epidermal growth factor receptors in glioblastoma cells , 2003, International journal of cancer.
[33] Edouard C. Nice,et al. Crystal Structure of a Truncated Epidermal Growth Factor Receptor Extracellular Domain Bound to Transforming Growth Factor α , 2002, Cell.
[34] J. Schlessinger. Cell Signaling by Receptor Tyrosine Kinases , 2000, Cell.
[35] Careen K. Tang,et al. Epidermal growth factor receptor vIII enhances tumorigenicity in human breast cancer. , 2000, Cancer research.
[36] H. Varmus,et al. A constitutively active epidermal growth factor receptor cooperates with disruption of G1 cell-cycle arrest pathways to induce glioma-like lesions in mice. , 1998, Genes & development.
[37] K. Mishima,et al. Heparin-binding epidermal growth factor-like growth factor stimulates mitogenic signaling and is highly expressed in human malignant gliomas , 1998, Acta Neuropathologica.
[38] H. Wiley,et al. The Enhanced Tumorigenic Activity of a Mutant Epidermal Growth Factor Receptor Common in Human Cancers Is Mediated by Threshold Levels of Constitutive Tyrosine Phosphorylation and Unattenuated Signaling* , 1997, The Journal of Biological Chemistry.
[39] O. Bogler,et al. A common mutant epidermal growth factor receptor confers enhanced tumorigenicity on human glioblastoma cells by increasing proliferation and reducing apoptosis. , 1996, Cancer research.
[40] R. B. Montgomery,et al. Transformational and altered signal transduction by a naturally occurring mutant EGF receptor. , 1996, Oncogene.
[41] P. Humphrey,et al. Epidermal growth factor ligand-independent, unregulated, cell-transforming potential of a naturally occurring human mutant EGFRvIII gene. , 1995, Cell growth & differentiation : the molecular biology journal of the American Association for Cancer Research.
[42] W. Cavenee,et al. A mutant epidermal growth factor receptor common in human glioma confers enhanced tumorigenicity. , 1994, Proceedings of the National Academy of Sciences of the United States of America.
[43] J. Barrett,et al. Immunocytochemical study of transforming growth factor expression in benign and malignant gliomas. , 1989, The American journal of pathology.
[44] Hermona Soreq,et al. Amplification, enhanced expression and possible rearrangement of EGF receptor gene in primary human brain tumours of glial origin , 1985, Nature.