Literature DB >> 24386505

Current Understanding on EGFR and Wnt/β-Catenin Signaling in Glioma and Their Possible Crosstalk.

Indranil Paul1, Seemana Bhattacharya1, Anirban Chatterjee1, Mrinal K Ghosh1.   

Abstract

Glioblastoma multiformes (GBMs) are extensively heterogeneous at both cellular and molecular levels. Current therapeutic strategies include targeting of key signaling molecules using pharmacological inhibitors in combination with genotoxic agents such as temozolomide. In spite of all efforts, the prognosis of glioma patients remains dismal. Therefore, a proper understanding of individual molecular pathways responsible for the progression of GBM is necessary. The epidermal growth factor receptor (EGFR) pathway is probably the most significant signaling pathway clinically implicated in glioma. Not surprisingly, anti-EGFR therapies mostly prevail for therapeutic purposes. The Wnt/β-catenin pathway is well implicated in multiple tumors; however, its role in glioma has only recently started to emerge. We give a concise account of the current understanding of the role of both these pathways in glioma. Last, taking evidences from a limited literature, we outline a number of points where these pathways intersect each other and put forward the possibility of combinatorially targeting them for treatment of glioma.

Entities:  

Keywords:  EGFR; crosstalk; glioma; signaling; β-catenin

Year:  2013        PMID: 24386505      PMCID: PMC3877660          DOI: 10.1177/1947601913503341

Source DB:  PubMed          Journal:  Genes Cancer        ISSN: 1947-6019


  199 in total

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Review 2.  Wnt/beta-catenin signaling in glioma.

Authors:  Kailiang Zhang; Junxia Zhang; Lei Han; Peiyu Pu; Chunsheng Kang
Journal:  J Neuroimmune Pharmacol       Date:  2012-03-28       Impact factor: 4.147

3.  EGFR-dependent migration of glial cells is mediated by reorganisation of N-cadherin.

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4.  Recombinant immunotoxins specific for a mutant epidermal growth factor receptor: targeting with a single chain antibody variable domain isolated by phage display.

Authors:  I A Lorimer; A Keppler-Hafkemeyer; R A Beers; C N Pegram; D D Bigner; I Pastan
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Review 5.  Targeted molecular therapy of malignant gliomas.

Authors:  Santosh Kesari; Naren Ramakrishna; Claire Sauvageot; Charles D Stiles; Patrick Y Wen
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6.  EGFR-AKT-Smad signaling promotes formation of glioma stem-like cells and tumor angiogenesis by ID3-driven cytokine induction.

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Review 7.  Wnt/beta-catenin signaling pathway as a novel cancer drug target.

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9.  Glycogen synthase kinases-3beta controls differentiation of malignant glioma cells.

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  70 in total

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2.  Functional IRGM polymorphism is associated with language impairment in glioma and upregulates cytokine expressions.

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3.  Wnt signaling regulation of stem-like properties in human lung adenocarcinoma cell lines.

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Journal:  Med Oncol       Date:  2015-04-04       Impact factor: 3.064

4.  Basic fibroblast growth factor activates β-catenin/RhoA signaling in pulmonary fibroblasts with chronic obstructive pulmonary disease in rats.

Authors:  Zhengxing Ge; Bo Li; Xun Zhou; Yi Yang; Jun Zhang
Journal:  Mol Cell Biochem       Date:  2016-10-13       Impact factor: 3.396

5.  Genomic Correlates of Exceptional Response to ErbB3 Inhibition in Head and Neck Squamous Cell Carcinoma.

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6.  The potential of neurotensin secreted from neuroendocrine tumor cells to promote gelsolin-mediated invasiveness of prostate adenocarcinoma cells.

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7.  Glioblastoma cells vampirize WNT from neurons and trigger a JNK/MMP signaling loop that enhances glioblastoma progression and neurodegeneration.

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8.  3D Mathematical Modeling of Glioblastoma Suggests That Transdifferentiated Vascular Endothelial Cells Mediate Resistance to Current Standard-of-Care Therapy.

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Review 9.  A critical overview of long non-coding RNA in glioma etiology 2016: an update.

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Journal:  Tumour Biol       Date:  2016-09-15

Review 10.  Extracellular vesicles shed by glioma cells: pathogenic role and clinical value.

Authors:  Dimitry A Chistiakov; Vladimir P Chekhonin
Journal:  Tumour Biol       Date:  2014-06-27
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