Targeting ErbB receptors in high-grade glioma.

Détails

ID Serval
serval:BIB_32B8FE26F80F
Type
Article: article d'un périodique ou d'un magazine.
Sous-type
Synthèse (review): revue aussi complète que possible des connaissances sur un sujet, rédigée à partir de l'analyse exhaustive des travaux publiés.
Collection
Publications
Titre
Targeting ErbB receptors in high-grade glioma.
Périodique
Current pharmaceutical design
Auteur⸱e⸱s
Berezowska S., Schlegel J.
ISSN
1873-4286 (Electronic)
ISSN-L
1381-6128
Statut éditorial
Publié
Date de publication
2011
Peer-reviewed
Oui
Volume
17
Numéro
23
Pages
2468-2487
Langue
anglais
Notes
Publication types: Journal Article ; Research Support, Non-U.S. Gov't ; Review
Publication Status: ppublish
Résumé
High-grade gliomas, including glioblastoma, are among the most malignant and treatment-refractory human neoplasms. The tumors show high levels of resistance to conventional therapies (i.e. surgery, irradiation, and chemotherapy), and despite treatment advances patient outcome remains poor. New therapeutic options are needed. An especially interesting idea is the rational development of new therapies targeting molecules in cancer specific signaling pathways, thereby ideally increasing treatment efficacy and minimizing toxicity. Clearly, rational design requires thorough understanding of the molecular pathogenesis and resistance mechanisms. One highly promising approach is the targeted inhibition of ErbB growth factor receptors, which are recognized as key signaling pathways in many types of human tumors, including high-grade glioma. The ErbB receptor family of tyrosine kinases comprises four members: epidermal growth factor receptor (EGFR/ErbB1/HER1), ErbB2 (HER2/neu), ErbB3 (HER3) and ErbB4 (HER4). Physiologically, signaling is induced by ligand initiated receptor homo- or heterodimerization, activating intracellular downstream signaling pathways and leading to increased cell proliferation, anti-apoptosis and migration. A truncated, constitutively activated mutant EGFR (EGFRvIII) is associated with poor survival in GBM. Thus, to date anti-ErbB approaches are mainly focused on EGFR. The two major classes of anti-ErbB therapeutics are monoclonal antibodies (e.g. cetuximab, panitumumab) and small molecule Tyrosine kinase inhibitors (TKI, e.g. gefitinib, erlotinib, lapatinib). Some compounds entered clinical trials already, but clinical efficacy needs to be enhanced. Here we review current therapeutic advances targeting ErbB receptors in high-grade gliomas, and give a concise overview on current understanding of ErbB biology in gliomas, paving the way to novel rational therapeutic development.
Mots-clé
Animals, Antineoplastic Agents/pharmacology, Antineoplastic Agents/therapeutic use, Brain Neoplasms/drug therapy, Brain Neoplasms/genetics, Brain Neoplasms/metabolism, Brain Neoplasms/pathology, ErbB Receptors/antagonists & inhibitors, ErbB Receptors/genetics, Glioblastoma/drug therapy, Glioblastoma/genetics, Glioblastoma/metabolism, Glioblastoma/pathology, Humans, Neoplasm Grading, Neoplastic Stem Cells/drug effects, Neoplastic Stem Cells/metabolism, Oncogene Proteins v-erbB/metabolism, Signal Transduction/drug effects
Pubmed
Web of science
Création de la notice
29/06/2020 12:12
Dernière modification de la notice
30/06/2020 5:26
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