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The epidermal growth factor receptor variant III ( EGFR v III ): where wild things are altered
Author(s) -
Gan Hui K.,
Cvrljevic An.,
Johns Terrance G.
Publication year - 2013
Publication title -
the febs journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.981
H-Index - 204
eISSN - 1742-4658
pISSN - 1742-464X
DOI - 10.1111/febs.12393
Subject(s) - epidermal growth factor receptor , internalization , downregulation and upregulation , exon , cancer research , biology , epidermal growth factor , mutant , mutation , gene , receptor , microbiology and biotechnology , genetics
The epidermal growth factor receptor ( EGFR ) is overexpressed in a variety of human epithelial tumors, often as a consequence of gene amplification. Tumors with EGFR gene amplification frequently contain EGFR gene rearrangements, with the most common extracellular domain mutation being EGFR v III . This mutation leads to a deletion of exons 2–7 of the EGFR gene and renders the mutant receptor incapable of binding any known ligand. Despite this, EGFR v III displays low‐level constitutive signaling that is augmented by reduced internalization and downregulation. Aberrant EGFR v III signaling has been shown to be important in driving tumor progression and often correlates with poor prognosis. It is clear that EGFR v III is expressed in a considerable proportion of patients with glioblastoma multiforme ( GBM ). The presence of EGFR v III in other tumor types, however, remains controversial. In this review, we critically analyze the evidence for the expression of EGFR v III in a range of tumor types and discuss recent findings pertinent to its function and biology in GBM .