Diversity and frequency of epidermal growth factor receptor mutations in human glioblastomas.

By L. Frederick, Xiao Wang, G. Eley, C. James. Cancer Research, 2000

706 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/3ad22d8667ade152827b11a2fccb6cce789da58b

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Citations in the corpus

Glioblastoma: pathology, molecular mechanisms and markers (2015, background): “In adult GBMs, high-level genomic amplification (~40 %) occurs in the EGFR gene, often along with constitutively activating mutations in this protein’s ectodomain mainly through the variant III (vIII) deletion event [46, 93, 114, 123, 178].”
Mechanism for activation of the EGF receptor catalytic domain by the juxtamembrane segment (2009, unknown): “Analysis of EGFR mutations in cancer patients has shown that deletion of the C-terminal tail can drive constitutive EGFR activation (Frederick et al., 2000).”
Malignant astrocytic glioma: genetics, biology, and paths to treatment. (2007, background): “An EGFR mutant allele with deletion of exons 2–7 (known variously as EGFR-vIII, (cid:5) EGFR, or EGFR*) occurs in 20–30% of all human GBM (and in 50%–60% of those that have amplified wild-type EGFR), making it the most common EGFR mutant (Sugawa et al. 1990; Frederick et al. 2000).”
ERBB receptors: From oncogene discovery to basic science to mechanism-based cancer therapeutics (2014, background): “EGFRc958 lacks amino acids 521–603 and displays increased, ligand-dependent kinase activity (Frederick et al., 2000).”
Epidemiologic and Molecular Prognostic Review of Glioblastoma (2014, background): “EGFRvIII (variant III) is the most common mutation among EGFR amplified GBMs and has been described in approximately 60–70% of these tumors (120, 122).”
Hypoxia and the hypoxia-inducible-factor pathway in glioma growth and angiogenesis. (2005, background): “EGFR gene amplifi cation and/or overexpression is seen frequently in a variety of tumors, including GBM, and is associated with a poor prognosis (Frederick et al., 2000).”
Prognostic value of epidermal growth factor receptor in patients with glioblastoma multiforme. (2003, background): “Our finding suggests the existence of other types of mutations that conserve the cytoplasmic domain near the COOH-terminal tails reported by others (34, 35, 66).”
The Epidermal Growth Factor Receptor Pathway: A Model for Targeted Therapy (2006, background): “Ligand-independent receptor activation occurs in some tumors that display forms of the EGFR and HER that have a deletion of the extracellular domain that result in constitutive receptor activation (5, 6).”