EGF receptor amplification and expression in human brain tumours

Chaffanet, Max; Chauvin, Christiane; Lainé, Michèle G.; Berger, François; Chedin, M; Rost, Nathalie; Nissou, Marie-France; Benabid, Alim Louis

doi:10.1016/0959-8049(92)90374-b

Cited by 93 publications

(38 citation statements)

References 18 publications

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“…EGFR is involved in oncogenic transformation, which can be caused by receptor overexpression, autocrine ligand loops, gene amplification, or activating mutations such as the EGFR type III deletion mutant (EGFRvIII; refs. [5][6][7][8].…”

Section: Introductionmentioning

confidence: 99%

Activation of the EGFR Gene Target EphA2 Inhibits Epidermal Growth Factor–Induced Cancer Cell Motility

Larsen

Pedersen

Stockhausen

et al. 2007

Molecular Cancer Research

125

118

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EphA2 overexpression has been reported in many cancers and is believed to play an important role in tumor metastasis and angiogenesis. We show that the activated epidermal growth factor receptor (EGFR) and the cancer-specific constitutively active EGFR type III deletion mutant (EGFRvIII) induce the expression of EphA2 in mammalian cell lines, including the human cancer cell lines A431 and HN5. The regulation is partially dependent on downstream activation of mitogen-activated protein kinase/extracellular signal -regulated kinase kinase and is a direct effect on the EphA2 promoter. Furthermore, EGFR and EphA2 both localize to the plasma membrane and EphA2 coimmunoprecipitates with activated EGFR and EGFRvIII. Ligand activation of EphA2 and EphA2 knockdown by small interfering RNA inhibit EGF-induced cell motility of EGFR-overexpressing human cancer cells, indicating a functional role of EphA2 in EGFR-expressing cancer cells. (Mol Cancer Res 2007;5(3):283 -93)

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Section: Introductionmentioning

confidence: 99%

Activation of the EGFR Gene Target EphA2 Inhibits Epidermal Growth Factor–Induced Cancer Cell Motility

Larsen

Pedersen

Stockhausen

et al. 2007

Molecular Cancer Research

125

118

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“…A role for PI3'K in tumorigenesis is underscored by the identi®cation of activating mutations in both upstream and downstream components of PI3'K signaling pathways in human cancer. For example, ampli®cation of members of the receptor tyrosine kinase family capable of activating PI3'K such as platelet-derived growth factor receptor (PDGFR) and epidermal growth factor receptor (EGFR) genes have been demonstrated in glioblastoma (Chaanet et al, 1992;Smits and Funa, 1998). Identi®cation of PKB/Akt, a transforming oncogene that causes thymic lymphomas in mice (see above), as a major target of PI3'K signaling further supports the importance of PI3'K/PKB in cancer.…”

Section: Importance Of Pi3'k Signaling In Cancermentioning

confidence: 99%

Modulation of cellular apoptotic potential: contributions to oncogenesis

1999

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“…Increased EGFR expression correlates with a poor clinical outcome in patients with cancer of the lung, bladder, oesophagus, breast, cervix and ovary (Hendler et al, 1989;Fox et al, 1994). Only in glial and head and neck tumours has EGFR over-expression been frequently associated with amplification of the gene (Libermann et al, 1985;Chaffanet et al, 1992;Wong et al, 1992), and on tumour cells expression levels can be increased by several orders of magnitude, suggesting the feasibility of therapeutic strategies that exploit the differential levels of EGFR expression on tumours vs normal cells. Like other growth factor receptors on tumour cells, EGFR may represent a suitable target molecule for antibody-driven therapy.…”

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confidence: 99%