Epidermal growth factor-related peptides and their receptors in human malignancies

Salomon, David; Brandt, Ralf; Ciardiello, Fortunato; Normanno, Nicola

doi:10.1016/1040-8428(94)00144-i

Cited by 2,409 publications

(1,570 citation statements)

References 386 publications

Supporting

Mentioning

1,524

Contrasting

Unclassified

Order By: Relevance

“…Three main results emerged from the study. Firstly, both EGFr protein and mRNA content varied widely in both neoplastic tissue and normal mucosa in our CRC patients, in agreement with IHC studies (Salomon et al, 1995;Goldstein and Armin, 2001). Secondly, EGFr expression in the apparently normal colorectal mucosa of our CRC patients supports the idea that EGFr expression may not be exclusive to CRC.…”

Section: Discussionsupporting

confidence: 88%

“…Aberrant regulation of EGFr signalling has been implicated in the development and progression of several different solid tumours (Rubin Grandis et al, 1996;Rusch et al, 1997;Goldstein and Armin, 2001). Colorectal cancer (CRC) is considered a tumour showing EGFr overexpression, but EGFr expression ranges between 25 and 75% (Salomon et al, 1995;Goldstein and Armin, 2001). The discrepancy in this range could be due to several factors.…”

mentioning

confidence: 99%

See 1 more Smart Citation

Molecular determination of epidermal growth factor receptor in normal and neoplastic colorectal mucosa

et al. 2006

View full text Add to dashboard Cite

show abstract

Section: Discussionsupporting

confidence: 88%

mentioning

confidence: 99%

Molecular determination of epidermal growth factor receptor in normal and neoplastic colorectal mucosa

et al. 2006

View full text Add to dashboard Cite

show abstract

“…EGFR is a factor with a key regulatory role in a wide variety of solid malignancies and EGFR signalling cascades have been implicated in cellular processes such as proliferation, angiogenesis, invasion and metastasis (Salomon et al, 1995). Manipulation of this receptor in combination with standard cancer therapies such as chemotherapy and radiotherapy might therefore offer the potential for increased efficacy of established treatments without significantly increasing overall cellular toxicity.…”

Section: Discussionmentioning

confidence: 99%

“…This results in receptor-associated tyrosine kinase activation, which triggers a cascade of downstream signalling pathways resulting in cell cycle progression, proliferation, angiogenesis and cell survival. A wide variety of human tumours including breast, NSCLC, bladder and SCC of the head and neck have been reported as expressing moderate to high levels of EGFR (Salomon et al, 1995). Activation of EGFR has been shown to result in accelerated tumour growth and is associated with a poor patient prognosis in many solid tumours (Nicholson et al, 2001).…”

mentioning

confidence: 99%

Differential radiosensitisation by ZD1839 (Iressa), a highly selective epidermal growth factor receptor tyrosine kinase inhibitor in two related bladder cancer cell lines

et al. 2004

View full text Add to dashboard Cite

The epidermal growth factor receptor (EGFR) is expressed in a wide variety of epithelial tumours including carcinoma of the bladder. Stimulation of the EGFR pathway is blocked by ZD1839 (Iressa), a highly selective EGFR tyrosine kinase inhibitor. Radical radiotherapy is an established organ sparing treatment option for muscle invasive bladder cancer and this study has explored the possibility for the use of ZD1839 as a radiosensitiser in this scenario. The effect of combination treatment with ZD1839 (0.01 mM) and ionising radiation in the established bladder cancer cell lines MGH-U1 and its radiosensitive mutant clone S40b was measured by clonogenic assays. A highly significant radiosensitising effect was seen in both cell lines (Po0.001 for MGH-U1 and S40b cell lines). This effect was independent of the concentration of the drug and the duration of exposure prior to treatment with ionising radiation. Cell cycle kinetics of both cell lines was not significantly altered with ZD1839 (0.01 mM) as a single agent. A modest induction of apoptosis was observed with ZD1839 (0.01 mM) as a single agent, but a marked induction was observed with the combination treatment of ZD1839 and ionising radiation. These results suggest a potentially important role for ZD1839 in combination with radiotherapy in the treatment of muscle invasive bladder cancer.

show abstract

“…The four ErbB family members (ErbB1, or EGFR; ErbB2 or Her2 or neu; ErbB3 or Her3; ErbB4 or Her4) are critical regulators of tumorigenesis (Salomon et al, 1995). They exert e ects by the activation of speci®c signal transduction cascades after exposure to various ligands such as heregulin and EGF family members EGF and transforming growth factor (TGF)a.…”

Section: Introductionmentioning

confidence: 99%

Phosphorylation and nuclear exclusion of the forkhead transcription factor FKHR after epidermal growth factor treatment in human breast cancer cells

et al. 2000

View full text Add to dashboard Cite

Akt, when activated by IGF/insulin, can phosphorylate forkhead transcription factors. We undertook this study to determine whether epidermal growth factor (EGF) treatment could produce a signaling cascade resulting in phosphorylation of the forkhead transcription factor FKHR in a breast cancer cell line, MDA-MB-231. After establishing ErbB1, cbl, PI3 kinase and Akt were activated in EGF treated MDA-MB-231, we determined by immunoblot with FKHR antiserum that the electrophoretic mobility of FKHR was retarded after EGF treatment. This mobility retardation was reversible by treatment with alkaline phosphatase, and immunoblot with phospho-Ser 256 FKHR antibody further con®rmed phosphorylation on an Akt consensus site after EGF treatment. EGF stimulated FKHR phosphorylation was blocked by the PI3 kinase inhibitor LY294002, and the ErbB1 inhibitor AG1478. FKHR immunoblotting after puri®cation of nuclear and cytoplasmic proteins showed that EGF induced a simultaneous increase of FKHR in the cytoplasm and decrease in the nucleus. This ®nding was con®rmed by immuno¯uorescence staining. Treatment of cells with pharmacological inhibitors of PI3 kinase or ErbB1 blocked this e ect. Thus, these results demonstrate the phosphorylation and nuclear exclusion of FKHR after EGF treatment by a PI3 kinase dependent mechanism, and represent the ®rst report of growth factor regulation of endogenous FKHR localization Oncogene (2000) 19, 4574 ± 4581.

show abstract

Epidermal growth factor-related peptides and their receptors in human malignancies

Cited by 2,409 publications

References 386 publications

Molecular determination of epidermal growth factor receptor in normal and neoplastic colorectal mucosa

Molecular determination of epidermal growth factor receptor in normal and neoplastic colorectal mucosa

Differential radiosensitisation by ZD1839 (Iressa), a highly selective epidermal growth factor receptor tyrosine kinase inhibitor in two related bladder cancer cell lines

Phosphorylation and nuclear exclusion of the forkhead transcription factor FKHR after epidermal growth factor treatment in human breast cancer cells

Contact Info

Product

Resources

About