Epidermal Growth Factor in the Oesophagus

Jankowski, Janusz; Tregaskis, B; Coghill, G.; Grant, A.; Fawkes, R; Hopwood, David A.; Wormsley, K. G.

doi:10.1042/cs080006p

Cited by 17 publications

(25 citation statements)

References 5 publications

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“…EGF-R are immunohistochemically de tectable throughout all the different layers of the oesophageal epithelium, being found in greatest density in the basal layer compared with more superficial layers of the oesopha geal epithelium [30]. Flow cytometry has con firmed these findings.…”

Section: Structure Of Egf Tgf-a and Egf-rsupporting

confidence: 50%

“…Flow cytometry has con firmed these findings. The EGF-R can also be demonstrated, by electromicroscopy, to be present in the lysosomes of oesophageal squames, presumably representing internal ised bound EGF-EGF-R complexes [30].…”

Section: Structure Of Egf Tgf-a and Egf-rmentioning

confidence: 99%

“…The amount of EGF immu nohistochemically detectable in capillaries is significantly reduced in sections with histo logical evidence of oesophagitis [26], Con versely. the EGF-R staining increases in the basal as well as parabasal layer of the inflamed oesophagus [30]. TGF-a expression appears not to alter with the presence of degree of oesophageal inflammation [31].…”

Section: Expression Of Egf Tgf-a and Egf-r In The Inflamed Oesophagusmentioning

confidence: 99%

“…The patients with the highest Ki-67 (a marker of dividing cells) labelling in dices [62] also had significant overexpression of TGF-a and EGF-R when compared with Barrett's mucosa showing low proliferative indices [31]. Dysplastic glandular Barrett's mucosa and also dysplastic gastric mucosa may show mitoses in the superficial epithe lium outside the proliferative zone [30], It is therefore of interest that there appears to be a significant correlation between TGF-a over expression and proliferating nuclear antigen (a marker for dividing or recently divided nuclei) [63] labelling, representing an index of proliferation in the superficial glandular mu cosa of highly dysplastic mucosa. In the stom ach, it seems that EGF-R expression in the neck cells of the normal proliferative zone of the gastric cells correlates well with Ki-67 labelling indices [40]…”

Section: Correlation Between Expression Of Egf Tgf-a and Egf-r With mentioning

confidence: 99%

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Expression of Epidermal Growth Factor, Transforming Growth Factor Alpha and Their Receptor in Gastro-Oesophageal Diseases

Jankowski

Hopwood

Wormsley³

1993

Dig Dis

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This article is a review of aspects of the expression of the regulatory peptides; epidermal growth factor (EGF), transforming growth factor alpha (TGF-α), and their receptor (EGF-R) in the epithelium of the human oesophagus and stomach in health and disease. It has become clear that TGF-α has increased expression in metaplastic, dysplastic and neoplastic tissue of the oesophagus compared with normal mucosa. The degree of abnormal expression becomes more marked as dysplasia increases. TGF-α expression is also increased in gastric neoplasias. EGF has a different pattern of expression, being decreased in oesophagitis and increased in gastritis. Although EGF is present in Barrett’s oesophagitis, the expression of EGF does not discriminate between dysplastic and neoplastic epithelium. EGF-R is normally expressed on all gastrointestinal epithelia, but its expression is increased in Barrett’s epithelium, as well as in adenocarcinomas of the oesophagus and the stomach. The two peptides bind to their receptors on the mucosal cell membranes, and the co-expression of peptide and receptor is positively associated with varying degrees of cellular proliferation. The density of receptor expression may modulate the proliferative stimulus, leading to either mitogenic (regulated) or oncogenic (unregulated) growth.

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Section: Structure Of Egf Tgf-a and Egf-rsupporting

confidence: 50%

Section: Structure Of Egf Tgf-a and Egf-rmentioning

confidence: 99%

Section: Expression Of Egf Tgf-a and Egf-r In The Inflamed Oesophagusmentioning

confidence: 99%

Section: Correlation Between Expression Of Egf Tgf-a and Egf-r With mentioning

confidence: 99%

See 2 more Smart Citations

Expression of Epidermal Growth Factor, Transforming Growth Factor Alpha and Their Receptor in Gastro-Oesophageal Diseases

Jankowski

Hopwood

Wormsley³

1993

Dig Dis

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“…Die Liganden dieser Rezeptoren, die Wachstumsfaktoren selbst, sind potente Mitogene. «Epidermal growth factor» (EGF) wird ebenso wie «transforming growth factor ␣» (TGF␣) in einer Vielzahl der Barrett-Karzinome exprimiert und könnte zur autokrinen Wachstumsstimulation beitragen [44,45]. Ein anderer Wachstumsfaktor, «acidic fibroblast growth factor» (aFGF) akkumuliert während der Progression von der Metaplasie zum Karzinom [46].…”

Section: Tumorsuppressorgeneunclassified

Pathogenese von Barrett-Ösophagus und Barrett-Karzinom

Halm¹,

Schoppmeyer²,

Mössner³

2001

Visc Med

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Pathogenesis of Barrett’s Esophagus and Barrett’s Carcinoma Patients with Barrett’s esophagus are at a significantly higher risk for developing an esophageal adenocarcinoma compared to the normal population. New epidemiologic data, however, indicate a lower risk than previously assumed. Gastroesophageal reflux disease is the most important risk factor for the development of Barrett’s esophagus. Numerous molecular abnormalities characterize the sequence from metaplasia to dysplasia and finally adenocarcinoma. Clonal expansion of diploid cells with alterations of p53 and/or p16 seems to precede further neoplastic development. Other changes in cell cycle regulation, expression of growth factors, and apoptosis are also important. So far, molecular and immunohistochemical markers have not replaced endoscopic-bioptic surveillance programs. Markers as Cyclin D1 and flow cytometry studies of ploidy may help to identify patients at risk for adenocarcinoma during surveillance.

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Intrinsic resistance triggered under acid loading within normal esophageal epithelial cells: NHE1- and ROS-mediated survival

et al. 2015

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The transition to a pathological phenotype such as Barrett's esophagus occurs via induction of resistance upon repeated contact with gastric refluxate in esophagus. This study examined the molecular changes within normal esophageal epithelial cells (EECs) under short-term acid loading and the role of these changes in defensive resistance against acidic cytotoxicity. After primary cultured EECs were exposed to pH 4-acidified medium (AM4), cell viability was determined by the MTT assay. Reactive oxygen species (ROS) and NAD(P)H oxidase (NOX) activity were measured. Activation of the mitogen-activated protein kinases (MAPKs) MEK/ERK1/2, p38 and JNK; phosphoinositol-3-kinase (PI3K)/Akt, and nuclear factor-kappa B (NF-κB) were detected by Western blot analysis or immunofluorescence staining. AM4 incubation induced intracellular ROS generation accompanied by increase in NOX activity, which was further increased by Na(+) /H(+) exchange-1 (NHE1)-dependent inhibition but was prevented by inhibition of NOX or mitochondria complex I. AM4 also induced phosphorylation of MEK/ERK1/2, p38 MAPK, PI3K/Akt, and nuclear translocation of NF-κB, and all these effects, except for p38 MAPK phosphorylation, were abolished by inhibition of ROS. ROS-dependent PI3K/Akt activation, which mediates NF-κB nuclear translocation, was inhibited by protein tyrosine kinase (PTK) inhibitors and NHE1-specific inhibitor. All inhibitors of NHE, ROS, PTK, PI3K, or NF-κB further decreased AM4-induced cell viability. Acid loading in the presence of NHE1-dependent protection induced ROS generation by activating NOX and mitochondria complex I, which stimulated PTK/PI3K/Akt/NF-κB-dependent survival in EEC. Our data indicate that normal EEC initially respond to acid loading through intrinsic survival activation.

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Epidermal Growth Factor in the Oesophagus

Cited by 17 publications

References 5 publications

Expression of Epidermal Growth Factor, Transforming Growth Factor Alpha and Their Receptor in Gastro-Oesophageal Diseases

Expression of Epidermal Growth Factor, Transforming Growth Factor Alpha and Their Receptor in Gastro-Oesophageal Diseases

Pathogenese von Barrett-Ösophagus und Barrett-Karzinom

Intrinsic resistance triggered under acid loading within normal esophageal epithelial cells: NHE1- and ROS-mediated survival

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