Epidermal growth factor in the oesophagus.

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

doi:10.1136/gut.33.11.1448

Cited by 53 publications

(14 citation statements)

References 33 publications

(7 reference statements)

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“…Acid, by acting as a mild irritant to the esophagus, triggers mucosal defensive mechanisms including increased cell proliferation and blood supply to the esophagus [12–14]. The mechanisms of these adaptive responses, albeit remain largely unknown, may be mediated by prostaglandins (PGs), nitric oxide (NO), epidermal growth factor, and capsaicin-sensitive afferent neurons [7,12–16].…”

Section: Introductionmentioning

confidence: 99%

Orally administered L-arginine and glycine are highly effective against acid reflux esophagitis in rats

et al. 2012

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SummaryBackgroundReflux esophagitis is caused mainly by excessive exposure of the mucosa to gastric contents. In the present study, we examined the effect of several amino acids on acid reflux esophagitis in rats.Material/MethodsAfter 18 h of fasting, acid reflux esophagitis was induced by ligating both the pylorus and the transitional region between the forestomach and the corpus under ether anesthesia, and the animals were killed 4 h later. The severity of esophagitis was reduced by the oral administration of omeprazole, a proton pump inhibitor, or pepstatin, a specific pepsin inhibitor.ResultsThe development of esophageal lesions was dose-dependently prevented by L-arginine and glycine, given intragastrically (i.g.) after the ligation, with complete inhibition obtained at 250 mg/kg and 750 mg/kg, respectively, and these effects were not influenced by the prior s.c. administration of indomethacin or L-NAME. By contrast, both L-alanine and L-glutamine given i.g. after the ligation aggravated these lesions in a dose-dependent manner. These amino acids had no effect on acid secretion but increased the pH of the gastric contents to 1.8~2.3 due to their buffering action.ConclusionsThe results confirmed an essential role for acid and pepsin in the pathogenesis of acid reflux esophagitis in the rat model and further suggested that various amino acids affect the severity of esophagitis in different ways, due to yet unidentified mechanisms; L-alanine and L-glutamine exert a deleterious effect on the esophagitis, while L-arginine and glycine are highly protective, independent of endogenous prostaglandins and nitric oxide.

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Section: Introductionmentioning

confidence: 99%

Orally administered L-arginine and glycine are highly effective against acid reflux esophagitis in rats

et al. 2012

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“…There is evidence that signaling through EGFR may play a role in Barrett carcinogenesis to stimulate growth. Protein expression of EGF and TGFα is increased to similar levels in BE and EAC, 35 , 36 suggesting that EGFR activation through these ligands via an autocrine signaling mechanism may be an early event in the BE metaplasia-dysplasia-EAC sequence. In BE, expression of TGFα was found to correlate with proliferation and TGFα immunoreactivity was found in the same areas as proliferating cells in BE glands showing high-grade dysplasia (HGD) 37 .…”

Section: Molecular Pathogenesis Of Eacmentioning

confidence: 97%

Signaling pathways in the molecular pathogenesis of adenocarcinomas of the esophagus and gastroesophageal junction

Clemons

Phillips

Lord

2013

Cancer Biology & Therapy

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Esophageal adenocarcinoma develops in response to severe gastroesophageal reflux disease through the precursor lesion Barrett esophagus, in which the normal squamous epithelium is replaced by a columnar lining. The incidence of esophageal adenocarcinoma in the United States has increased by over 600% in the past 40 years and the overall survival rate remains less than 20% in the community. This review highlights some of the signaling pathways for which there is some evidence of a role in the development of esophageal adenocarcinoma. An increasingly detailed understanding of the biology of this cancer has emerged recently, revealing that in addition to the well-recognized alterations in single genes such as p53, p16, APC, and telomerase, there are interactions between the components of the reflux fluid, the homeobox gene Cdx2, and the Wnt, Notch, and Hedgehog signaling pathways.

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“…EGF and binds to the EGF receptor, has been shown to increase IGF/BP-3 protease levels, which separate Higher levels of EGF and EGF receptors are found in the esophageal mucosa of patients with Barrett's the IGF-I from the binding protein [26]. EGF may also increase protease levels leading to an increase in the esophagus when compared to normal mucosa [20,21]. IGF-I has been shown to stimulate epithelial prolifera-pool of available IGF-I over an extended period of time.…”

Section: Igf-i/bp-3 Complex Actionmentioning

confidence: 99%

EGF and IGF-I Synergistically Stimulate Proliferation of Human Esophageal Epithelial Cells

Qureshi

Tchórzewski

Duncan

et al. 1997

Journal of Surgical Research

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Epidermal growth factor in the oesophagus.

Cited by 53 publications

References 33 publications

Orally administered L-arginine and glycine are highly effective against acid reflux esophagitis in rats

Orally administered L-arginine and glycine are highly effective against acid reflux esophagitis in rats

Signaling pathways in the molecular pathogenesis of adenocarcinomas of the esophagus and gastroesophageal junction

EGF and IGF-I Synergistically Stimulate Proliferation of Human Esophageal Epithelial Cells

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