Growth regulatory peptides in gastric mucosa

Jankowski, Janusz; Al-Rawi, Hoda; Johnston, D.; Hopwood, David A.; Filipe, M. I.; Coghill, G.; Wormsley, K. G.

doi:10.1042/cs0820581

Cited by 22 publications

(18 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Fas or soluble Fas ligand was used in two studies [119, 120]. As markers for cell proliferation associated with gastric inflammation, four studies use Ki-67 staining [115, 116, 118, 121] and two studies use proliferating cell nuclear antigen (PCNA) staining [117, 122]. …”

Section: Growth Factors Apoptosismentioning

confidence: 99%

“…Six studies used growth factors as a marker of gastric inflammation [87, 121,124,125,126,127]. Among them, three studies used epidermal growth factor (EGF) or EGF receptor [121, 125, 126], two studies used hepatocyte growth factor (HGF) [87, 128], two used transforming growth factor-β (TGF-β) [125, 126], one study used insulin-like growth factor-1 (IGF-1) [127], and one study used vascular endothelial growth factor (VEGF) [129], for a marker of gastric inflammation. One study dealt with serum trefoil factor 3 (TFF3) as a marker of gastrointestinal inflammation and/or ulceration [130].…”

Section: Growth Factors Apoptosismentioning

confidence: 99%

See 1 more Smart Citation

Biomarkers in Patients with Gastric Inflammation: A Systematic Review

et al. 2005

View full text Add to dashboard Cite

Background: The importance of examining the status of gastric inflammation has been acknowledged; the new classification by the updated Sydney system (USS) allows us to evaluate the quantitative status of gastric inflammation. However, this system is based on the histological classification derived from biopsy specimens. Therefore, more convenient, objective and practical biomarkers are recommended. Aim: We undertook a systematic review to find out potential biomarkers by summarizing the relationship between biomarkers and grades of inflammation. Methods: By a primary search via Medline up to December 2004, we extracted a total of 6,526 papers that described biomarkers for human gastric inflammation. All papers were screened by title and abstract. The authors then retrieved 435 citations for complete review; ultimately 231 were appropriate for inclusion criteria. These papers were subclassified into several categories and summarized by each author. Results: In addition to standard markers such as pepsinogens, we confirmed the close relationship between the levels of several biomarkers including gastrin, interleukin-8, HLA class II molecules, reactive oxygen species, and the histological grades. Conclusions: This review provides valuable information describing the clinical implication of these biomarkers for evaluating the static conditions or dynamic alterations of human gastric inflammation.

show abstract

Section: Growth Factors Apoptosismentioning

confidence: 99%

Section: Growth Factors Apoptosismentioning

confidence: 99%

Biomarkers in Patients with Gastric Inflammation: A Systematic Review

et al. 2005

View full text Add to dashboard Cite

show abstract

“…It is possible that factors unique to the chronic inflammatory cell infiltrate are involved in the promotion of cell proliferation, 5 6 for example the increased expression of epidermal growth factor (EGF) in the proliferative zone. 6 EGF receptor (EGFr) is strongly expressed in the proliferative compartment and EGF expression is increased in gastritis. 6 EGF and transforming growth factor (TGF ), a ligand to EGFr, also have increased expression in gastric carcinoma.…”

mentioning

confidence: 99%

“…6 EGF receptor (EGFr) is strongly expressed in the proliferative compartment and EGF expression is increased in gastritis. 6 EGF and transforming growth factor (TGF ), a ligand to EGFr, also have increased expression in gastric carcinoma. 23 24 The finding that there is no correlation between glandular atrophy and reduced epithelial cell proliferation is of particular interest.…”

mentioning

confidence: 99%

Correlation between epithelial cell proliferation and histological grading in gastric mucosa.

et al. 1999

View full text Add to dashboard Cite

Aim-To determine if there is a correlation between the histological findings in the gastric mucosa and the degree of cell proliferation in gastric antral biopsies. Methods-Cell proliferation in gastric antral biopsies was determined by in vitro bromodeoxyuridine labelling. Histological sections were assessed using the Sydney System. Results-There was a positive correlation between antral mucosal cell proliferation and the acute inflammatory cell infiltrate (r = 0.29; p = 0.03). There was a stronger correlation with the chronic inflammatory cell infiltrate (r = 0.53; p < 0.0001) and the density of H pylori colonisation (r = 0.54; p < 0.0001). There was no correlation between gastric epithelial proliferation and the degree of atrophy. Stepwise multiple regression indicates that the only independent predictor of epithelial cell proliferation is the density of H pylori colonisation (p < 0.0001). Conclusions-H pylori increases gastric epithelial cell proliferation through the mucosal inflammatory response and probably by other means. The strong correlation between epithelial proliferation, the chronic inflammatory cell infiltrate, and the density of H pylori colonisation may have implications for gastric carcinogenesis. (J Clin Pathol 1999;52:367-371) Keywords: gastritis; epithelial kineticsWe have shown previously that epithelial proliferation is increased in H pylori gastritis aVecting antral and corpus mucosa.1 2 Eradication of the organism results in antral cell proliferation returning to normal, in contrast to persistent infection where cell proliferation remains increased on long term follow up.1 The increased cellular proliferation may be caused by the inflammatory response stimulated by H pylori infection. In order to establish whether there is a relation between the two, we have studied the relation of both the density of H pylori colonisation of the gastric epithelium and the histological changes within the gastric mucosa with the degree of cell proliferation. We have also explored the relation between antral and corpus epithelial kinetics, and the eVect of patient age, sex, and cigarette smoking. MethodsPatients undergoing routine diagnostic endoscopy were recruited following informed consent. Those taking non-steroidal antiinflammatory drugs, antibiotics, or bismuth salts were excluded from the study. At endoscopy, biopsies were taken from the antrum (2) and corpus (2) for in vitro bromodeoxyuridine labelling and routine histological processing. This study was approved by the hospital ethics committee. BROMODEOXYURIDINE LABELLINGTwo antral biopsies for immunostaining were put immediately into RPMI medium without L-glutamine (Gibco) containing bromodeoxyuridine (5 mg/10 ml) and placed in a water bath for 60 minutes at 37°C. They were then placed on filter paper and fixed in formalin. Using a three step immunoperoxidase technique, sections were stained with antibromodeoxyuridine (Dakopatt) antibody (1:20 dilution) for 60 minutes.

show abstract

“…Growth factors are important regulators of cell differentiation and proliferation and play an important role in maintaining the integnty of the epithelium. Increased expression in cells or aberrant topographical distribution of the growth-regulatory peptides epidermal growth factor (EGF) and transforming growth factor X (TGF-uc) and their receptor (EGFR) has been described in the gastrointestinal epithelium associated with mitogenesis and carcinogenesis (Goodlad and Wright, 1990;Jankowski. 1992;Nasim et al.…”

mentioning

confidence: 99%

Expression of transforming growth factor alpha, epidermal growth factor receptor and epidermal growth factor in precursor lesions to gastric carcinoma

Filipe

Osborn²,

Linehan³

et al. 1995

Br J Cancer

View full text Add to dashboard Cite

Summary Epidermal growth factor (EGF). its related peptide transforming growth factor (TGF-a) and their common receptor (EGFR) have been implicated in the control of cell proliferation and differentiation in the gastrointestinal epithelium and may play an important role in gastric carcinogenesis. We compared the immunohistochemical expression and topographic distribution of these peptides using Western blot analysis in gastric carcinoma precursor lesions and in non-cancer tissue. We observed: (i) increased and extended expression of TGF-a in normal mucosa and hyperplasia in carcinoma fields compared 'with non-cancer controls: (ii) increased expression of EGFR in intestinal metaplasia (IM) from carcinoma fields compared with controls; (iii) EGF expression was not detected in normal mucosa and only weakly in IM; (iv) coexpression of TGF-a EGFR and EGF EGFR was higher in intestinal metaplasia in carcinoma fields than in non-cancer controls. We conclude that altered expression of TGF-a EGFR is associated with morphological changes dunrng gastric carcinogenesis. In this regard increased expression of TGF-a is a very early event which is subsequently followed by up-regulation of EGFR and this has important biological and clinical implications.Keywords growth factors; precancer lesions, gastric carcinoma Gastric carcinogenesis is a stepwise process which starts with molecular changes in normal cells resulting in phenotypic adaptation. In this regard chronic gastritis is one of the earliest identifiable histological abnormalities and may lead to intestinal metaplasia (IM), dysplasia and ultimately adenocarcinoma (Correa, 1988). The underlying mechanisms that control this process are not as yet fully understood. The majority of gastric carcinomas appear to be caused by environmental factors resulting in mucosal damage and repair (Parsonnet et al., 1991; UK Subgroup of the ECPEuronut-IM Study Group, 1992;Pignatelli et al., 1993). This pleomorphic response is regulated in part by inhibitory and stimulatory molecules derived from proto-oncogenes and tumour-suppressor genes (Tahara, 1993). Growth factors are important regulators of cell differentiation and proliferation and play an important role in maintaining the integnty of the epithelium. Increased expression in cells or aberrant topographical distribution of the growth-regulatory peptides epidermal growth factor (EGF) and transforming growth factor X (TGF-uc) and their receptor (EGFR) has been described in the gastrointestinal epithelium associated with mitogenesis and carcinogenesis (Goodlad and Wright, 1990;Jankowski. 1992;Nasim et al.. 1992;Filipe and Jankowski, 1993). Human TGF-a has been mapped to chromosome 2 to the short arm region 2pll -2pl3. and it is known that chromosome 2 contains other genes that are involved in growth regulation and tumorigenesis. EGFR has been found to be overexpressed at high frequency in a wide range of tumours. Increased expression of TGF-x is frequent in gastric carcinoma (60% ). particularly the intestinal type of carcinoma, but EGFR...

show abstract

Growth regulatory peptides in gastric mucosa

Cited by 22 publications

References 0 publications

Biomarkers in Patients with Gastric Inflammation: A Systematic Review

Biomarkers in Patients with Gastric Inflammation: A Systematic Review

Correlation between epithelial cell proliferation and histological grading in gastric mucosa.

Expression of transforming growth factor alpha, epidermal growth factor receptor and epidermal growth factor in precursor lesions to gastric carcinoma

Contact Info

Product

Resources

About