Prospects for intervention in gastric carcinogenesis: reversibility of gastric atrophy and intestinal metaplasia

Mf, Dixon

doi:10.1136/gut.49.1.2

Cited by 81 publications

(61 citation statements)

References 28 publications

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“…Lesions of the excluded stomach have been reported and the diagnosis of this possibility is difficult, onerous, not always available and, as a result of that, gastric diseases, such as ulcers and malignant neoplasms in the excluded stomach may not be diagnosed (18,21,39) . H. pylori is associated to gastric diseases, such gastritis, ulcer, epithelial atrophy, intestinal metaplasia, lymphoma, adenocarcinoma (9,31) . The prevalence of infection caused by the H. pylori in Latin America is around 60%, varying from 30% to 90% (5) .…”

Section: Discussionmentioning

confidence: 99%

“…This inflammation consists initially in recruitment of neutrophils, followed by lymphocytes, with later epithelial damage (15) . The chronic inflammatory process increases the turnover of epithelial cells and apoptosis (cellular death), evolving to epithelial atrophy and intestinal metaplasia (9) . The development of gastric cancer involves several stages and can start with chronic gastritis, atrophy, intestinal metaplasia, dysplasia and finally invasive cancer (6) .…”

Section: Discussionmentioning

confidence: 99%

“…Studies have shown the increased incidence of gastric cancer in the population infected by the H. pylori, as well as a positive correlation between intestinal metaplasia and stomach cancer (27,31,37) . Eradication of the H. pylori leads to a regression of the inflammation, reduction of cellular turnover, increase in the acid secretion, which are important factors for the prevention of gastric cancer (9,14,22,24) . Some studies have concluded for the irreversibility of the carcinogenic process, even with the eradication of the H. pylori, basically when intestinal metaplasia of the stomach was present (13,14,20) .…”

Section: Discussionmentioning

confidence: 99%

See 2 more Smart Citations

Prevalence of upper digestive endoscopy and gastric histopathology findings in morbidly obese patients

Dietz¹,

Ulbrich-Kulcynski

Souto³

et al. 2012

Arq. Gastroenterol.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Prevalence of upper digestive endoscopy and gastric histopathology findings in morbidly obese patients

Dietz¹,

Ulbrich-Kulcynski

Souto³

et al. 2012

Arq. Gastroenterol.

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“…The evolution of H. pylori-associated gastric cancer begins with superficial gastritis that progresses to chronic gastritis, atrophy with islands of IM, development of dysplasia, and finally frank carcinoma (13,14). Since SHH is one of the peptide morphogens expressed in the parietal cells of normal human stomachs, the loss of fundic glands due to H. pylori-related atrophic changes or IM is accompanied by the loss of Shh expression (5,15,16).…”

Section: Discussionmentioning

confidence: 99%

Effect of Helicobacter pylori infection on the sonic hedgehog signaling pathway in gastric cancer cells

et al. 2010

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Abstract. This study aimed to investigate the effect of Helicobacter pylori (H. pylori) infection on the sonic Hedgehog (Shh) signaling in gastric cancer. Shh, Patched (Ptch), and transcription factor Gli1 were overexpressed in H. pyloriinfected gastric cancer cells. The oncoprotein, CagA positive H. pylori resulted in significantly higher Shh expression. Pretreatment with MG-132 or PDTC significantly lowered Shh expression. Significant overexpression of Shh and Gli1 were noted in H. pylori-infected compared to non-infected gastric cancer tissues. Conclusively, H. pylori activated the Shh signaling pathway in CagA-dependent manner partly through the NF-κB pathway in gastric cancer cells.

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“…Paneth cells are not found in type II and type III intestinal metaplasia; therefore the lesions have been designated as incomplete intestinal metaplasia. It has been suggested that intestinal metaplasia might be a preneoplastic hyperproliferative lesion of the stomach (Cahill et al, 1996;Correa, 1988;De Bolos et al, 2001;Dixon, 2001;Endoh et al, 1999;Morson, 1955;Rokkas et al, 1991;Rouzier and Robine, 2001;Wong et al, 2000;Tahara, 1995). However, cellular differentiation and proliferative status of Paneth cells in complete intestinal metaplasia (type I metaplasia) of the stomach has not been extensively examined.…”

Section: Discussionmentioning

confidence: 99%

Expression of Calnexin Reflects Paneth Cell Differentiation and Function

Gaßler

Schnölzer

Rohr

et al. 2002

Laboratory Investigation

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SUMMARY:It has been suggested that the behavior and function of Paneth cells in metaplasia are different from those found in normal intestinal mucosa. In this study, we investigated whether calnexin, a protein involved in secretory pathways, might be associated with differentiation and function of Paneth cells in normal small intestine, in complete intestinal metaplasia of the stomach, and in Paneth cell-rich adenomas. Differentiation and function of Paneth cells was monitored by Ki67, lysozyme, and morphologic features. Using a newly established monoclonal antibody, we found that calnexin is regularly synthesized by Paneth cells of normal small intestine. In these cells, the staining intensity of calnexin was inversely correlated with their content of secretory granules (lysozyme). In contrast, Paneth cells of intestinal metaplasia and Paneth cell-rich adenomas showed a reduced immunostaining of both calnexin and lysozyme. Moreover, these Paneth cells synthesized the proliferation marker Ki67, a phenomenon that was never observed in Paneth cells of normal small intestine. In vitro experiments using CaCo2 cells showed that the expression of calnexin is not directly affected by the induction of mitosis. In conclusion, calnexin probably reflects the status of Paneth cell differentiation and function. The results do not necessarily indicate that calnexin has a function in Paneth cell proliferation. (Lab Invest 2002, 82:1647-1659.T he four principal epithelial cell types of the human small intestinal mucosa (absorptive, goblet, Paneth, and endocrine cells) derive from a multipotent stem cell located near the base of crypts of Lieberkühn. In contrast to absorptive and goblet cells, which migrate in approximately 5 days from the crypt depths to the surface, endocrine cells and Paneth cells differentiate during a downward migration to the base of crypts. Paneth cells reside there for approximately 20 days (Bry et al, 1994). Paneth cells are generally recognized in hematoxylin and eosinstained sections by their large eosinophilic apical secretory granules and their characteristic ultrastructural pattern (Otto, 1973). Functions that have been attributed to Paneth cells include modulation of the intestinal microflora and maintenance of the mucosal defense barrier through production and secretion of several antimicrobial peptides, such as lysozyme, secretory phospholipase A 2 , and ␣-defensins (Nevalainen et al, 1998;Ouellette, 1999;Ouellette and Bevins, 2001). In addition, Paneth cells can also produce further regulatory molecules including growth factors, suggesting that Paneth cells may regulate the proliferation and differentiation programs of epithelial cell lineages by short-circuit paracrine loops (Bry et al, 1994;Ganz, 2000).In humans, Paneth cell metaplasia is preferentially found in atrophic gastritis (Wong et al, 2000). Other nonmalignant pathologic conditions associated with Paneth cell metaplasia are diversion colitis, ulcerative colitis, and collagenous colitis (Goff et al, 1997;Shah et al, 1998;Stamp et al, ...

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Prospects for intervention in gastric carcinogenesis: reversibility of gastric atrophy and intestinal metaplasia

Cited by 81 publications

References 28 publications

Prevalence of upper digestive endoscopy and gastric histopathology findings in morbidly obese patients

Prevalence of upper digestive endoscopy and gastric histopathology findings in morbidly obese patients

Effect of Helicobacter pylori infection on the sonic hedgehog signaling pathway in gastric cancer cells

Expression of Calnexin Reflects Paneth Cell Differentiation and Function

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