Simple atrophic gastritis and gastric carcinoma

Walker, I. R.; Strickland, R. G.; Ungar, Berta; Mackay, Ian R.

doi:10.1136/gut.12.11.906

Cited by 138 publications

(51 citation statements)

References 30 publications

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“…49 Australian researchers followed 40 patients with atrophic gastritis for a mean 15 years and observed that gastric cancer occurred in four (10%) of them. 50 A large Japanese study followed 3914 patients with endoscopical signs of atrophic gastritis for a mean 4.4 years. 51 Scoring atrophy macroscopically during endoscopy is an accepted and reportedly adequate method in Japan.…”

Section: Atrophy Metaplasia and Gastric Cancer: Prospective Studiesmentioning

confidence: 99%

Relationship between Helicobacter pylori, atrophic gastritis and gastric cancer

Kuipers

1998

Aliment Pharmacol Ther

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Section: Atrophy Metaplasia and Gastric Cancer: Prospective Studiesmentioning

confidence: 99%

Relationship between Helicobacter pylori, atrophic gastritis and gastric cancer

Kuipers

1998

Aliment Pharmacol Ther

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“…

(Schindler, 1965; Siurala etal., 1966;Walker et al, 1971). Numerous authors have investigated cell proliferation kinetics in normal and atrophic stomach mucosa.

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mentioning

confidence: 99%

“…Atrophic gastritis is a pathological condition that may predispose to the development of gastric cancer (Schindler, 1965;Siurala etal., 1966;Walker et al, 1971). Numerous authors have investigated cell proliferation kinetics in normal and atrophic stomach mucosa.…”

mentioning

confidence: 99%

Nuclear binding of tritiated actinomycin in surface epithelial cells from normal stomach and atrophic gastritis.

Stoffels¹,

Preumont²,

Reuck³

1978

Gut

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(Schindler, 1965; Siurala etal., 1966;Walker et al., 1971). Numerous authors have investigated cell proliferation kinetics in normal and atrophic stomach mucosa. An increased proliferation of the epithelial cells in the latter has been described (Deschner and Lipkin, 1976), while in cases of intestinalisation of the gastric mucosa, which is found in over 90% of gastric cancers (Morson, 1959), the same authors have described an impairment of epithelial cell maturation.Earlier work has reported an increased nuclear fixation of tritiated actinomycin (3H-AM) in cancer cells as compared to the corresponding normal cells Pileri et al., 1972;Heenen et al., 1973). This technique has been shown to be a valid method for the rough evaluation of the number of free DNA sites: the fixation of labelled actinomycin by the nuclei is closely linked to the degree of repression in chromatin (Brachet and Ficq, 1965;Brachet, 1971).'Address for correspondence: Dr G. Stoffels, H6pital Universitaire Brugmann, 4, Place Van Gehuchten, 1020 Bruxelles.Received for publication 4 May 1978 In this study, we have compared the binding of 3H-AM to chromatin in epithelial cells in normal stomachs and in atrophic gastritis by autoradiographs. Significant increases of 3H-AM binding would suggest that these cells are in a depressed state. MethodsTwenty-five patients were studied; eight had a normal gastric mucosa and 17 had a atrophic gastritis as defined by the histological criteria described by Whitehead et al. (1972).The grades of gastritis were (1) superficial, and (2) atrophic with three grades: mild, moderate, and severe. Superficial gastritis is characterised by mononuclear and polymorphonuclear cell infiltration located in the surface epithelium and gastric pit region. In mild atrophic gastritis the infiltration occurs into all layers of lamina propria with a slight reduction of parietal and chief cells. Moderate and severe atrophic gastritis includes all the above signs, in addition to a greater reduction in parietal and chief cells, and the presence of intestinal metaplasia and regenerative nodules.It must be remembered that in this classification 'active atrophic gastritis' signifies the presence of 870 on 25 March 2019 by guest. Protected by copyright.

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“…Very recently, a meta-analysis showed that Hp eradication reduced the risk of gastric cancer (32). However, also the other type of gastritis, the so-called autoimmune gastritis affecting only the oxyntic mucosa predisposes to gastric cancer (33). Thus, it seems that the gastritis and not Hp itself is the carcinogenic mechanism.…”

Section: Predisposing Conditions For Gastric Cancermentioning

confidence: 99%

“…However, it seems logical to focus on the gastritis since also the so-called autoimmune gastritis predisposes to gastric cancer (33). Moreover, oxyntic gastric atrophy is a common feature in conditions causing gastric cancer (36), and therefore, we recently proposed that hypergastrinemia could be the factor incriminated in Hp gastric carcinogenesis (89).…”

Section: Gastrin and Gastric Carcinomasmentioning

confidence: 99%

Gastrin and gastric cancer

Waldum¹,

Petersen²,

Brenna³

1993

European Journal of Gastroenterology & Hepatology

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Gastric cancer although occurring in reduced frequency is still an important disease, partly because of the bad prognosis when occurring in western countries. This decline in occurrence may mainly be due to the reduced prevalence of Helicobacter pylori (Hp) infection, which is the most important cause of gastric cancer. There exist many different pathological classifications of gastric carcinomas, but the most useful seems to be the one by Lauren into intestinal and diffuse types since these types seldom transform into the other and also have different epidemiology. During the nearly 30 years that have passed since the groundbreaking description of Hp as the cause of gastritis and gastric cancer, a continuous search for the mechanism by which Hp infection causes gastric cancer has been done. Interestingly, it is mainly atrophic gastritis of the oxyntic mucosa that predisposes to gastric cancer possibly by inducing hypoacidity and hypergastrinemia. There are many arguments in favor of an important role of gastrin and its target cell, the enterochromaffin-like cell, in gastric carcinogenesis. The role of gastrin in gastric carcinogenesis implies caution in the long-term treatment with inhibitors of gastric acid secretion inducing secondary hypergastrinemia, in a common disease like gastroesophageal reflux disease.Keywords: carcinogenesis, classification of cancer, gastric cancer, gastrin, hormones, neuroendocrine neoplasia Gastric cancer has been one of the most prevalent cancers and combined with a high mortality, gastric cancer has been among the leading causes of cancer death. However, there has been a continuous decline in the prevalence of gastric cancers during the last decades. Unfortunately, in spite of widespread use of upper gastrointestinal endoscopy, the prognosis in patients affected in the western world has not been much improved. This is in contrast to Japan where gastric cancer often is diagnosed at an early phase allowing removal and a better prognosis (1, 2). This is partly due to special screening programs in Japan having a high prevalence of gastric cancer (1, 2), resulting in diagnoses at a curable stage. In most western countries, the prevalence is much lower (3), and therefore, no such program has been implemented. The cause of the geographical differences in the prevalence of gastric cancer most probably is increased prevalence of Helicobacter pylori (Hp) in East Asia as well as a higher frequency of atrophic oxyntic gastritis (4). The prognosis of gastric cancer is better in patients from East Asia even when living in the west possibly due to less aggressive biology (5). In this review, we will focus on the role of gastrin in the etiology of gastric cancer and at the same time give an explanation of the decline in frequency. We will only cover cancers originating from epithelial cells (carcinomas) and will not discuss the importance of Epstein-Barr virus that plays a role neither in gastric carcinogenesis (6) nor in human papilloma virus, which has a less established impact (7).

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Simple atrophic gastritis and gastric carcinoma

Cited by 138 publications

References 30 publications

Relationship between Helicobacter pylori, atrophic gastritis and gastric cancer

Relationship between Helicobacter pylori, atrophic gastritis and gastric cancer

Nuclear binding of tritiated actinomycin in surface epithelial cells from normal stomach and atrophic gastritis.

Gastrin and gastric cancer

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