Limited value of type III intestinal metaplasia in predicting risk of gastric carcinoma.

Ramesar, K.; Sanders, D. S. A.; Hopwood, David A.

doi:10.1136/jcp.40.11.1287

Cited by 65 publications

(42 citation statements)

References 14 publications

(1 reference statement)

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“…In these patients, we therefore suggest a thorough endoscopic follow-up or, preferably, treatment of the promotor of regeneration, the HP gastritis. This holds true especially when IM of the enterocolic type (type III), which is said to show a greater risk for the development of gastric carcinoma, is detected [19,20,23,[51][52][53][54], The results reported by other groups, however, have failed to support this hypothesis [55][56][57][58][59], In conclusion, we might state that, although the causative role of HP in the development of IM cannot be proven, and other factors like NSAID and duodenogastral bile reflux surely have to be taken into account, our data do support the hypothesis that HP plays an important part in the development of antral IM. Another important ques tion urgently awaiting an answer is whether by eradicating HP the development of IM might be reduced.…”

Section: Discussioncontrasting

confidence: 42%

Antral Intestinal Metaplasia in Helicobacter pylori Gastritis

Eidt

Stolte²

1994

Digestion

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The prevalence of antral intestinal metaplasia (IM) in underlying Helicobacter pylori (HP) gastritis was studied in biopsy specimens of the antral mucosa obtained from 2,692 patients with histologically proven HP gastritis. The prevalence of IM varied in the groups investigated: 47.4% in gastric ulcers, 30.5% in pyloric ulcers, 16.8% in duodenal ulcers, 21.8% in gastritis with no lesions and 9.8% in chronic antral erosions (p < 0.001). A hypothetical model for the role of HP in the development of IM is presented: HP probably promotes mucosal regeneration. The prolonged stimulatory effect on regeneration could then, in the course of time, lead to an increasing likelihood of IM developing.

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Section: Discussioncontrasting

confidence: 42%

Antral Intestinal Metaplasia in Helicobacter pylori Gastritis

Eidt

Stolte²

1994

Digestion

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“…IM type I in these studies has been found to be more frequently associated with benign gastric conditions, while type 111 was more often associated with stomach cancer (Sipponen et al, 1980;Silva and Filipe, 1986;Rokkas et al, 1991;Filipe et al, 1985;Turani et al, 1986;Kini et al, 1990). Although 2 earlier cohort studies concluded that subtyping of IM in endoscopic biopsies was of only limited value in identifying patients who required longterm follow-up, this was based on a case or two without statistical evaluation (Ectors and Dixon, 1986;Ramesar et al, 1987) and therefore is not convincing evidence.…”

Section: Discussionmentioning

confidence: 94%

Intestinal metaplasia types and the risk of gastric cancer: A cohort study in Slovenia

Filipe

Muñóz

Matko

et al. 1994

Intl Journal of Cancer

418

328

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Between 1967 and 1976, 1,525 Slovenian patients with a histological diagnosis of intestinal metaplasia (IM) were classified according to subtype of IM based on morphology and mucin staining; 518 cases were diagnosed with type I, 197 with type II and 275 with type III, but in 291 the diagnosis of IM was not confirmed. Patients who had developed cancer or died up to 1986 were identified by record linkage at the Slovenia Cancer Registry and the Central Population Registry in Slovenia. A total of 34 incident cases of gastric cancer occurring at least 6 months after the diagnosis of IM were identified. The standardised incidence ratio (SIR) for stomach cancer was 2.23 in the whole cohort. It was highest for IM type III, followed by type II and IM-unconfirmed, but not increased for type I. The relative risk (RR) of developing gastric cancer based on Cox's proportional hazards model was 2.14 for type II and 4.58 for type III, compared with type I. The RR was especially increased for a subgroup of type III secreting sulphomucins in their goblet cells in comparison with types I-II negative to sulphomucins. Our results confirm that subtyping of IM is useful for identifying individuals at high risk for gastric cancer.

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“…The risk of gastric cancer is proportional to the extent of metaplasia [49]. However, follow-up studies of type III metaplasia did not show an increased risk of gastric carcinoma [51]. Examination of microcarcinomas less than 5 mm in diameter revealed that prominent metaplasia accompa- nied tubular carcinoma but not mucocellular (signet-ring cell) carcinoma [52].…”

Section: Intestinal Metaplasia (Im)mentioning

confidence: 99%

Cellular and molecular pathology of gastric carcinoma and precursor lesions: A critical review

Ming

1998

Gastric Cancer

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Abstract:The cellular and molecular pathology of gastric cancer and its precursors are reviewed and discussed. Gastric carcinogenesis is a multistep phenomenon, beginning with precancerous conditions. Among these, adenoma is a direct precursor, because of the dysplastic nature of its cells. However, gastric adenoma is relatively rare. Chronic atrophic gastritis (CAG) is the most common precancerous condition, in which intestinal metaplasia often occurs. Carcinoma develops in CAG through stages of hyperplasia and dysplasia involving both metaplastic and non-metaplastic glands. Molecular alterations, including replication error and p53 and APC gene mutation and aneuploidy have been found in some of these conditions, confirming their role in carcinogenesis. Carcinomas of the stomach are heterogeneous in cellular composition. Both intestinal and gastric types of cells are found in all types of tumors, indicating the unique characteristics of gastric cancer. Many molecular lesions have been found in gastric carcinomas. Basic changes involve replication errors, telomerase activity, and aberrant CD44 transcripts. Many other changes often show differences in the frequency of their occurrence between the two major histological types of gastric carcinoma: well differentiated versus poorly differentiated, or intestinal type versus diffuse type. The timing and frequency of these changes in the stomach differ from the timing and frequency in colonic carcinogeneis. Pathological evaluation remains reliable and meaningful, in basic research as well as clinical management. To obtain correlation with molecular alterations, the need for detailed pathologic classification of gastric carcinoma is recognized, taking into account its biologic behavior and grades of cell differentiation.The cellular and molecular pathology of gastric cancer and its precursors are reviewed and discussed. Gastric carcinomas are unique in their heterogeneity in both cellular composition and molecular changes.

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Limited value of type III intestinal metaplasia in predicting risk of gastric carcinoma.

Cited by 65 publications

References 14 publications

Antral Intestinal Metaplasia in <i>Helicobacter pylor</i><i>i</i> Gastritis

Antral Intestinal Metaplasia in <i>Helicobacter pylor</i><i>i</i> Gastritis

Intestinal metaplasia types and the risk of gastric cancer: A cohort study in Slovenia

Cellular and molecular pathology of gastric carcinoma and precursor lesions: A critical review

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