Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.2.1.26 (invertase)
 4,927 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The gastric- and intestinal-type properties of 15 human gastric cancers, which were transplanted into nude mice, were studied biochemically and histologically. Enzyme activities were determined in the crude extracts of cancer tissues: pepsinogen isozymes as gastric marker enzymes; and sucrase, aminopeptidase (microsomal), and alkaline phosphatase as intestinal marker enzymes. By hematoxylin and eosin staining and paradoxical concanavalin A staining, gastric cancer tissues were classified into gastric type (pyloric gland cell type and surface mucous cell type) and intestinal type (goblet cell type and intestinal absorptive cell type). On the basis of their properties, human gastric cancers were classified into four types: (a) intestinal type; (b) gastric type; (c) intestinal plus gastric type; and (d) unclassified type, showing no gastric- or intestinal-type properties. Of six well-differentiated adenocarcinomas, four were of intestinal type, one of gastric type, and one of intestinal plus gastric type. All of the intestinal-type carcinomas showed sucrase activity. Of the three signet ring cell carcinomas, one was classified as a gastric type, one as an intestinal plus gastric type, and one as an unclassified type. Of the six poorly differentiated adenocarcinomas, five were of the intestinal type and one of the unclassified type. The present results clearly showed the appearance of intestinal-type properties in gastric cancer cells not only in so-called intestinal-type carcinomas, but also in diffuse-type carcinomas.
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PMID:Gastric- and intestinal-type properties of human gastric cancers transplanted into nude mice. 669 75

Intestinal metaplasia is defined as the appearance of intestinal epithelium in the stomach. Intestinal metaplasia is frequently found in populations with a high incidence of gastric cancer. Macroscopic demonstration of sucrase and trehalase with Tes-tape in many resected stomachs yielded new information for understanding the nature of intestinal metaplasia. Intestinal metaplasia can be classified into two types, complete and incomplete. The former is associated with the presence of sucrase, trehalase, leucine aminopeptidase, alkaline phosphatase, goblet cells and Paneth cells, and the latter with that of sucrase, leucine aminopeptidase and goblet cells, but not trehalase or Paneth cells. Goblet cells in the complete type of intestinal metaplasia contain sialomucin, as does the small intestine, while those in the incomplete type contain sulphomucin and sialomucin, as does the large intestine. Well-differentiated adenocarcinoma is closely related to intestinal metaplasia, especially the incomplete type. Atypical epithelium of intestinal metaplasia has been proposed as a more proximate stage of gastric cancer. Intestinal metaplasia can be diagnosed by staining with dye under endoscopic observation. A reduced level of pepsinogen I in the blood reflects the presence of severe intestinal metaplasia, which is understood to be a sign of high risk of gastric cancer. Intestinal metaplasia is supposed to be produced by components of food. Mutagens/carcinogens such as N-methyl-N'-nitro-soguanidine and N-propyl-N'-nitro-N-nitrosoguanidine can produce intestinal metaplasia in the glandular stomach of rats and gastric cancers. The formation of intestinal metaplasia precedes the appearance of adenocarcinoma in the glandular stomach. Intestinal metaplasia, which is a kind of host reaction to environmental agents, may result either from genetic change - change in DNA structure - or from epigenetic change - change in the differentiation mechanism. Preventive measures could be developed to suppress the development of intestinal metaplasia and to suppress the process of conversion of metaplastic cells to cancer cells.
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PMID:Intestinal metaplasia of the stomach as a precancerous stage. 675 88

The clinicopathological significance of colonic and small-intestinal phenotypes has hitherto remained unclear in gastric cancers. The purpose of the present study was therefore to examine 86 gastric carcinomas histologically and phenotypically using several phenotypic markers, including colon-specific carbonic anhydrase 1 (CA1) and sucrase as small-intestine specific marker. Of 86 gastric cancers, sucrase and CA1 expression was observed in 12 (14.0%) and only in two cases (2.3%), respectively, associated with other intestinal markers such as villin and mucin core protein (MUC)2. In the sucrase cases, expression appeared independent of the stage. However, CA1 expression was observed only in two advanced cases. No association was observed between colonic and small-intestinal phenotypes, and lymph node metastasis and postoperative survival in the advanced gastric cancer cases with intestinal phenotypic expression. Cdx2 appeared to be linked to upregulation of both CA1 and sucrase. In conclusion, the data suggest that colonic phenotype occurs rarely in gastric carcinogenesis. Colonic and small-intestinal phenotypes appear with expression of several intestinal phenotypic markers under the control of Cdx2 and presumably other related transcription factors.
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PMID:Colonic and small-intestinal phenotypes in gastric cancers: relationships with clinicopathological findings. 1618 90