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Query: UMLS:C0024623 (gastric cancer)
 36,219 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Morphological and biochemical changes reflecting the process of genesis of experimental stomach cancer were studied and compared in experiments carried out on 170 rats to whom N-methyl-N'-nitro-N-nitrosoguanidine had been given in drinking water. The concentration of the compound in drinking water was 167 mg/l. Malignization mostly developed during the ingrowth of the epithelial complexes involved in the process of carcinogenesis into the submucous membrane, in rare cases, into the mucous membrane itself. The results of experiments showed that biochemical changes preceded morphological alterations. The signs of inhibition of the synthesis of the isoenzyme spectrum of pepsinogen-pepsin revealed the qualitative changes of biochemical processes of the epithelium. A possible dependence of morphological features of the process of carcinogenesis on the evolutionally-established functional peculiarities of rat stomach epithelium is discussed.
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PMID:Morphological and biochemical changes induced in rat stomach by N-methyl-N'-nitro-N-nitrosoguanidine. 47 27

Up to 19--20 fractions of separate RNA species and groups have been revealed in malignant tumors of the stomach and mucous membrane of patients with stomach cancer, ulcer and polyposis of the stomach by means of the method of analytical and preparative electrophoresis in 2.5% polyacrylamide gel. A more intensive incorporation of 14C uridine both into the nuclear and separate fractions of cytoplasmic RNA was observed in stomach tumors in comparison with the stomach mucous membrane of man. Pepsinogen-pepsin was synthesized by bound polysoms of the stomach mucous membrane. In stomach malignant tumors of man the polysomes were not capable of synthesizing this enzyme. Fractions of messenger RNA with sedimentation constants 16S-17S, possessing the ability to stimulate pepsinogen-pepsin synthesis in vitro, have been isolated from cytoplasmic RNA of a pig stomach mucous membrane.
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PMID:Realization of genetic information programming the synthesis of pepsinogen-pepsin in the mucous membrane and tumors of the stomach in man. 79 Feb 10

In children and adolescents from two areas of Costa Rica with contrasting gastric cancer risks, two factors suspected to be linked to the natural history of the disease were tested: serum antibodies to Helicobacter pylori and serum pepsinogen levels. One hundred fifty-five subjects from the high-risk area of Turrubares were compared to 127 from the low-risk area of Hojancha. No significant differences were found in the prevalence of IgG or IgA antibodies to Helicobacter pylori between the two regions. The prevalence of IgG was 65.8% in the high-risk area and 72.4 in the low-risk area, and that of IgA was 43% in both areas. The levels of pepsinogen, especially pepsinogen C, were significantly elevated in subjects with H. pylori antibodies in their serum. The mean levels of pepsinogen C in those negative, positive, and strong positive for H. pylori antibodies were 8.7, 14.3, and 21.1 ng/ml. These findings suggest that H. pylori-associated gastritis, predominantly of antral localization, is very prevalent in Costa Rican children and adolescents. Such gastritis might be associated with a high prevalence of intestinal metaplasia and a high gastric cancer risk in the inland, but not the coastal rural populations. H. pylori may therefore be an insufficient cause whose role in gastric carcinogenesis is contingent upon the presence of other factors.
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PMID:Antibodies to Helicobacter pylori and pepsinogen levels in children from Costa Rica: comparison of two areas with different risks for stomach cancer. 130 56

The chief cell mass and serum pepsinogen I (PGI) have been evaluated in 18 patients with gastric cancer of intestinal type of the body-fundus. Moreover, a correlation with the parietal cell mass and the maximal acid output it has been effected. The patients have been subdivided in relation to histologic condition of the fundic mucosa. In case of gastric cancer with preatrophic fundic gastritis it has been revealed hypozymogenism with normoPGI and hypoparietalism with hypochlorhydria, in case of gastric cancer with atrophic fundic gastritis it has been revealed hypozymogenism with hypoPGI and hypoparietalism with hypochlorhydria. From this experience it emerges a similar anatomic-functional profile between gastric cancer of the body-fundus and chronic fundic gastritis without cancer. In particular, it emerges that serum PGI is a good marker of atrophic fundic gastritis, but it is not discriminant between atrophic fundic gastritis and atrophic fundic gastritis associated to gastric cancer.
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PMID:[Zymogenic cell mass and serum pepsinogen I: the cell secretory correlations in patients with gastric intestinal-type cancer of the corpus-fundus]. 143 99

The serum pepsinogens in man have been reviewed with respect to clinical and physiological significance. The many places of synthesis of pepsinogen (PG A) and progastricsin (PG C) are described. The major part of serum pepsinogen and progastricsin is synthezized in the stomach, and the findings after antrectomy indicate that the majority of the pepsinogens in serum originates from the corpus of the stomach. The concentrations of pepsinogen and progastricsin in serum in relation to stomach diseases, e.g. ulcer disease, gastritis, and cancer of the stomach, are described. Despite typical findings, i.e. hyperpepsinogenemia in duodenal ulcer disease, or hypopepsinogenemia in atrophic gastritis or stomach cancer, there is a big overlap in serum concentrations between the groups reducing the clinical value of routine measurements of pepsinogens. Most promising are the findings in stomach cancer disease, where the combined measurement of pepsinogen levels and the isozymogen Pg5 is found to be highly indicative for the presence of a gastric carcinoma. Reports state that pepsinogens are excellent markers of recurrence of gastric cancer somewhere in the body after total gastrectomy. Genetical studies have--concerning pepsinogen--proved the multiple gene/multiple loci model. There is only a single progastricsin gene in humans and no genetic heterogenity has been found. Finally, the relationship between gastric infection with the bacterium Helicobacter pylori, and elevated pepsinogen and progastricsin levels in the blood, and the search for serologic markers of gastric diseases is discussed.
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PMID:Clinical implications of serum pepsinogen and progastricsin in man. 145 83

The possibility that urinary pepsinogen I is a tumor marker of stomach cancer after total gastrectomy was examined. To decide the cutoff level of urinary pepsinogen I after total gastrectomy, urine samples from 15 patients who had undergone total gastrectomy for stomach cancer in the early or advanced stages and had been free from recurrence for more than 5 years were examined by pepsinogen I-specific radioimmunoassay. The mean concentration of urinary pepsinogen I was 17.5 +/- 7.4 ng/ml and the cutoff level of urinary pepsinogen after total gastrectomy was set at 32 ng/ml (mean + 2 SD). Twenty-two of 74 cases who had undergone total gastrectomy for stomach cancer were regarded as positive. And 20 of these 22 positive cases had definite clinical signs of recurrence of stomach cancer. There were only two false-positive cases. These results suggest that urinary pepsinogen I will be an useful tumor marker in detecting the recurrence of stomach cancer after total gastrectomy.
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PMID:Urinary pepsinogen I as a tumor marker of stomach cancer after total gastrectomy. 164 90

The gastric and intestinal phenotypic expressions of tumor cells in 18 adenomatous hyperplasias, 33 well-differentiated adenocarcinomas, and 16 undifferentiated adenocarcinomas (4 poorly differentiated adenocarcinomas, 10 signet-ring cell carcinomas and 2 mucinous adenocarcinomas) induced by N-methyl-N'-nitro-N-nitrosoguanidine or 4-nitroquinoline-1-oxide in the rat glandular stomach were studied by histochemical stainings for mucin and immunohistochemical staining for pepsinogen isozyme 1 (Pg 1). By histochemical staining for mucin [by the paradoxical concanavalin A method, the modified method with labeled peanut lectin, the galactose oxidase-Schiff (GOS) reaction, and the sialidase-GOS reaction] and immunohistochemical staining of Pg 1, gastric cancer cells of each histological group could be clearly classified into a gastric type, including mucous neck cell pyloric gland cell, and surface mucous cell subtypes, and an intestinal type, including goblet-cell, and intestinal absorptive cell subtypes. All tumors examined in this work consisted mainly of gastric-type cells but intestinal-type tumor cells were occasionally found among the gastric-type tumor cells. The incidences of intestinal-type cells in adenomatous hyperplasias (11.1%) and small well-differentiated adenocarcinomas (28.6%) were significantly less (P less than 0.05) than that in large well-differentiated adenocarcinomas (68.4%). The incidence of intestinal-type cells in small undifferentiated adenocarcinomas (25.0%) was also less than that in large ones (58.3%). The present results suggest the occurrence of change of phenotypic expression of tumor cells from the gastric type to the intestinal type during growth of tumors.
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PMID:Cellular differentiation and histogenesis of rat glandular stomach cancers. 169 50

Chief cell mass and type I serum pepsinogen (PGI) were calculated in 19 advanced antral gastric cancer of intestinal type. Comparisons were also made with parietal cell mass and acid secretion. In gastric cancer of the antrum there is a significant decrease of the chief cell mass and of serum pepsinogen I. The patients were subdivided according to the histological findings of the fundic mucosa. In cases of antral gastric cancer with superficial fundic gastritis there is normozymogenism with hyperpepsinogenemy; with preatrophic fundic gastritis there is hypozymogenism with normopepsinogenemy; with atrophic fundic gastritis there is hypozymogenism with hypopepsinogenemy. Similar behavior of the chief cell mass between antral gastric cancer and fundic atrophic gastritis without cancer has become recognized and while the validity of PGI as a marker of fundic atrophic gastritis has emerged it does not allow discrimination between atrophic fundic gastritis and atrophic fundic gastritis associated with gastric cancer of the antrum.
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PMID:Advanced gastric cancer of the antrum: anatomic-functional correlation between chief cell mass and serum pepsinogen I. 175 90

The possibilities to screen atrophic corpus gastritis with serum pepsinogen I (S-PGI) and serum gastrin (S-gastrin) concentrations have been studied in 774 subjects: 71 index subjects selected from a general population at random, 353 of their first-degree relatives, 276 first-degree relatives of patients with gastric cancer, 53 patients with pernicious anaemia, and 21 of their relatives. Discrimination function analysis was calculated from members of random and gastric carcinoma families. S-PGI less than 30 ng/ml had a high sensitivity for severe diffuse atrophic corpus gastritis (SDAG) alone (89.5%) and SDAG + severe patchy atrophic corpus gastritis (SPAG) (89.1%). Respective figures for specificity were 91.5% and 94.8%. The discriminatory power of S-PGI less than 30 ng/ml and S-PGI less than 25 ng/ml was of the same order. The sensitivity of low S-PGI decreased sharply in detection of slighter forms of atrophic corpus gastritis. The sensitivity of S-gastrin greater than 100 pmol/l to discriminate SDAG was 57.9% and SDAG+SPAG 58.7%. Respective figures for specificity were 90.2% and 92.2%. Diffuse and patchy atrophic changes behaved similarly regarding S-PGI and S-gastrin mean concentrations. Accordingly, the biopsy specimen with the severest atrophic changes indicates the degree of atrophy, which associates closely with the changes in S-PGI and S-gastrin. In conclusion, severe atrophic (diffuse or patchy) corpus gastritis may be screened from a general population with high sensitivity and specificity by low S-PGI less than 30 ng/ml, whereas an increased level of S-gastrin is too insensitive for this.
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PMID:Serum pepsinogen I and serum gastrin in the screening of severe atrophic corpus gastritis. 175 17

Serum pepsinogen I (S-PGI) and serum gastrin (S-gastrin) were examined in the screening of three types of atrophic gastritis with inherent high risk of gastric cancer: in 102 cases with severe atrophic corpus gastritis (SACG), in 5 cases with severe atrophic antrum gastritis (SAAG), and in 15 cases with severe atrophic pangastritis (SAPG) (atrophy both in corpus and in antrum) found among 916 subjects from three family series (265 from gastric cancer families, 425 from randomly selected control families and 226 from pernicious anaemia families). There is no way to screen directly atrophic gastritis restricted to the antral mucosa. In pangastritis atrophy of antral glands causes a failure of the hypergastrinemic reaction of achlorhydria. The combination of S-PGI less than 25 micrograms/l + S-gastrin less than 200 pmol/l detected 80.0% of our cases with SAPG, and only 17 subjects of 794 (2.1%) were false positives i.e. who had not advanced atrophic gastritis. The risk of gastric cancer may be significantly higher in SAPG than in SACG. The estimated prevalence of SAPG was 3% in random-family members over 60 years. The combination of S-PGI and S-gastrin is recommended when the cost/benefit ratio in the screening program of gastric cancer is considered and people from a general population are selected for endoscopic studies.
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PMID:Serum pepsinogen I and serum gastrin in the screening of atrophic pangastritis with high risk of gastric cancer. 175 19


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