Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0024623 (gastric cancer)
 36,219 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Prospective epidemiologic studies among Hawaii Japanese indicate that serum PG I levels below 20 micrograms/1 are highly specific for the presence of intestinal metaplasia and the intestinal type of gastric cancer; but this test shows a low level of sensitivity. Substitution of the PG I/PG II ratio for the PG I level results in a modest improvement in the level of sensitivity at the expense of some loss in specificity. Antral gastritis and intestinal metaplasia are gastric cancer precursors in this population. Abnormally low values of serum PG I or the PG I/PG II ratio predict high stage tumors in the majority of cases. It therefore does not seem likely that estimates of serum pepsinogen are likely to increase the frequency of the diagnosis of early intestinal type carcinoma of the antral portion of the stomach in this population.
 ...
PMID:The relation of serum pepsinogen to gastric cancer and its precursors in Hawaii Japanese men: a progress report. 398 94

Duodenal ulcer has not been observed in full-heritage Pima Indians, while gastric cancer is relatively frequent. To investigate possible underlying factors for this phenomenon, we determined gastric acid output, gastric emptying rate, and plasma levels of gastrin, pepsinogen I, and pepsinogen II in apparently healthy Pima Indians and in Caucasian controls. The Pimas had significantly lower basal and stimulated outputs of gastric acid and higher fasting and postprandial plasma gastrin concentrations than the Caucasians. Plasma pepsinogen I levels were similar in the two groups, but plasma pepsinogen II was significantly higher and the ratio of pepsinogen I to pepsinogen II was significantly lower in the Pima Indians. In addition, gastric emptying of acaloric liquid meal was significantly delayed in the Pimas. The results suggest that the absence of duodenal ulcer in Pima Indians may be related to low gastric acid production and a slow rate of gastric emptying in this population. The associated findings of hypergastrinemia, hyperpepsinogenemia II, and a low ratio of pepsinogen I to pepsinogen II suggest that the hypochlorhydria may reflect an increased prevalence of chronic gastritis in full-heritage Pima Indians. This, in turn, could represent a risk factor for the development of gastric cancer in this population.
 ...
PMID:Low acid output in Pima Indians. A possible cause for the rarity of duodenal ulcer in this population. 646 10

Since the origin of group I pepsinogen (PG I) is no other than gastric mucosa, PG I has been considered to disappear in total gastrectomized patients. We, however, have found proteolytic activity in the urine of one-half of total gastrectomized patients and the activity has proven to be PG I by both gel chromatography and agar gel electrophoresis. Serum and urine PG I levels also have been determined by radioimmunoassay in 40 subjects. PG I was detected in almost all of them and the mean level of serum was 4.17 ng/ml and that of urine was 32.2 ng/ml. The levels had no relation to age and sex but elevated in the patients with recurrent gastric cancer after total gastrectomy. A few possibilities can be considered as to the source of PG I after total gastrectomy, in which heterotopic gastric mucosa or gastric gland metaplasia is most possible. An interesting result in this study was that both serum and urine PG I levels elevated in the recurrent patients. This phenomena suggests that gastric cancer may produce PG I.
 ...
PMID:[Group I pepsinogen (PG I) in the serum and urine after total gastrectomy]. 649 92

In order to evaluate its clinical usefulness, serum pepsinogen I level was measured in a prospective study in unselected patients affected by endoscopically and histologically confirmed gastric or duodenal diseases. The mean level in controls was 63 +/- 26 ng/ml (M +/- SD) with no statistical difference between males and females, while it was significantly higher in smokers than in non-smokers (respectively 69 +/- 25 and 56 +/- 25 ng/ml). On the average in gastric ulcer patients it overlapped with controls (69 +/- 34 ng/ml), but in prepyloric ulcers its value was higher (81 +/- 45 ng/ml) than that found in ulcer of the gastric corpus (66 +/- 30 ng/ml). Serum pepsinogen I level was significantly higher in duodenal ulcer patients (81 +/- 33 ng/ml), in males as compared to females and in smokers as compared to non-smokers (respectively 91 +/- 32 and 67 +/- 26 ng/ml). Higher than normal values were found in one subject affected by the Zollinger-Ellison syndrome, and in patients with severe renal failure. Low and very low levels were found after partial and total gastrectomies and in A type atrophic gastritis. In the case of duodenal ulcer, serum pepsinogen I determination showed a 16 p. 100 sensitivity and a 96 p. 100 specificity, while for atrophic gastritis it showed an 87 p. 100 sensitivity and a 100 p. 100 specificity. It is concluded that, at present, the most important clinical application seems to be its screening value in the detection of atrophic gastritis and consequently its potential use to detect populations at increased risk for gastric cancer.
 ...
PMID:Diagnostic usefulness of serum group I pepsinogen determination. 662 12

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.
 ...
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.
 ...
PMID:Intestinal metaplasia of the stomach as a precancerous stage. 675 88

Changes in pepsinogen isoenzyme patterns were examined in the pyloric mucosae of the stomachs of noninbred male Wistar rats after short-term administration of gastric carcinogens. N-Methyl-N-nitro-N-nitrosoquanidine, N-ethyl-N1-nitro-N-nitrosoguanidine, and N-propyl-N-nitro-N-nitrosoguanidine, which induce stomach cancer in rats, decreased the content of pepsinogen isoenzyme 1 )Pg 1), which was separated by poly-acrylamide gel electrophoresis. They also decreased the pepsingoen content of the pyloric mucosa. 4-Nitroguinoline 1-oxide, which induces a low incidence of stomach cancer in rats, rarely decreased the Pg 1 content or the pepsinogen content of the pyloric mucosa, and the incidence of such decreases was not statistically significant. However, diethylnitrosamine and dimethylnitrosamine, which do not induce stomach cancer in rats, did not cause any decrease in pepsinogen content. Ethyl methanesulfonate, a direct-acting carcinogen used as a control, also did not decrease the pepsinogen content.
 ...
PMID:Induction of changes in the pepsinogen content and the pepsinogen isoenzyme pattern of the pyloric mucosa of the rat stomach by short-term administration of stomach carcinogens. 679 78

The paper deals with the description of a simple, time-saving and sufficiently precise procedure of determining the activity and level of pepsinogen-pepsin in the gastric juice of healthy subjects and those at high risk for stomach carcinoma by means of photography. The level of pepsinogen-pepsin in the gastric juice of stomach cancer patients is generally found to be very low or nil. A considerable drop in the enzyme's activity is also observed in cases of polyposis of gastric mucosa as well as in ana- and hypoacidic states. The procedure may be used for assessment of the secretory function of gastric mucosa and screening for groups at high risk for stomach carcinoma.
 ...
PMID:[Use of the pepsinogen-pepsin test in examining persons at high risk of stomach cancer]. 679 18

Among 7498 Japanese men who were examined from 1967 to 1970, 48 were subsequently diagnosed with stomach cancer and had premorbid stored sera available for serum pepsinogen I analysis. The median interval between serum collection and diagnosis of cancer was 44.5 months (range, 3 to 103 months). A low pepsinogen I level was found in 15 of the 48 patients with stomach cancer and in only six (6.3%) of 96 matched control subjects (p < 0.001). All 15 patients with low pepsinogen I levels belonged to the subgroup of 38 who had the intestinal-mixed-other histologic types of gastric cancer. This finding indicates that a low serum pepsinogen I level is a subclinical marker of increased risk for these histologic types of gastric cancer.
 ...
PMID:Serum pepsinogen I as a predictor of stomach cancer. 743 85

The incidence rate of gastric cancer among men of Japanese ancestry living in Hawaii is about one-third as high as that of their counterparts living in Japan. Because of this difference, a prospective study was conducted to identify factors related to the development of gastric cancer in Hawaii. Eight thousand and six (8,006) men born from 1900-1919 were examined from 1965 to 1968 and followed for over 25 years. During this time, 250 incident cases of gastric cancer were identified. The study has found the following: 1) prior infection with Helicobacter pylori bacteria increased the risk for stomach cancer; 2) cigarette smoking was positively associated with gastric cancer with age at which smoking started being an important risk factor; 3) after taking cigarette smoking into account, alcohol intake was not related to stomach cancer risk; 4) a low pepsinogen I level identified subjects at increased risk for the intestinal histologic type of gastric cancer; 5) a low serum ferritin level was a marker for increased risk of stomach cancer; 6) there was a weak indication that the intake of vegetables and fruits was inversely related to gastric cancer; 7) there was no association of stomach cancer with levels of serum cholesterol, serum uric acid, serum micronutrients (retinol, beta-carotene or alpha-tocopherol) or blood hematocrit; 8) there was also no association of gastric cancer with body mass index or physical activity.
 ...
PMID:Gastric cancer among the Japanese in Hawaii. 749 9


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>