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

A sample of 219 primary stomach cancers, 143 advanced cancers and 76 early cancers were examined for mucin histochemical staining (the paradoxical concanavalin A method, the galactose oxidase-Schiff [GOS] reaction, and the sialidase-GOS reaction) and immunohistochemical reactivity (pepsinogen [Pg] I, Pg II, SH-9 and TKH-2). Gastric cancer cells were clearly classified according to mucin histochemistry into a gastric type, including mucus neck cell, pyloric gland cell and surface mucus cell types, and an intestinal type, including goblet-cell, and intestinal absorptive cell types. TKH-2 monoclonal antibody, which recognizes the mucin-associated sialosyl-Tn antigen, reacted with the mucin of goblet cells in both the normal small intestine and in the intestinal metaplasia of the stomach. Sixty-five of 106 (61%) differentiated adenocarcinomas and 76 of 113 (67%) undifferentiated adenocarcinomas had over 10% of their cancer cells positive for TKH-2. The TKH-2-positive cancers were primarily classified as a goblet-cell type by mucin-histochemical staining and the other immunohistochemical staining methods. Therefore, it is concluded that sialosyl-Tn is an excellent marker of small intestinal mucins and is indicative of a small intestinal type of differentiation in two-thirds of gastric cancers.
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PMID:Expression of sialosyl-Tn in intestinal type cancer cells of human gastric cancers. 831 Aug 25

In order to adopt pepsinogen levels as a screening indicator of gastric cancer, the serum pepsinogen I (PG I) and serum pepsinogen II (PG II) levels were studied using one thousand samples from a rural area and their ratios PG I/PG II were calculated. Samples were collected by stratified random sampling of the residents in S town with a population of about 10,000. The collected data was statistically analyzed to determine distributions by respective categories of sex and age. The following results were obtained. 1. The distributions of PG I, PG II and their ratio PG I/PG II levels largely deviated from normal distributions. Therefore, it is recommended that non-parametrical method is used to analyze this data. 2. The median of PG I level (49.3 micrograms/l) in males was statistically higher than that (43.6 micrograms/l) in females. On the other hand, a statistically significant difference between males and females was not observed in either the PG II value or the ratio PG I/PG II, respectively. 3. The pattern for changes in PG I values with age was different between males and females. While PG I levels were almost constant until the sixties, after the seventies levels showed a marked decrease in male subjects. In female subjects, an age effect in levels was not observed for PG I. On the other hand, PG II levels increased with age except for age group seventies, and the PG I/PG II ratios showed a decreasing tendency in both males and females.
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PMID:[Distribution of serum pepsinogen I, II values and their ratios in residents of a rural area]. 832 51

In a cross-sectional study of 634 men aged 40 to 49 years, randomly selected from five areas of Japan with different rates of gastric cancer mortality, 121 men of 624 evaluated were diagnosed as having atrophic gastritis through serum pepsinogen I < 70 ng/ml and the pepsinogen I (PGI)/pepsinogen II (PGII) ratio < 3.0. We examined the relation of Helicobacter pylori (H. pylori) antibodies and dietary factors, including plasma level of antioxidant micronutrients, to the presence of atrophic gastritis. Presence of H. pylori IgG antibodies was associated with increased risk of atrophic gastritis (odds ratio [OR] = 1.9, 95 percent confidence interval [CI] = 1.1-3.3). As the level of plasma beta-carotene increased, we found a steady decrease in the risk of atrophic gastritis (OR for second quartile = 0.7, third quartile = 0.6, fourth quartile = 0.4, with CI = 0.2-0.8). Frequent intake of yellow vegetables also was associated with lower risk, while frequent intake of soybean products was related to increased risk. Although H. pylori antibodies, beta-carotene level, and intake of soybean products were all significant in the multivariate analysis, these factors did not explain the differences in atrophic gastritis prevalence among the five regions. The analysis of these risk factors in relation to each pepsinogen marker showed that although both H. pylori infection and low plasma beta-carotene were associated with the decreased level of serum PGI/II ratio, the former was derived from the increase of PGII, which is common in early stage of atrophic gastritis, and the latter from the decrease of PGI, which is specific to severe atrophic gastritis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Helicobacter pylori, dietary factors, and atrophic gastritis in five Japanese populations with different gastric cancer mortality. 834 78

The recent discussions about the relationship between helicobacter-pylori-infection, gastritis and the occurrence of stomach cancer caused us to analyse blood sera of 543 participants randomly selected from the general population in the age of 25 to 34 and of 55 to 64 years from Mosbach (Neckar-Odenwald-Kreis), the county of Deggendorf (Lower-Bavaria) and Augsburg (Upper-Bavaria) regarding IgG-antibodies against helicobacter pylori and the concentrations of the pepsinogens A and C. The latter were used as markers for the presence of chronic gastritis without atrophy and with severe atrophy. The prevalence of helicobacter pylori infection and of forms of gastritis showed no particular differences regarding region or gender. Notable differences in the prevalences were observed with respect to the two age strata. The helicobacter pylori prevalence of the regions being studied ranged for males from 13% to 75% and for females from 22% to 76%. The prevalences of chronic gastritis without atrophy in the investigated areas, derived from the pepsinogen titers, were found to be for males between 24% and 70% and for females between 28% and 61%. Chronic gastritis with severe atrophy appeared mainly in the age group of 55 to 64 years, ranging from 2% to 11% in males and 4% to 10% in females, depending upon region. The helicobacter pylori prevalence and the prevalence of chronic gastritis without atrophy were found to be highly correlated. Chronic gastritis with severe atrophy was also found to be associated with helicobacter pylori prevalence. However, this association did not reach statistical significance.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Prevalence of Helicobacter pylori and gastritis in southern Germany. Results of a representative cross-sectional study]. 837 30

With respect to the inverse association of serum ferritin level (SFL) with the risk of gastric cancer (GC) observed in some recent epidemiologic studies, possible mediation by achlorhydria as well as atrophic gastritis (AG), both of which are strongly associated with GC risk at not only the individual but also the population level, was examined in a cross-sectional study of 634 men aged 40 to 49 years randomly selected from 5 populations in Okinawa, Iwate, Nagano, Akita and Tokyo. AG and achlorhydria were serologically diagnosed based on the criteria of pepsinogen (Pep) I level < 70 ng/ml and Pep I/Pep II ratio < 3.0, as described previously, and a serum gastrin level of over 140 pg/ml, respectively. In the results, while the mean SFL for all the subjects differed significantly by area, similar areal differences in SFL were also found even when only the non-AG cases were considered. However, both of the above differences were eliminated with the exception of those between Okinawa and each of the other 4 areas, when adjustments were made for medical histories of diabetes mellitus, ulcers and liver disease, body mass index and gamma-glutamyltranspeptidase level. Therefore, no correlation among the 5 areas was observed between the adjusted areal mean SFLs and GC mortality in either case.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Does high gastric cancer risk associated with low serum ferritin level reflect achlorhydria? An examination via cross-sectional study. 840 48

In a survey of 930 adults aged 35-74 years randomly sampled from the general population of four areas of Italy, two at low and two at high risk for gastric cancer, plasma levels of Helicobacter pylori IgG antibodies were assayed in order to investigate associations with the geographical distribution of gastric cancer and other dietary and life-style factors, as assessed by personal interview. H. pylori positivity (antibody titer above or equal to 10 micrograms/ml), 45% overall, increased with age and was inversely associated with social class but showed little geographical variation or association with dietary variables and blood nutrients. H. pylori positivity was also associated with increased blood levels of pepsinogens, particularly pepsinogen II. The authors discuss these findings in relation to those from a previous case-control study of gastric cancer in the same areas.
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PMID:Helicobacter pylori antibodies in areas of Italy at varying gastric cancer risk. 842 Jun 10

To verify the hypothesis that chronic atrophic gastritis (CAG) is a precancerous lesion for gastric cancer, we investigated the correlation between the prevalence rates for CAG determined by levels of serum pepsinogens (I and II) of randomly selected, healthy, blood donors and the mortality rates for gastric cancer among four prefectures (Akita, Iwate, Miyagi, and Okinawa) in Japan. The prevalence rates for CAG according to a criterion that the level of pepsinogen I is below 70 ng/ml and the pepsinogen I to pepsinogen II ratio is below 3.0, were the highest in Akita for both sexes (38.8 percent in males, 37.8 percent in females) and the lowest in Okinawa (13.9 percent in males, 12.3 percent in females), where mortality rates for gastric cancer are the highest and the lowest in Japan, respectively. The correlation between the prevalence rates for CAG and the standardized mortality ratios for gastric cancer among these four prefectures was statistically significant in males (r = 0.97, P = 0.03), but less significant in females (r = 0.92, P = 0.08). These data strongly support the hypothesis that CAG is a precancerous lesion. The limitations of our cross-sectional study and the advantages of measuring the levels of serum pepsinogens in epidemiologic studies and in mass-screening programs for gastric cancer are discussed.
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PMID:Correlation between the prevalence of gastritis and gastric cancer in Japan. 843 26

The aim of this study was to estimate the validity of mass screening for gastric cancer using serum pepsinogens (PG test). The study subjects were 4876 workers aged from 40 to 61 years old. Sera were obtained at the time of the health checkup and serum pepsinogen levels (PG I and PG II) were measured at the same time. PG I < 50 ng/ml and PG I/PG II ratio < 3.0 were adopted as the criteria for a positive result for the PG test. PG test-positive subjects were examined, in principle, by endoscopy. Furthermore, all subjects were followed up for a year to check for occurrence of gastric cancer. Among the total subjects, 911 (18.7%) were positive for the PG test and 650 (71.4%) among the positive subjects underwent further examinations, which revealed 11 cases of gastric cancer. Seven gastric cancer cases were diagnosed during the follow-up period within one year after the PG test. When the results of one years's follow-up from the time of screening were defined as the gold standard, the sensitivity and specificity of the PG test were estimated at 66.7% and 81.5%, respectively. The authors conclude that the validity of the PG test as a mass screening method may be comparable to that of X-ray screening, if optimum criteria of a positive test are selected.
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PMID:Sensitivity and specificity of mass screening for gastric cancer using the measurment of serum pepsinogens. 863 12

This study is aimed at a role of Helicobacter pylori (HP) infection in reflux esophagitis of the elderly. 46 patients with reflux esophagitis aged at older than 60 years are selected for this study with informed consent. 43 patients without reflux esophagitis, peptic ulcer, and gastric cancer are used as a control group. In reflux esophagitis, gastric mucosal atrophy is judged as closed type of endoscopic findings in all cases. In control, 27 of 43 patients were judged as open type. Serum pepsinogen I, II ratio is 4.73 +/- 1.28 which is higher significantly than 3.39 +/- 1.69 in control. Serological positive rate of HP antibody is 39.1% in reflux esophagitis. This rate is significantly lower than 62.7% in control. In conclusion, low frequency of chronic HP infection protects gastric mucosa from atrophy, and keeps secretion of gastric acid, resulting in reflux esophagitis of the elderly accompanied with various abnormal esophago-gastric functions.
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PMID:[Gastric mucosal atrophy and prevalence of Helicobacter pylori in reflux esophagitis of the elderly]. 865 65

Helicobacter pylori infection has been suggested to be associated with an increased risk of gastric cancer, and low levels of serum pepsinogen I (PG I) have been linked to atrophic gastritis, which is a risk factor for gastric cancer. In Finland, 39,268 persons from 25 cohorts participated during 1968-1972 in a health examination survey and were followed for up to 13 years. A nested case-control study was performed on 84 stomach cancer patients identified from the Finnish Cancer Registry and 146 controls matched for age, sex, and municipality. Serum samples drawn at the baseline study were analyzed. An elevated level of serum anti-H. pylori immunoglobulin A (IgA) antibodies (a titer > or = 70) and a low serum PG I level ( < 49 micrograms/liter) were associated with an increased risk of gastric cancer. The odds ratios were 2.52 (95% confidence interval (CI) 1.14-5.57) for high IgA and 2.68 (95% CI 1.35-5.30) for low PG I. For high immunoglobulin G (IgG) ( > or = 700), the odds ratio was only 1.50 (95% CI 0.70-3.22). When both high IgA and low PG I were present, the odds ratio was 5.96 (95% CI 2.02-17.57). The association of H. pylori infection with cancer became stronger with longer follow-up times, whereas that of low PG I was strongest at shorter follow-up times. Our findings support the hypothesis that H. pylori infection is a prevalent and potentially preventable cause of gastric cancer. They stress the value of IgA antibody determinations and provide new evidence for a pathogenesis leading from prolonged infection through atrophic gastritis to gastric cancer.
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PMID:Circulating anti-Helicobacter pylori immunoglobulin A antibodies and low serum pepsinogen I level are associated with increased risk of gastric cancer. 867 45


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