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

Gastric cancer is still a major cause of mortality due to cancer worldwide. The most common type of gastric cancer is intestinal type carcinoma, which usually occurs in stomachs containing chronic atrophic gastritis. Individuals with chronic atrophic gastritis are considered to be at increased risk for developing intestinal type carcinoma of the stomach. To examine the association between chronic atrophic gastritis and other gastric cancer risk factors, a cross-sectional study was conducted using serum samples and questionnaire information collected from 776 persons of full Japanese ancestry in the greater Seattle area in 1994. The presence of chronic atrophic gastritis and Helicobacter pylori infection was determined by measurement of serum pepsinogen levels and H. pylori antibodies, respectively. Based on multiple logistic regression, the significant predictors of chronic atrophic gastritis were age over 50 years, H. pylori infection, and 20 years or more lived in Japan. Alcohol consumption, smoking, prior peptic ulcer, and history of gastric cancer in parents were not significantly associated with chronic atrophic gastritis. The results imply that H. pylori infection since earlier life and other unknown exposure factors in Japan might have played an important role in the development of chronic atrophic gastritis.
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PMID:Chronic atrophic gastritis and Helicobacter pylori infection among Japanese Americans in Seattle. 1096 79

The role of Helicobacter pylori infection in gastric cancer was evaluated in a high-risk population in Venezuela using serological assays in a study of 302 cases and 483 neighborhood controls. To investigate the claim that assays for H. pylori should use antigens derived from local strains, four different assays derived from Venezuelan and European strains were used. Prevalence of IgG H. pylori antibodies in controls was very high, with estimates between 72 and 92%. Prevalence was similar in cases and controls. However, cases had lower antibody titers. This effect was observed only in subjects with low pepsinogen (PG) levels PGI/PGII <3.0), which suggested that extensive atrophy in cases causes a loss of H. pylori infection, with a consequent reduction in antibody titer. In addition, advanced cases (stage II or higher) had lower antibody titers than less advanced cases, which indicated that the lower antibody titers in cases may be attributable partially to a diminished immune response. All of the four assays for anti-H. pylori antibodies gave similar results. No evidence was found for the superiority of the assay based on Venezuelan strains. These results are consistent with other case-control studies in high-risk populations and highlight the difficulties of investigating H. pylori infection in retrospective studies.
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PMID:Helicobacter pylori and stomach cancer: a case-control study in Venezuela. 1100 15

A low level of serum pepsinogen I (Pg I) is a risk factor for gastric cancer (GC); low levels of Pg I and the pepsinogen ratio (Pg I:Pg II) are correlated with chronic atrophic gastritis. We report serum Pg levels and compare the degree of association with GC among Japanese and non-Japanese Brazilians. Sera were cross-sectionally ascertained from 93 Japanese Brazilian patients category matched by age and sex with 110 controls, and 228 non-Japanese Brazilian patients individually matched by age and sex with one control. Among non-Japanese Brazilians, GC was associated with a Pg I level <30 ng/ml (odds ratio [OR], 2.5; 95% confidence interval [CI], 1.7-3.8) and a Pg I:Pg II ratio < 3.0 (OR, 3.4; 95% CI, 2.2-5.3). However, among Japanese Brazilians, the association was present with a level of Pg I < 30 ng/ml (OR, 3.5; 95% CI, 1.9-6.3), and was weak with a Pg I:Pg II ratio < 3.0 (OR, 1.3; 95% CI, 0.73-2.4). Serum Pg I may be preferred to the Pg I:Pg II ratio to study the association between Pg and GC among Japanese Brazilians.
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PMID:Ethnic differences in serum pepsinogen levels among Japanese and non-Japanese Brazilian gastric cancer patients and controls. 1119 70

cagA gene, the best known virulence factor of Helicobacter pylori, codes for an immunodominant CagA protein. In this study, CagA antibodies of the IgG class were measured by immunoblot or enzyme immunoassay in subjects with positive H. pylori serology, and the presence of CagA antibodies was compared with that of H. pylori antibodies of IgA and IgG classes. Serum samples were available for a total of 1,481 subjects, including gastroscopied patients with biopsy-verified H. pylori infection, smoking men with a normal or low serum pepsinogen I level indicating atrophic corpus gastritis, and subjects who later developed gastric cancer and their matched controls. CagA antibodies were significantly more prevalent among individuals with elevated H. pylori antibody titres of the IgA class than in those with IgG antibodies only, with the exception of a small subgroup of individuals who later developed gastric cancer. CagA-positive H. pylori strains seem to induce an immune response with a markedly higher frequency of IgA than what is found in inflammation caused by CagA-negative strains. The presence of serum IgA antibodies to H. pylori seems to indicate a higher risk for CagA-positive H. pylori infection and possibly more severe late sequelae of the disease.
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PMID:Association of CagA-positive infection with Helicobacter pylori antibodies of IgA class. 1120 73

Intestinal-type gastric adenocarcinomas usually are preceded by chronic atrophic gastritis. Studies of gastric cancer prevention often rely on identification of this condition. In a clinical trial, we sought to determine the best serological screening method for chronic atrophic gastritis and compared our findings to the published literature. Test characteristics of potential screening tests (antibodies to Helicobacter pyloni or CagA, elevated gastrin, low pepsinogen, increased age) alone or in combination were examined among consecutive subjects enrolled in a study of H. pylori and preneoplastic gastric lesions in Chiapas, Mexico; 70% had chronic atrophic gastritis. English-language articles concerning screening for chronic atrophic gastritis were also reviewed. Sensitivity for chronic atrophic gastritis was highest for antibodies to H. pylori (92%) or CagA, or gastrin levels >25 ng/l (both 83%). Specificity, however, was low for these tests (18, 41, and 22%, respectively). Pepsinogen levels were highly specific but insensitive markers of chronic atrophic gastritis (for pepsinogen I <25 microg/l, sensitivity was 6% and specificity was 100%; for pepsinogen I:pepsinogen II ratio <2.5, sensitivity was 14% and specificity was 96%). Combinations of markers did not improve test characteristics. Screening test characteristics from the literature varied widely and did not consistently identify a good screening strategy. In this study, CagA antibodies alone had the best combination of test characteristics for chronic atrophic gastritis screening. However, no screening test was both highly sensitive and highly specific for chronic atrophic gastritis.
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PMID:Screening markers for chronic atrophic gastritis in Chiapas, Mexico. 1121 66

The present investigation aims at defining the functional status of several gastric cancer cell lines in order to assess their usefulness as adequate cellular models to study the regulation of gastric digestive functions. Compared to AGS, Hs746t and KATO-III cells, NCI-N87 exhibited an unique differentiation status. They formed coherent monolayers expressing E-cadherin and ZO-1 junctional proteins; their integrity and epithelial morphology were maintained at post-confluency for up to 10 days. All cell lines synthesized PAS-reactive (mucous-type) glycoconjugates. However, only NCI-N87 cells expressed MUC6 glycoprotein suggesting a mucopeptic phenotype. Immunostaining, enzymatic assays, Western blotting and Reverse Transcriptase polymerase chain reaction (RT-PCR) revealed that all cell lines contained varying levels of pepsinogen (Pg5) and human gastric lipase (HGL). Only NCI-N87 cells were able to express zymogens at higher levels, in granule-like structures, and to efficiently secrete both HGL and Pg5. The addition of epidermal growth factor (EGF) to post-confluent NCI-N87 cells, which exhibit an abundant membrane staining for EGF-receptors, modulated HGL activity without affecting Pg5. In conclusion, this investigation enlightens the potential usefulness of the gastric cell line NCI-N87 as a model for elucidating the cellular and molecular mechanisms involved in the regulation of human gastric epithelial functions.
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PMID:Gastric cancer cell lines as models to study human digestive functions. 1124 64

Serum pepsinogen (sPG) levels are used in gastric cancer screening programs. However, modification of sPG levels by smoking habit, according to the status of Helicobacter pylori (H. pylori) infection has been little investigated. This study investigated the effects of smoking on serum levels of pepsinogen I (PG I), pepsinogen II (PG II), and gastrin by IgG titer of antibody against H. pylori (Hp-IgG titer) using the data from 356 current-smokers and 262 non-smokers (133 never-smokers and 129 ex-smokers) in a cross-sectional study of 618 men aged 40 to 49 years. PG I, PG II, PG I / PG II ratio and gastrin were significantly associated with Hp-IgG titer in never-smokers [Spearman's correlation coefficient (95% confidence interval): 0.23 (0.07, 0.39), 0.52 (0.41, 0.63), -0.40 (-0.54,-0.27), and 0.25 (0.10, 0.41), respectively]. However, the correlation coefficients of PG I and PG II decreased in current-smokers, 0.02 (-0.1, 0.13) and 0.32 (0.22, 0.42), respectively. In H. pylori seronegative and low titer cases, the mean PG I level was significantly (P < 0.01) higher in current-smokers, compared with non-smokers. However, in high titer cases, the mean PG I level was lower in current-smokers. Mean PG II and gastrin levels, and PG I / PG II ratio did not differ according to smoking habits by Hp-IgG titer. The gastrin level was significantly correlated with PG II, but not PG I. These data indicate that current smoking influences the serum PG I level depending on Hp-IgG titer and the associations between sPGs and Hp-IgG titer. Gastrin is not involved in the modification of PG I levels by smoking.
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PMID:Effect of smoking on serum pepsinogen I level depends on serological status of Helicobacter pylori. 1126 33

BACKGROUND: We conducted a case-control study to evaluate whether patients with severe gastric atrophy (indicated by serum pepsinogen concentration) have a high risk of gastric cancer.METHODS: At the time of diagnosis of gastric cancer, sera from 301 patients (cases) and 602 sex- and age-matched cancer-free individuals (controls) were tested for the presence of anti- Helicobacter pylori IgG antibody (HM-CAP enzyme-linked immunoassay [ELISA] kit; Kyowa Medix, Tokyo, Japan) and serum pepsinogen (PG) levels (PG I and II Riabead Kits; Dainabot, Tokyo, Japan). We defined positivity for pepsinogen a pepsinogen I concentration of less than 70 ng/mL and a PG I/II ratio of less than 3.0. We categorized the subjects according to serum pepsinogen levels and anti- Helicobacter pylori IgG antibody, creating four categories.RESULTS: Of the 301 cancer cases, 177 had positive serum pepsinogen levels, and 172 were positive for anti- Helicobacter pylori IgG antibody. The category in which subjects had positive serum pepsinogen levels and were negative for anti- Helicobacter pylori IgG antibody had the highest proportion (76.9%) of individuals with gastric cancer and the highest odds ratio (4.20) of the four categories. The odds ratios were 2.55 (95% confidence interval; 1.92-3.88) for positive serum pepsinogen levels and 0.93 (95% confidence interval; 0.63-1.27) for positive anti- Helicobacter pylori IgG antibody.CONCLUSION: These results suggest that patients with positive serum pepsinogen levels who are negative for IgG antibody to Helicobacter pylori, constitute a high-risk group for gastric cancer. Helicobacter pylori infection is associated with the development of gastric cancer by providing a suitable environment i.e., severe gastric atrophy, for carcinogenesis of the gastric mucosa.
Gastric Cancer 1998 Mar
PMID:Severe atrophic gastritis with Helicobacter pylori infection and gastric cancer. 1195 55

There are two markers, pepsinogen isoenzymes and antibody against Helicobactor pyroli, for screening of high-risk group for gastric cancer. Most of markers are used in diagnosis, staging, monitoring and differentiating subgroups of gastric cancer. Markers in ascitic fluid are used for diagnosing peritoneal invasion of gastric cancer.
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PMID:[Tumor markers in gastric cancer]. 1197 55

In Japan, mass screening for gastric cancer with photofluorography was initiated in 1960. At present, over 6 million people are screened annually. The sensitivity and specificity of photofluorography are 70%-90% and 80%-90%, respectively. The 5-year survival rate is 15%-30% better in screen-detected cancers than in symptom-diagnosed cases. Although no randomized controlled trials have been reported, cohort and case-control studies generally showed a decreased risk of mortality from gastric cancer in the screened subjects. The summary odds ratio (95% confidence interval) of three case-control studies for ever screened versus never screened subjects was 0.39 (0.29-0.52) for men and 0.50 (0.34-0.72) for women. Substantial evidence indicates that the Japanese screening program with photofluorography is effective in reducing the mortality from gastric cancer. The measurement of serum pepsinogens has recently drawn attention as an alternative to photofluorography, given its lower cost and simplicity. Some studies have suggested a comparable accuracy for the two methods. However, these investigations may have overestimated the relative sensitivity of serum pepsinogen testing compared with photofluorography, because serum pepsinogen testing was conducted as prevalent screening, while photofluorography was done as incident screening. Furthermore, no studies have directly examined whether the screening with serum pepsinogens reduced gastric cancer mortality. Therefore, at present, evidence is insufficient to determine the benefit of this program.
Gastric Cancer 2000 Aug 04
PMID:Screening for gastric cancer in Japan. 1198 3


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