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)

This study was carried out to determine the cutoff levels of serum pepsinogen (PG) I, II and their ratio of PG I/PG II for gastric cancer to establish a better screening system. Optimal cutoff levels for gastric cancer screening using serum pepsinogens were determined using Youden's index. The sensitivity, specificity and Youden's index for gastric cancer cases were calculated according to sex, age and the stage of gastric cancer, and the maximum Youden's index in each category was adopted as the cutoff level for gastric cancer screening using serum pepsinogens. The maximal Youden's index in all gastric cancer cases was 0.37, corresponding to a cutoff level of PG I < 40 (micrograms g/l) and PG I/PG II < 3.5. The sensitivity and specificity for gastric cancer cases of these cutoff levels were 0.50 and 0.87, respectively. In future, better criteria for gastric cancer screening have to be examined with the estimation of Youden's index in addition to other epidemiological methods such as ROC (receiver operating characteristic) curves and/or cost benefit analyses.
 ...
PMID:Evaluation of cutoff levels for screening of gastric cancer using serum pepsinogens and distributions of levels of serum pepsinogen I, II and of PG I/PG II ratios in a gastric cancer case-control study. 933 12

H. pylori is thought to be a stomach carcinogen. Since no experimental model has hitherto been established to clarify the relationship between H. pylori and stomach carcinogenesis, the effects of infection with the bacteria on experimental carcinogenesis in the glandular stomach of mice were investigated. BALB/c mice were given salty diet or N-methyl-N-nitrosourea (MNU) and administered broth culture of H. pylori. The incidence of pepsinogen-altered pyloric glands, considered as precancerous lesions, was increased in the H. pylori inoculated group pre-treated with MNU. The findings provide the new experimental model demonstrating the relationship between stomach cancer and H. pylori.
 ...
PMID:Helicobacter pylori promotes development of pepsinogen-altered pyloric glands, a preneoplastic lesion of glandular stomach of BALB/c mice pretreated with N-methyl-N-nitrosourea. 946 Oct 19

The number of people examined in "the Japanese Stomach Cancer Examination" programs under "Health Services Law for the Aged" has not increased, and a strategy is needed to increase participation in the programs. We have thought out a plan to persuade people to the programs by using serum pepsinogen tests without changing the framework of the programs. The plan is as follows: The subjects are those who undergo phlebotomy in "the General Health Examination" programs and who do not undergo the Stomach Examination programs. Serum pepsinogen levels are measured using the sera and those with high risk for stomach cancer are persuaded to attend "the Stomach Examination" programs. To estimate the effect of the plan, we asked several local governments to complete a questionnaire on the numbers of subjects. The ratio of the number of the subjects in the plan to the number of screenees in recent Stomach Examination programs was 0.61. An increase of about 15% was expected in screenees of the Stomach Examination Programs, if 40% of the subjects in the plan were diagnosed as high risk and 60% of the high risk subjects attended the Stomach Examination programs. From the economical stand point, it was expected that detection rate would increase and that the plan did not raise the cost for detecting a patient with stomach cancer. We also conducted a questionnaire survey of those who would be the subjects of the plan. Eighty-two percent of the subjects answered that they would attend the Stomach Examination programs, if they were told that their risk of stomach cancer was high by the serum pepsinogen tests. These results seem to suggest that more people would participate in cancer examination programs when informed that their risk for cancer is high as determined by blood tests.
 ...
PMID:[Effectiveness and feasibility of a strategy for increasing participation in the Japanese Stomach Cancer Examination programs by incorporating serum pepsinogen tests]. 969 65

Gastric cancer is a rather common disease worldwide. In Italy it still accounts for 15,000 deaths annually. A sharp drop in the incidence rate of Lauren's intestinal histotype has been reported, whereas the frequency of the diffuse histotype is relatively steady. If the histogenesis of the latter is still somewhat obscure, the intestinal type confirms the sequence: atrophic gastritis--intestinal metaplasia--dysplasia--neoplasia. These different stages of development can nowadays be singled out through a series of indicators, the most reliable of which are the pepsinogen I/pepsinogen II ratio, the presence of sulphomucins and Lewis antigens in the gastric juices and NOR (Nucleolar Organizer Regions), cell ploidy and oncogenes determination. The genes involved in the neoplastic transformation are mostly oncosuppressors, the most frequent alterations being those relative to the APC gene, p53 and c-myc. In addition to the by now indispensable pathological staging of the disease, the modern prognostic factors are arising great interest: the most significant are the immunohistochemical examination of the peritoneal washing, and cell ploidy. Surgery is still the only potentially curative treatment: the earlier surgery is performed in the course of disease, the greatest the curative potential. The Authors' experience, which includes 400 operated cases with complete follow-up records, is here reported. The resectability rate turned out to be 84%, overall operative mortality was 6.5% with that due to surgical causes along being 3.7%. Overall survival at 5 years was 36%, while that of the curative operations 47%. Good results were obtained with the association surgery + intraoperative radiotherapy which resulted in a significant decrease in local recurrences of the disease.
 ...
PMID:Gastric cancer. Clinico-biological updating and analysis of 400 operated cases. 970 May 78

Following a phase I study, a phase II study was conducted to evaluate the effects of two different doses of tea polyphenols on serum pepsinogen levels. Subjects were patients aged 40 to 69 years who had undergone gastroscopy between 1995 and 1997 at Aichi Cancer Center Hospital, and had been found to have no disease requiring medication. Those with pepsinogen I < 70 ng/ml and pepsinogen I/II ratio < 6 were included in this study. Capsules containing 100 mg of tea polyphenols were administered for 1 year: 1 capsule per day for 101 patients (42 males and 59 females), and 6 capsules (equivalent to 10 cups) per day for 83 patients (30 males and 53 females). The enrollment of the 1 capsule group preceded that of the 6 capsule group, in which re-participation was allowed. Blood samples were obtained 1 year after participation from 86 participants of the 1 capsule group and 77 participants (43 new participants and 34 re-participants) of the 6 capsule group. The compliance in polyphenol capsule intake ranged from 11.4 to 105.7% (87.6% on average) of the scheduled amount for the 1 capsule group and 3.2 to 112.3% (77.8% on average) for the 6 capsule group. No serious polyphenol-related adverse effects were reported. The difference in pepsinogen I between before and after 1 year intake of the polyphenol was 3.1 ng/ml for the 43 participants of the 6 capsule group, but 3.5 ng/ml for the 1 capsule group. The mean pepsinogen I/II ratio for the 43 participants increased from 2.37 by 0.08. This increase was not larger than that for the 1 capsule group (from 2.61 by 0.11). Among 34 participants in both interventions, no significant increase in pepsinogen I and I/II ratio for the 6 capsule intervention was observed. This result suggests that additional polyphenol intake for 1 year in Japanese does not improve pepsinogen levels, which are considered to reflect stomach atrophy, a high-risk condition for stomach cancer.
 ...
PMID:Tea polyphenol intake and changes in serum pepsinogen levels. 1018 83

The role of the Helicobacter pylori in the induction of gastric carcinogenesis seems to be certain. The exact pathomechanism is not yet known, although the special genetic conditions both of the microbe and the host just as the imbalance of the apoptotic and proliferative processes caused by the chronic inflammation are assumed to be involved. The latter one can be proved by the use of different cell proliferative and apoptotic markers. The results are inconsistent whether the eradication therapy causes the regression of premalignant atrophic gastritis. The regression of the MALT-associated lymphoma after the eradication therapy seems to be more convincing. The need of the eradication to prevent gastric cancer can be judged by the follow-up of some biomarkers (e.g. HLA II genotype, PCNA index, anti HP-IgA titer and the serum pepsinogen level), although their diagnostical application could be hardly introduced in the everyday practise so far.
 ...
PMID:[Effect of Helicobacter pylori infection on the apoptotic and cell proliferative processes of the gastric mucosa]. 1022 45

The effects of low dose catechol administration in the diet on stomach carcinogenesis in mice after initiation with N-methyl-N-nitrosourea (MNU) in the drinking water were investigated. Male, 6-week-old, BALB/c mice were given MNU in the drinking water intermittently for 1-week periods at 1-week intervals for a total of 3 weeks at a concentration of 120 ppm (groups 1 and 3). Groups 2 and 4 served as non-initiated controls. From week 7, groups 1 and 3 were divided into four subgroups and the mice were fed on a diet containing 4 ppm (groups la and 3a), 20 ppm (groups 1b and 3b), 100 ppm (groups 1c and 3c), 500 ppm (groups 1d and 3d) or 0 ppm (groups 2 and 4) catechol for 44 weeks. At week 50, appreciably enhanced development of pepsinogen 1 altered pyloric glands (PAPG) was noted in groups 1c and 1d. The incidences of adenomatous hyperplasia and carcinomas were not affected in any of the catechol-treated groups as compared with corresponding controls on a basal diet. Thus, the administration of catechol in the diet at low doses enhanced only preneoplastic lesion development and not neoplastic lesion development. From these results, we conclude that the biological significance of the catechol promoting effect at probable human exposure levels on gastric cancer is probably limited, while the PAPG may be a sensitive endpoint lesion for mouse glandular stomach carcinogenesis.
 ...
PMID:Effects of low dose catechol on glandular stomach carcinogenesis in BALB/c mice initiated with N-methyl-N-nitrosourea. 1039 74

Fundic gland polyps (FGPs) are tiny multiple sessile polyps of the acid-secreting gastric mucosa. They have been described both in a sporadic form, mainly in middle-aged females, and in a syndromic form, associated with familial adenomatous polyposis (FAP)-Gardner's syndrome and attenuated variants (AFAP). They share the same histology, characterised by superficial and deep cystic dilatations, shortened gastric pits, with an inconspicuous lamina propria. They have been for a long time described as innocuous lesions, but some recent reports have shown that FGPs may harbour dysplastic foci and ultimately (particularly syndromic polyps) gastric cancer. Factors influencing their genesis are unknown. A circulating factor in FAP patients has been postulated and a role of female hormones has been suggested for sporadic FGPs. Whereas patients with sporadic FGPs have normal basal acid output, normal fast serum levels of gastrin and pepsinogen I, the role of gastrin seems crucial for the development of cystic changes in flat body-fundus mucosa, and for the appearance of FGPs in patients with Zollinger-Ellison syndrome. A role of H. pylori induced gastritis has been excluded. Actually, patients with both sporadic and syndromic FGPs appear consistently free from H. pylori colonisation, again for an unknown factor(s). Some recent reports have claimed a role for omeprazole in the genesis of FGPs, a highly controversial issue. Ultimately, the nature of FGPs is still debated: some have interpreted them as hamartomatous lesions, others as a peculiar form of hyperplastic polyp.
 ...
PMID:Fundic gland polyps: a still elusive entity on the eve of the year 2000. 1083 97

Serum pepsinogen values are markers of gastric mucosal status and of gastric cancer risk. The effect of Helicobacter pylori infection and sibship size on change of serum pepsinogen values over a seven-year span was investigated. Data from 2584 subjects with phlebotomy were analyzed both in 1989 and in 1996. The subjects were classified by H. pylori serology and sibship size (1 - 3 vs. 4 and more). Pepsinogen I (PG I) to II (PG II) ratio in '96 minus that in '89 was defined as DeltaPG I / II and compared among the groups. DeltaPG I / II was lower and decrease of PG I / II was more frequent among H. pylori-positive subjects than among negative subjects. The difference was owing to a decrease of PG I in all subjects and owing to an increase of PG II in those not younger than 30 years in '89. In H. pylori-positive subjects, those with a larger sibship size showed lower DeltaPG I / II and higher frequency of PG I / II decline. H. pylori infection exerts a reducing effect on PG I / II during the seven-year span. The effect of H. pylori is stronger among those with a larger sibship size, who are expected to have been infected with H. pylori in childhood. Inducing atrophy of gastric mucosa, which is reflected by a decline of PG I / II, may be one of the mechanisms through which H. pylori elevates the risk of gastric cancer.
 ...
PMID:Long-term effect of Helicobacter pylori infection on serum pepsinogens. 1083 90

Blood serum in stomach cancer and chronic gastritis has been compared. A sharp decrease in pepsinogen 1 level both in cancer and gastritis patients was found as compared with healthy subjects. Pepsinogen 1 level in poorly-differentiated tumor (37.4 ng/ml) was lower than in well-differentiated one (58.2 ng/ml).
 ...
PMID:[Radioimmunoassay of serum pepsinogen I in chronic gastritis and stomach cancer]. 1085 11


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