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

The results of biochemical blood analysis in 75 patients with I-II stage gastric cancer have been analysed. The control group was comprised of 210 patients with gastritis, callous ulcer and polyps of the stomach. By means of a correlation-regression analysis, the non-linear relations between I-II stage gastric cancer and biochemical indices of the blood were revealed. The highly significant indices for diagnosis of the disease in mass examination of the population have been developed.
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PMID:[The value of biochemical indices of the blood in early diagnosis of gastric cancer]. 128 26

Helicobacter pylori has now been recognized as one of the most common chronic human infections. It has been accepted as an important aetiologic agent in non-immune chronic gastritis and plays a key role in the aetiology of duodenal ulcer. It may also be involved in the pathogenesis of gastric cancer.
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PMID:Helicobacter pylori: past, present, and future. 129 43

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

H. pylori infection is strongly associated with chronic gastritis and is probably the main course of chronic inflammation in the gastric mucosa. Acquisition of the infection will lead to gastritis and the eradication of the bacterium results in healing and final cure of the gastritis. Chronic gastritis and H. pylori infection may occur in antrum and/or corpus, and will gradually result in atrophy of the underlying mucosa in a great number of affected persons. Correspondingly, impairments in several important functions of the gastric mucosa are consequences of the atrophy and inflammation. Hp infection and gastritis associate with important gastroduodenal diseases, such as peptic ulcer diseases and gastric cancer. There are reasons to suggest that the infection and subsequent gastritis precede these diseases, and that they are important risk factors for both disorders. In fact, peptic ulcer can be seen a late frequent complication of an H. pylori infection. In addition, the type and grade of gastritis can be used in prediction of the ulcer risk if adequate biopsy specimens are available for microscopy from both antrum and corpus mucosa (Table II). An association between chronic gastritis and Helicobacter pylori (Hp) infection is strong. Clearly more than 80% of cases with chronic gastritis are related to coexistent Hp infection. Furthermore, both Hp and gastritis are extremely common in patients with peptic ulcer supporting the view that they are causally related to the ulcer disease. Correspondingly, similar suggestions may also be presented about the links between Hp and gastritis in the pathogenesis of gastric cancer.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Helicobacter pylori, chronic gastritis and peptic ulcer. 130 46

A series of 60 gastric endocrine tumors comprised 44 body-fundus argyrophil carcinoids, of which 23 arose in a background of hypergastrinemia and type A chronic atrophic gastritis (A-CAG), mainly with histologic patterns suggestive of an autoimmune process. Only 22 percent (compared with 19 percent of 58 tumor-free A-CAG cases) of 36 carcinoids and 21 percent of 19 A-CAG carcinoids investigated had Helicobacter pylori (HP) colonization, against 50 percent of 14 CAG-associated neuroendocrine carcinomas or mixed endocrine-exocrine tumors, 84 percent of 150 cases with early gastric cancer (p < 0.001 versus carcinoids), mostly with B- or AB-type CAG, 76 percent of 97 tumor-free AB-CAG, and 95 percent of 151 tumor-free B-CAG cases. Secondary hypergastrinemia and local mechanisms activated by chronic autoimmune gastritis are among factors involved in the pathogenesis of relatively indolent CAG-associated carcinoids, whereas active HP gastritis in cooperation with environmental carcinogens may likely cause more severe epithelial transformation, leading to ordinary cancer and, possibly, to neuroendocrine carcinomas or mixed endocrine-exocrine tumors.
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PMID:Distinct patterns of chronic gastritis associated with carcinoid and cancer and their role in tumorigenesis. 134 Oct 79

Helicobacter pylori has been shown to be the cause of chronic active gastritis and the evidence that it is involved in the development of peptic ulcer disease and gastric cancer is compelling. Narrow host range, tissue specificity, and chronic inflammation are hallmarks of infection. The study of virulence determinants has just begun but it seems likely that urease, adhesins, cytotoxins, and mediators of inflammation will prove to be important.
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PMID:Helicobacter pylori and gastroduodenal disease: pathogenesis and host-parasite interaction. 134 68

Contents of the progesterone receptors (PgR) and estrogen receptors (ER) in 18 gastric adenocarcinoma tissues were determined using both the dextran-coated charcoal (DCC) assay and enzyme immunoassay (EIA). PgR were found in 15 cancer tissues (range, 1.0-58.8 fmol/mg protein) and 12 normal mucosal tissues (range, 1.4-26.8 fmol/mg protein) by DCC assay, whereas only 6 cancer tissues (ranged, 0.2-3.3 fmol/mg protein) and 7 normal mucosal tissues (range, 0.1-0.8 fmol/mg protein) had measurable PgR by EIA analysis. Similar results were observed for ER. DCC assay found ER in 12 cancer tissues (range, 2.9-112.6 fmol/mg protein) and 12 normal mucosal tissues (range, 1.2-36.6 fmol/mg protein), whereas EIA measured ER in 16 cancer tissues (range, 0.1-3.5 fmol/mg protein) and 15 normal mucosal tissues (range, 0.1-4.8 fmol/mg protein). No significant correlation between DCC and EIA was observed for either PgR or ER. DCC assay and its modified procedures including 5% DCC stripping of cytosol and/or the addition of sodium molybdate in buffer were simultaneously measured in 5 gastric adenocarcinoma tissues and 1 gastritis cystica polyposa tissue (a precancerous lesion). Higher receptor levels were found by the modified procedures than by conventional method. Using the DCC procedure with addition of sodium molybdate in buffer for receptor analysis, PgR and ER were found in gastric tissues in six patients, with significantly increased levels of measurable PgR. The results suggest that PgR and ER may be involved in the physiology of normal and gastric cancer tissues; their clinical implications are worthy of further study.
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PMID:The nontransformed progesterone and estrogen receptors in gastric cancer. 137 95

The effectiveness of a fluorescent analysis in the diagnosis of gastric cancer was studied in 280 patients. Fluorescence of a tumor was noted in 87% of cases. Dependence of fluorescence of a tumor on its sizes was revealed: in tumor diameter less than 1 cm, fluorescence was revealed in 94% of cases, more than 4 cm--in 76%. In infiltrative growth, only 74% of tumors were fluorescent. To define the possibility of the use of a fluorescent analysis in the differential diagnosis of gastric diseases, 490 patients with presumptive diagnosis of chronic gastritis, gastric ulcer disease, polyposis were examined. In diagnosis of +malignant polyps in 91.5% of cases, results of the fluorescent analysis concurred with the findings of histologic study. Probability of establishing the correct diagnosis by the data of fluorescent analysis in ulcer disease is equal to 87.5%, in chronic gastritis--86%.
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PMID:[Use of the fluorescent analysis in early diagnosis of cancer of the stomach]. 138 May 85

This study aimed to examine the association between Helicobacter pylori, histological gastritis, and intestinal metaplasia in gastric cancers of different histological types. A total of 169 gastrectomy specimens received in one pathology department were studied. Altogether 156 were adenocarcinomas (intestinal type 87, diffuse type 50, mixed type 19). Gastritis occurred in 137 of 163 body specimens (84%) and in 126 of 131 antral specimens (96%). Its presence was unrelated to tumour histology. Atrophic gastritis was more common in both body and antral mucosa in intestinal type compared with diffuse type carcinoma. This was also true for intestinal metaplasia of the body, but not of the antral mucosa. H pylori was present in 101 of 163 (62%) body specimens and 56 of 131 (43%) antral specimens. In intestinal type carcinoma, H pylori was found in 52/84 (62%) body specimens and in 24/70 (34%) antral specimens, while the corresponding figures for diffuse type carcinoma were 29/48 (60%) and 17/38 (45%) respectively. Tumour histology therefore had no influence on the occurrence of H pylori. Tumour site had no effect on the presence or absence of gastritis, atrophic changes, intestinal metaplasia, or H pylori. While both H pylori and gastritis are associated with gastric cancer, the association is unrelated to tumour histology and may not be a causal one.
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PMID:Helicobacter pylori and gastric cancer: correlation with gastritis, intestinal metaplasia, and tumour histology. 139 26

Hypergastrinemia is a very important clinical condition for the reason that a growing body of evidence obtained from animal and human experiments has revealed gastric carcinoids induced by hypergastrinemia. We investigated 35 patients with Basedow's disease (BD) to elucidate the mechanism of hypergastrinemia associated with BD as well as the relationship between type A gastritis and BD. Fasting serum gastrin levels in BD (296.1 +/- 251.4 pg/ml; mean +/- S.D.) were significantly (p less than 0.001) higher than those in age-matched 27 healthy subjects (106.1 +/- 69.2), and in the BD group, significant positive correlation was detected between fasting serum gastrin levels and thyroid hormones (i.e. T3 and free T4). In the hyperchlorhydria group in BD with hypergastrinemia, the levels of fasting serum gastrin were normalized after euthyroidism was attained due to antithyroidal drugs. On the other hand, in the achlorhydria group in BD significant hypergastrinemia was persisted in spite of normalization of thyroid function. Twenty % of the BD patients had histologically proved type A gastritis with achlorhydria, and all patients with type A gastritis were older than 60 years old. Endoscopic examination revealed that one patient with type A gastritis had an early gastric cancer. However, no gastric carcinoids were demonstrated in this study. In conclusion, the results described as above suggested, 1) hypergastrinemia observed in patients with BD may be induced by gastrin hypersecretion due to hyperthyroidism as well as type A gastritis, 2) BD patients with type A gastritis were recommended to undertake regular endoscopic examination for detecting gastric cancers as well as gastric carcinoids.
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PMID:[Hypergastrinemia and type A gastritis in Basedow's disease]. 140 86


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