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

Plantwide analyses of the mortality experience of 8147 foundrymen revealed excesses for several diseases including lung cancer. Using indirect measures of smoking, it appeared that most, if not all, of the excess of lung cancer deaths could be explained by smoking habits. To explore further the possible association between these mortality excesses and foundry exposures, jobs were grouped into six work areas on the basis of similarities in production processes. The findings of analyses by work areas support the inferences from plantwide observations. No evidence was found of a relationship between lung cancer and foundry exposures. The pattern of mortality from emphysema and cerebrovascular disease in the different work areas paralleled that of lung cancer, suggesting that mortality from these diseases may have been influenced by a common etiologic agent, probably tobacco smoke. The data also reveal possible associations between metal pattern-making and colon cancer, silica or metal dust and stomach cancer, and carbon monoxide and ischemic heart disease.
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PMID:Mortality of iron foundry workers. II. Analysis by work area. 801 21

Triptolide (Tri) is a diterpenoid triepoxide isolated from Tripterygium wilfordii Hook F. The effects of Tri on the colony formation of breast cancer cell lines MCF-7 and BT-20, stomach cancer cell lines MKN-45, MKN-7, and KATO-III, and promyelocytic leukemia cell line HL-60 were reported. Using Hamburger-Salmon's double layer agar technique with certain modifications, cancer cells were cultured in 0.3% agar in a highly humidified atmosphere of 5% CO2 at 37 degrees C for 14-21 d. Colonies were counted on d 14 (occasionally d 21) with the colony analyzer system CA-7A. Of the 5 solid tumor cell lines tested, 4 showed diminished colony formation in soft agar by greater than 70% of control value in Tri 10(-8) mol.L-1 (continuous exposure). The magnitudes of the inhibitory effect of Tri on most breast and stomach cancer cell lines were similar to that on the leukemia cell line HL-60. IC50 were 0.504-1.22 micrograms.L-1. The clinically achievable peak plasma concentration (PPC) of Tri was estimated as 0.15 mg.L-1, being 72-126 times higher than the IC70 of the cancer cell lines except KATO-III. The results suggest that Tri might have a potential therapeutic effect on some types of solid tumors, e.g., breast and stomach cancers.
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PMID:Inhibitory effect of triptolide on colony formation of breast and stomach cancer cell lines. 181 94

Respiratory gas exchange was evaluated using indirect calorimetry during total body hyperthermia (TBH) in 7 postoperative patients with disseminated gastric cancer to the peritoneal cavity. TBH was induced using veno-venous bypass and extracorporeal circuit incorporating a heat exchanger to keep pulmonary arterial temperature 42 degrees C. The high temperature was maintained for 3 hours under general anesthesia with droperidol (0.15 mg.kg-1), morphine (1 mg.kg-1) and enflurane (less than 0.5%). Oxygen consumption (VO2) was also calculated using the Fick equation and thermodilution cardiac output. Hyperthermia for three hours increased both VO2 and carbon dioxide output (VCO2) values to 1.5 times as compared to the control values before heating, respectively. VO2 values measured by indirect calorimetry correlated well with the values calculated from the Fick equation when respiratory and cardiovascular system were relatively stable during the procedure. Gradual but statistically insignificant increase in respiratory quotient was observed after recooling started. These results suggest that indirect calorimetry was valuable to measure respiratory gas exchange continuously during hyperthermic state as well as normothermic state. However, RQ value observed in the present study may be modified by several factors including lactate accumulation in the blood, and may not reflect substrate utilization during the hyperthermic state.
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PMID:[Respiratory gas exchange during total body hyperthermia in man]. 238 95

In an attempt to define the mechanism of weight loss in cancer patients, fat and carbohydrate oxidation rates were calculated in 93 patients. Seventy patients with colorectal or gastric cancer were compared with a control group of 23 patients with nonmalignant illness. Twenty-seven patients with cancer and 13 control patients had lost more than 10% of their pre-illness body weight. Fat and carbohydrate oxidation rates were derived from measurements of oxygen consumption, carbon dioxide production, and urinary nitrogen excretion. Patients with cancer had significantly higher fat oxidation rates (p less than 0.01) and significantly lower carbohydrate oxidation rates (p less than 0.05) when compared with controls. Weight-losing cancer patients had significantly higher fat oxidation rates when compared with weight-stable cancer patients (p less than 0.02), weight-stable controls (p less than 0.01), and weight-losing controls (p less than 0.02). Cancer patients with liver metastases (N = 14) had significantly higher fat oxidation rates (p less than 0.01) and significantly lower carbohydrate oxidation rates (p less than 0.01) compared with cancer patients who had localized disease. There were no significant differences among the groups with respect to resting energy expenditure when expressed as kilocalorie per kilogram lean body mass per day. The presence of cancer appears to be associated with abnormal fat and carbohydrate metabolism. The increased rate of fat oxidation seen in patients with cancer, especially those with weight loss or liver metastases, may be a significant factor in the development of cancer cachexia.
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PMID:The oxidation of body fuel stores in cancer patients. 378 35

A sensitivity test of antitumor drugs using primary shortterm culture with 3H-thymidine was performed on stomach cancer patients. Stomach cancer tissues, which were removed in the operating room, were cut into cubes of 1 to 2 mm. Thereafter, they were put on a stainless steel mesh which was placed in a small petri dish (40 X 15 mm) and they were moisted with the cultivating medium. An appropriate dose of antitumor drugs (MM-C, 5-FU, cytosine arabinoside) was added at the onset of cultivation and 3H-thymidine was further added 24 hours later. At the end of cultivation in a CO2 incubator for about 3 days, the specimens were homogenized in an ice-cold homogenizer with 5% trichloroacetic acid. DNA fraction of the specimens was extracted by Schmidt-Thannhauser method. The isotope activity in DNA fraction was measured in a scintillation counter and was represented as cpm/microgram DNA. Sensitivities of antitumor drugs can be determined by comparison between isotope incorporations into the specimens tested and those into control specimens. Bacterial and fungal contaminations were observed in primary stomach cancer tissues.
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PMID:[Sensitivity test of antitumor drugs by the use of isotope]. 718 15

To investigate ornithine decarboxylase (ODC) activity and proliferating cell nuclear antigen (PCNA) in gastric cancer, ODC activity and PCNA were measured in 50 resected samples. The relationship between both and clinicopathologic factors was examined. ODC activity was 473.3 +/- 54.7 pmol CO2/60 min/mg protein in tumors, and 273.5 +/- 38.3 pmol CO2/60 min/mg protein in normal mucosa. ODC activity in tumors was significantly higher than that of normal mucosa. ODC activity in tumors was significantly high in gross type 4, maximum diameter more than 10 cm, depth se, infiltrative growth (INF) gamma, positive lymph vessel invasion and positive lymph node metastasis. PCNA-LI was 24.7 +/- 1.5% in tumors, and 13.9 +/- 1.1% in normal mucosa. PCNA-LI of tumors was significantly higher than that of normal mucosa. PCNA-LI of tumors was significantly high in gross type 2, histological type tub 2 and por, depth ss beta and se, IFN beta, positive lymph vessel invasion, positive venous invasion, and positive lymph node metastasis. ODC activity and PCNA-LI were closely related in normal mucosa, showing a correlation coefficient of 0.730. On the other hand, their relationship was weak in tumors, showing a correlation coefficient of 0.417. These results suggest the differentiation of value between ODC activity and PCNA-LI in gastric cancer. In gastric cancer, ODC activity and PCNA-LI in tumors may be good markers of lymph node metastasis. Furthermore, PCNA-LI may be a good marker of hematogenous metastasis.
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PMID:[A ornithine decarboxylase activity and proliferating cell nuclear antigen in gastric cancer]. 782 96

Recently many reports have shown a strong association between Helicobacter pylori infection in the stomach and recurrent peptic ulcer. Moreover, prospective cohort serological studies showed that H. pylori infected individuals have significantly increased rate of gastric cancer in the USA. H. pylori is a gram-negative spiral organism which has urease activity and produces ammonia and CO2 from urea, and nestles in the gastric pits and overlaying mucus gel layer. Many diagnostic methods of H. pylori infection are available; ie bacterial culture, 13C-urea breath test, histology, serum IgG antibody against H. pylori. We developed a new method, ie tissue IgA antibody against H. pylori and detection of H. pylori DNA in the gastric juice by PCR method. Triple therapies with metronidazole, bismuth compounds, and amoxicillin or tetracyclin are difficult to use in Japan because of their sever side effects. Thus, new methods with proton pump inhibitor (PPI) and amoxicillin have been introduced. We treated 14 patients of whom were H. pylori positive-active peptic ulcer with 30 mg/day of lansoprazole, a new PPI, plus 1,500 mg/day of amoxicillin for 2 weeks and 8 (57%) patients were eradicated. Gastric carcinogenesis are multi-steps and multifactorials process. Hypothetical sequence of intestinal type of gastric cancer is that superficial gastritis-->atrophic gastritis-->intestinal metaplasia-->dysplasia-->gastric cancer and H. pylori infection may play a role in the early stage of the sequence. We examined mucosal IgA antibody against H. pylori in chronic gastritis and intestinal metaplasia detected by the Tes-Tape method in 25 resected specimens after gastrectomy for gastric cancer. Positivity rates of tissue H. pylori IgA antibody were lower in the mucosa of intestinal metaplasia than in non-metaplastic gastric mucosa and were negative in carcinoma. Causal relationship between H. pylori infection and gastric cancer is not proven and factors other than H. pylori infection are also important in the gastric carcinogenesis. Finally we introduce 2 reports: (1) NIH Consensus Conference: Helicobacter pylori in peptic ulcer disease (JAMA. 1994; 272: 65-69). The consensus panel concluded that 1. ulcer patients with H. pylori infection require treatment with antimicrobial agents in addition to antisecretory drugs whether on first presentation with the illness or on recurrence; 2. the value of treating nonulcerative dyspepsia patients with H. pylori infection remains to be determined; and 3. the interesting relationship between H. pylori infection and gastric cancer requires further exploration. (2) World Health Organization: Working Group Meeting (Reported in World Congress of Gastroenterology, Los Angeles, 1994). H. pylori plays a causal role in the chain of events leading to cancer of the stomach. Group I: definite carcinogen.
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PMID:[Helicobacter pylori in peptic ulcer and gastric cancer]. 785 88

Helicobacter pylori has been implicated as an agent in the pathogenesis of antral gastritis, gastric and duodenal ulcer and probably in gastric cancer. The C13 urea breath test is a diagnostic method quick to perform, sensitive, reliable and non invasive. It is based on the presence of Helicobacter pylori urease activity, which permits to detect it in the infected mucosa. A substrate (urea) labelled with Carbon 13 is administered to the patient and exhaled breath is collected to detect the possible catabolism product (CO2 labelled with C13). In the European protocol, patients in fasting condition are given a test meal to delay gastric emptying and five minutes later a solution which contents 100 mg of C13 labelled urea. Breath samples are collected before and 30 minutes after urea was given. In our first year of experience, 363 patients with Helicobacter pylori infection detected by histology or urease were studied by C13 urea breath test, with a sensitivity and specificity of 95 and 96%. False negatives may occur if the test is used after antibiotics and other antiulcer drugs. Its main indication is to monitor eradication therapy after treatment. Its possible use as a quantitative test still remains unclear.
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PMID:[C13 urea breath test in the diagnosis of Helicobacter pylori infection in the gastric mucosa. Validation of the method]. 864 14

Helicobacter pylori is a spiral Gram-negative microaerophilic bacterium that causes one of the most common infections in humans; approximately 30-50% of individuals in Western Europe are infected and the figure is nearly 100% in the developing world. It is recognized as the major aetiological factor in chronic active type B gastritis, and gastric and duodenal ulceration and as a risk factor for gastric cancer. H. pylori normally inhabits the mucus-lined surface of the antrum of the human stomach where it induces a mild inflammation, but its presence is otherwise usually asymptomatic. A variety of virulence factors appear to play a role in pathogenesis. These include the vacuolating cytotoxin VacA, cytotoxin-associated proteins, urease and motility. All are under intense study in an attempt to understand how the bacterium colonizes and persists in the gastric mucosa, and how H. pylori infections lead to the disease state. Although an explosion of research on H. pylori has occurred within the past 15 years, most efforts have been directed at aspects of the bacterium and disease process which are of direct clinical relevance. Consequently, our knowledge of many aspects of the physiology and metabolism of H. pylori is relatively poor. This should change rapidly now that the complete genome sequence of a pathogenic strain has been determined. This review focuses attention on these more fundamental areas of Helicobacter biology. Analysis of the genome sequence and some detailed metabolic studies have revealed solute transport systems, an incomplete citric acid cycle and several incomplete biosynthetic pathways, which largely explain the complex nutritional requirements of H. pylori. The microaerophilic nature of the bacterium is of particular interest and may be due in part to the involvement of oxygen-sensitive enzymes in central metabolic pathways. However, the biochemical basis for the requirement for CO2 has not been completely explained and a major surprise is the apparent lack of anaplerotic carboxylation enzymes. Although genes for glycolytic enzymes are present, physiological studies indicate that the Entner-Doudoroff and pentose phosphate pathways are more active. The respiratory chain is remarkably simple, apparently with a single terminal oxidase and fumarate reductase as the only reductase for anaerobic respiration. NADPH appears to be the preferred electron donor in vivo, rather than NADH as in most other bacteria. H. pylori is not an acidophile, and must possess mechanisms to survive stomach acid. Many studies have been carried out on the role of the urease in acid tolerance but mechanisms to maintain the protonmotive force at low external pH values may also be important, although poorly understood at present. In terms of the regulation of gene expression, there are few regulatory and DNA binding proteins in H. pylori, especially the two-component 'sensor-regulator' systems, which indicates a minimal degree of environmentally responsive gene expression.
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PMID:The physiology and metabolism of the human gastric pathogen Helicobacter pylori. 988 78

The effect of gastrin on stimulating tumour proliferation has been evaluated on human pancreas cancer cells in culture and in tumours transplanted to nude mice. The presence of CCK-B/gastrin-like receptor responsible for that effect of gastrin has been proved in colonic (WiDr, HT-29, YAMC) and pancreatic (PANC-1, BON) cell lines. The aim of our study was to examine the stimulating effect of gastrin and pentagastrin on the growth of human gastric adenocarcinoma cell line. The human gastric adenocarcinoma cell line (AGS, CRL-1739) was purchased from ATCC (Rockville, MA, USA). Gastrin-17 was purchased from Sigma-Aldrich (Budapest, Hungary), pentagastrin was from Zeneca Limited (Macclasfield, UK). The cells were incubated in DMEM containing 10% FCS on 96-well culturing plate with 10(4) cells/well starting cell number at 37 degrees C with 5% CO2. The proliferation rates were detected: by the measurements of the metabolically active cells with Owen's reagent and the determination of protein content, and by cell counting in a haemocytometer at several incubation times. As a result, we detected similar proliferation rates using gastrin-17 or pentagastrin in the incubation medium. The stimulating effect of gastrin/pentagastrin on cell line proliferation was in correlation with its concentration. Our results proved that pentagastrin is a 10 times less effective stimulator of proliferation of gastric cancer than gastrin-17, and that AGS human adenocarcinoma cell line might be CCK receptor positive.
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PMID:Gastrin and pentagastrin enhance the tumour proliferation of human stable cultured gastric adenocarcinoma cells. 1076 93


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