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)

This study was performed to evaluate changes in Magnesium (Mg) and Calcium (Ca) levels in blood and cancerous stomach tissue of patients with stomach cancer, who were classified into four stages of malignancy and three groups of metastatic category. Mg and Ca were determined with atomic absorption spectrophotometer after blood and stomach tissue were digested with nitric and perchloric acid. Significantly high Mg levels in the early stages were found both in plasma and in whole blood. On the other hand, significantly low Ca levels were found in blood plasma in most stages and in all metastatic groups. By contrast, significantly high Ca levels were observed in whole blood in later malignant stages and in two metastatic groups. Significantly high Mg and low Ca levels were found in cancerous stomach tissue in patients with stomach cancer, as compared to their normal stomach tissue. The same tendencies were observed in each malignant stages and metastatic groups. These changes in Mg and Ca levels in blood and cancerous stomach tissue may reflect inherent peculiarities of stomach cancer.
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PMID:[Changes in magnesium and calcium levels in blood and stomach tissue of patients with stomach cancer]. 142 7

Gastrin is known as a trophic factor for some stomach and colorectal cancer cells; however, the roles of gastrin receptors and the intracellular signal transduction pathways by which gastrin regulates cell growth are still unknown. The authors examined the effect of synthetic human gastrin-17 on growth of human stomach cancer cells (the parent line, AGS-P, and two different clones, AGS-10 and AGS-12), which were established (and have been maintained) in our laboratory. Gastrin stimulated growth of AGS-P and AGS-10 cells, which have gastrin receptors, in a dose-dependent fashion. A highly selective gastrin receptor antagonist, JMV 320, inhibited the growth-stimulatory effect of gastrin on AGS-P cells in a dose-dependent fashion. Concentrations of gastrin (10(-8) to 10(-6) M), which stimulated growth of AGS-P cells, did not affect either cyclic adenosine monophosphate production or phosphatidylinositol hydrolysis. Gastrin (10(-11) to 10(-5) M) mobilized calcium from the intracellular organelles to increases intracellular calcium level in AGS-P cells. The AGS-12 clone has no gastrin receptors, and gastrin did not affect growth or mobilization of intracellular calcium in these cells. Our findings indicate that gastrin stimulates growth of AGS cells through a mechanism that involves binding to specific gastrin receptors that are linked to the system for mobilization of intracellular calcium.
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PMID:The effect of gastrin on growth of human stomach cancer cells. 161 89

Blood magnesium (Mg) and calcium (Ca) concentrations were determined in patients with stomach cancer and in normal subjects. The patients were classified into four stages of malignancy and three metastatic categories. High Mg levels were found in plasma and whole blood of patients in the early stages of stomach cancer, while low Ca levels were found in blood plasma in most stages and in all metastatic groups. By contrast, high Ca levels were observed in whole blood in the later malignancy stages and in two of the metastatic categories. The calcium level in blood plasma does not therefore seem to depend on the stage of malignancy and metastasis, while the calcium level in whole blood and the Mg level in blood plasma and whole blood do appear to depend on the stage of malignancy or metastasis.
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PMID:Changes in blood magnesium and calcium concentrations in patients with stomach cancer. 213 75

Calcium intake inhibits growth of colon cancer in vivo, the mechanisms of which are not fully elucidated. The objective of this study was to determine whether Ca2+ directly affects the growth of colon cancer cells in vitro and to compare the effects of Ca2+ on the growth of several gastroenteropancreatic cancer cells, including mouse colon cancer (MC-26), human colon cancer (LoVo and WIDR), human gastric cancer (AGS and SII), and human pancreatic cancer (PANC-1 and MIA) cells. All tumor cell lines tested grew in medium containing low concentration (approx 0.16 mM) of Ca2+. Higher concentrations of Ca2+ significantly inhibited the growth of all three colon cancer cell lines tested but had no significant effect on proliferation of the stomach and pancreatic cancer cell lines. Growth of AGS cells, in the presence of 0.1 or 0.5 mM EGTA (resulting in the loss of the extracellular Ca2+) was similar to that observed in the absence of EGTA, indicating that AGS cells were relatively insensitive to loss of extracellular Ca2+. In the presence of TMB-8, an inhibitor of intracellular Ca2+ release, the growth of colonic cancer cell lines was inhibited in a dose-dependent manner, indicating that a minimum basal level of intracellular Ca2+ was required for continued proliferation of colon cancer cells. The stomach cancer cell lines (AGS) was once again less sensitive to the effects of TMB-8 than were the colon cancer cells, indicating an inherent difference in Ca2+ requirements and sensitivity to Ca2+ for growth of different gastroenteropancreatic cancer cells in vitro.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Differential effects of Ca2+ on proliferation of stomach, colonic, and pancreatic cancer cell lines in vitro. 221 99

We examined the effect of concomitant use of anticancer drugs such as Carmofur or 5-FU and Nicardipine, a Ca2+ antagonist, on human gastric cancer transplanted into nude mice, and obtained the following results: 1. Combined administration of Carmofur or 5-FU together with Nicardipine caused potentiation of an antitumor effect. 2. After Carmofur was used together with Nicardipine, the FU level in the tumor tissue was significantly elevated. In conclusion, it was found that in the combined use of Carmofur or 5-FU together with Nicardipine, a Ca2+ antagonist, caused a higher level of the FU in tumor tissue and potentiation of an antitumor effect on human gastric cancer transplanted into nude mice.
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PMID:[Effect of concomitant use of anticancer drugs and a Ca2+ antagonist, on human gastric cancer transplanted into nude mice]. 232 91

The antitumor effect of combined use of UFT and verapamil, a calcium antagonist, was examined in gastric cancer transplanted to BALB/c athymic nude mice. Four experimental groups included Group I (Control) which was administered 3% Gummi Alabicum (p.o.), Group II (UFT) which was administered 64.8 mg/kg UFT (p.o.), Group III (UFT + verapamil) which was administered UFT and 10 mg/kg verapamil (s.c.) and Group IV (verapamil) which administered same doses of verapamil. All mice were sacrificed at the day of 12 and pathological and flow cytometric studies were performed to those tumors. At the day of 8, significant retardation of tumor growth was observed in Group II and Group III compared with Group I (P less than 0.05). The ratio of tumor retardation of Group III was more predominant than that of Group II at the day of 9 (p less than 0.05). However, no difference in pathological and flow cytometric changes was observed between Group II and Group III. Weight loss and death, as side effects, were found in Group II and III. It was assumed that this may be depend on the over dose of UFT or methods of administration. These results suggested that combination chemotherapy of UFT and verapamil was effective in the retardation of gastric cancer, however the doses of UFT and verapamil have to be reexamined in order to control the side effect.
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PMID:[Experimental study on combination chemotherapy of UFT and calcium antagonist in gastric cancer]. 249 67

Pepsin is a potent proteolytic enzyme stored and secreted by chief cells in an inactive precursor form, pepsinogen. Its secretion is modulated by both cAMP and calcium-dependent mechanisms. Abnormalities in levels of pepsinogen and its various isozymogens have been linked clinically, epidemiologically, and experimentally to peptic ulcer disease and gastric carcinoma. The ulcerogenesis of pepsin stems from its ability to breach gastroduodenal mucosal barriers. Furthermore, certain isozymogens seems abundant and hyperactive in patients with peptic ulcer disease. The etiology and significance of low pepsinogen levels with disproportionate elevations of pepsinogen II and pepsin 5 in gastric cancer and its precursors is less clear. Further exploration of the patho-physiologic role of pepsin is likely to be of considerable importance in initiating further advances in the understanding and treatment of upper gastrointestinal disease.
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PMID:Pepsinogen. Prolate ellipsoid or unrecognized pathogen? 330 25

A case-control investigation involving interviews with 564 stomach cancer patients and 1131 population-based controls was conducted to evaluate reasons for the exceptionally high rates of stomach cancer in Linqu, a rural county in Shandong Province in northeast China. Daily consumption of sour pancakes, a fermented indigenous staple, was associated with a 30% increase in risk. Risks of stomach cancer were also increased by 2- to 3-fold among persons with prior chronic gastritis or gastric ulcer, by 80% among those with stomach cancer in a family member, by 50% among men who smoked one or more packs of cigarettes/day, by 40% among those who preferred salty foods, and by 50% among families with moldy grain supplies. In contrast, risks tended to decrease in proportion to increasing consumption of fresh vegetables and fruits. This protective effect was more pronounced for vegetables, with those in the highest quartile of intake at less than one-half the risk of those in the lowest. Stomach cancer risks also declined with increasing dietary intake of carotene, vitamin C, and calcium, but not retinol. These findings provide leads to dietary factors that contribute to the high rates in Linqu, where stomach cancer is the leading cause of cancer and has not yet begun to decline as in other parts of the world.
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PMID:Diet and high risk of stomach cancer in Shandong, China. 337 Jun 45

DNAs from 21 human stomach cancers, 16 metastatic stomach cancers to lymph nodes, and 21 apparently noncancerous specimens of stomach mucosae from a total of 26 patients with stomach cancer were tested for their ability to induce neoplastic transformation of NIH 3T3 cells on transfection by the calcium phosphate precipitation technique. Three samples of DNA were shown to have transforming activity; one was from a primary stomach cancer of one patient, the second was from a noncancerous portion of stomach mucosa of the same patient, and the third was from a lymph node metastasis of stomach cancer from another patient. These transformants were tumorigenic in nude mice, and DNAs from the cells could induce secondary transformants. A portion of the transforming gene from the stomach cancer of one patient, which contained the sequences expressed in the NIH 3T3 transformants, was cloned. The transforming gene did not have any homology with the transforming sequences reported previously. We have applied the term hst to this novel human transforming gene. The transforming gene, hst, was found to be present in all the primary and secondary transformants induced by the other two samples of DNA.
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PMID:Transforming gene from human stomach cancers and a noncancerous portion of stomach mucosa. 345 65

We made a retrospective review of the patients with cancer of the digestive organs who died between January 1, 1975 and December 31, 1985, at Shinshu University Hospital. Of 183 patients with such cancers 15 (8.2%) had hypercalcemia. Hypercalcemia was defined as serum calcium level greater than 11.0 mg/dl on at least two determinations. The incidence of hypercalcemia by site was 5 of 74 (6.8%) liver, 1 of 16 (6.3%) biliary tract, 4 of 33 (12.1%) pancreas, 3 of 15 (20.0%) esophagus, 0 of 37 stomach, 0 of 2 duodenum, 2 of 5 colon, and 0 of 1 rectum carcinomas. There was no sexual or age predisposition to hypercalcemia. Bone scans and/or x-ray results were positive in three of eight, negative in five of eight, and were not evaluated in the remaining seven patients. Of five patients tested, four had low to normal serum parathyroid hormone (PTH) levels, and one had a serum PTH level high by C-terminal assay but normal by N-terminal assay. Serum chloride levels at the late stage of hypercalcemia were less than 102 mEq/L in all patients. Therefore, hyperproduction of PTH was unlikely to be a causative factor for hypercalcemia. Indomethacin was given to four patients with hypercalcemia with no effect on serum calcium levels in any cases. Survival from the diagnosis of hypercalcemia ranged from 2 to 96 days (mean 33 days). We conclude that hypercalcemia is a complication not infrequent at the late stages of cancers of the digestive organs, with the exception of gastric cancer, and a portent of a poor prognosis.
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PMID:Hypercalcemia of cancer in the digestive tract. 355 19


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