Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0596263 (carcinogenesis)
 64,820 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cryostat sections of clinicopathologically characterized breast cancer tissues were eluted with phosphate-buffered 0.9% sodium chloride solution, pH 7.2. The proteins were then characterized by polyacrylamide gel electrophoresis with and without prior treatment with sodium dodecyl sulfate. Approximately 65% of the brease cancer tissue eluates contained a prominent protein fraction with a molecular weight of 47,000 to 55,000 (p50). No such component was found in 15 of 17 eluates of benign breast tissue. Charge density studies disclosed that the p50 component included three populations of proteins that could be characterized according to the migration relative to gp55 derived from RIII murine mammary tumor virus, namely, fast (F-p50), intermediate (I-p50), and slow (S-p50). Prognostically favorable pathological characteristics, i.e., stage, nuclear grade, and lymphoreticuloendothelial responses, were proportionately most frequently found among S-p50 bbreast cancers and were least frequently found among F-p50 breast cancers. It appears that the S-p50 component acts in vivo as a prognostically significant immunogen. Further knowledge of the relationship between protein characteristics and clinicopathological features of human breast cancers would contribute to our understanding of mammary carcinogenesis and biological behavior.
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PMID:Prognostically significant protein components of human breast cancer tissues. 18 41

We previously showed that 5% sodium L-ascorbate (Na-AsA) in the diet promotes rat urinary bladder carcinogenesis, whereas 5% ascorbic acid (AsA) and 1% sodium chloride (NaCl) in the diet do not. In order to cast light on basic properties of these compounds regarding the rat urinary bladder, we examined membrane potential levels in the bladder epithelium of F344 rats treated with 5% Na-AsA, 5% AsA or 1% NaCl in the diet for 2, 4 or 8 weeks. Microelectrode measurement showed Na-AsA to induce hyperpolarization of the membrane potential, which was, however, lacking with AsA and NaCl from week 2 until the end of experiment. Thus a good correlation between the effects on membrane potential and tumor promoting activity could be established.
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PMID:Change of membrane potential in rat urinary bladder epithelium treated with sodium L-ascorbate. 155 3

The effects of calcium chloride on glandular stomach carcinogenesis induced by N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) and sodium chloride were investigated in male outbred Wistar rats. Animals were given MNNG solution (100 p.p.m.) as drinking water and simultaneously fed a diet supplemented with 5% sodium chloride for 8 weeks. Matched negative controls received neither MNNG nor sodium chloride. Rats were then fed basal diet and given calcium chloride solution (1 or 0.2%) or tap water for the following 52 weeks. The incidences and multiplicities of preneoplastic hyperplasias in the glandular stomachs of rats given MNNG/sodium chloride followed by 1 and 0.2% calcium chloride were significantly lower than those in rats given MNNG/sodium chloride alone. The inhibitory effects of calcium were exerted in a dose-dependent manner. Calcium treatment also showed a tendency to inhibit the development of gastric adenocarcinomas although this was not statistically significant. Rats without carcinogen treatment had neither carcinomas nor preneoplastic hyperplasias in the glandular stomach. Calcium intake also significantly reduced the levels of malondialdehyde, a measure of lipid peroxidation, in the gastric mucosa and urine, the former in a dose-dependent manner. Thus, calcium chloride exerted inhibitory effects when given during the post-initiation phase of two-stage glandular stomach carcinogenesis in rats.
Carcinogenesis 1992 Jul
PMID:Inhibitory effect of calcium chloride on gastric carcinogenesis in rats after treatment with N-methyl-N'-nitro-N-nitrosoguanidine and sodium chloride. 163 81

Since Sugimura and Fujimura (1967) succeeded in selectively inducing gastric carcinomas in rats by N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) (1), similar models for the induction of gastric carcinomas in other species by using MNNG and its ethyl derivative N-ethyl-N'-nitro-N-nitrosoguanidine (ENNG) have been established. The susceptibility to gastric carcinogenesis, the histologic types of gastric carcinomas induced, and their biological behavior depend on the mode of treatment, species, strain and/or sex. The organ specificity of MNNG correlates well with the level of DNA methylation in target and non-target tissues following oral administration in rats. The high concentration of methylated DNA bases in the stomach mucosa appears to result from thiol-mediated acceleration of the decomposition of MNNG. Experimental gastric carcinogenesis is markedly modified by various factors and agents, including bile reflux, bile acids, sodium chloride, and ulceration, indicating that both host and environmental factors contribute significantly to gastric carcinogenesis by chemical carcinogens.
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PMID:Experimental gastric cancer. 174 32

The effect of calcium carbonate (CaCO3) on the initiation of gastroduodenal carcinogenesis induced by N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) was examined under the conditions with and without sodium chloride. Male Wistar rats were given drinking water containing MNNG (100 mg/liter) and one of the following diets during the first 20 weeks ad libitum. Group 1 was given basal diet; group 2, diet with 10% NaCl; group 3, diet with 10% NaCl and 2.5% CaCO3; group 4, diet with 10% NaCl and 7.5% CaCO3; group 5, diet with 7.5% CaCO3. During the next 20 weeks, all groups were fed with the basal diet and tap water. The carcinogenic incidences of glandular stomach between the nonsalted diet groups, 1 and 5 (15% and 16% respectively), were not significantly different at the 40th week. The incidences in the salted diet groups 2, 3, and 4 were 59, 63, and 43%, respectively, indicating no statistical difference among them. Thus, CaCO3 showed no anticarcinogenic effect on gastroduodenal carcinogenesis. In the groups 3 and 4, however, increased incidence of duodenal cancer was observed.
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PMID:Effect of calcium on rat gastric carcinogenesis induced by N-methyl-N'-nitro-N-nitrosoguanidine. 181 37

To assess the possibility of establishing an in vivo, medium-term bioassay system for gastric carcinogens and promoters, a total of 220 male WKY rats were divided into two groups. Group 1 animals were treated first with a single dose of N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) (160 mg/kg body wt) and starting 2 weeks later administrated one of five gastric carcinogens, a gastric promoter, one of five non-gastric carcinogens or no treatment, as a control, for 14 weeks. Saturated sodium chloride solution (1 ml) treatments were given by gastric intubation at weeks 4, 6, 8 and 10. Group 2 rats received 1 ml of DMSO instead of MNNG and were then treated in the same way as group 1. Analysis of pyloric mucosa sections for pepsinogen altered pyloric glands (PAPG) detected immunohistochemically after the animals were killed at week 16 revealed increased lesion numbers in group 1, with all gastric carcinogens and promoters examined. However, none of the five non-gastric carcinogens exerted any significant modification of PAPG development. The results strongly suggest that the experimental protocol consisting of the following four components: (i) adoption of PAPG as the end-point marker lesion; (ii) single dose of MNNG as initiator; (iii) test chemical administration for 14 weeks; and (iv) administration of saturated sodium chloride solution during the test chemical exposure, could be used effectively for the detection of gastric carcinogens as well as promoters of gastric carcinogenesis in a relatively short time period.
Carcinogenesis 1990 Nov
PMID:Enhancing effects of various gastric carcinogens on development of pepsinogen-altered pyloric glands in rats. 222 29

Catechol and N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) are gastric carcinogens in rats. Catechol, sodium chloride and bile salts have enhancing effects on gastric carcinogenesis induced by MNNG in rats. The effects of these compounds on proliferation of pyloric mucosa cells in male F344 rats were examined immunohistochemically using bromodeoxyuridine (BrdU) and anti-BrdU monoclonal antibody. Rats were given MNNG (83 micrograms/ml in their drinking water), catechol (0.8% in their diet), sodium taurocholate (0.3% in their diet), sodium taurodeoxycholate (0.3% in their diet), or sodium chloride (10% in their diet or by intragastric administration of 1 ml of saturated solution once a week) for 4 weeks. All these treatments markedly enhanced cell proliferation of the pyloric epithelium, suggesting the importance of enhanced cell proliferation in the development of gastric cancer.
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PMID:Effects of 4-week treatment with gastric carcinogens and enhancing agents on proliferation of gastric mucosa cells in rats. 275 82

Glyoxal and methylglyoxal were tested for tumor-promoting potential in a two-stage stomach carcinogenesis model. Male outbred Wistar rats were initially given N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) in the drinking water (100 mg/l) along with a 10% sodium chloride dietary supplement for 8 weeks. Thereafter, they were returned to basal diet and maintained on drinking water containing no addition or either 0.5% glyoxal or 0.25% methylglyoxal for 32 weeks and then killed for necropsy and histological examination at week 40. Glyoxal treatment significantly increased the incidence of adenocarcinomas in the pylorus of the glandular stomach of rats pretreated with MNNG and sodium chloride. Furthermore, although methylglyoxal did not enhance the development of adenocarcinomas, the incidence of hyperplasias in the pylorus was significantly increased. The results indicate that glyoxal exerts tumor promoting activity on rat glandular stomach carcinogenesis and that methylglyoxal might also have promoting potential.
Carcinogenesis 1989 Oct
PMID:Effects of glyoxal and methylglyoxal administration on gastric carcinogenesis in Wistar rats after initiation with N-methyl-N'-nitro-N-nitrosoguanidine. 279 Dec 8

Calcium chloride (CaCl2) inhibits stimulation of replicative DNA synthesis (RDS) induced in the pyloric mucosa of male Fischer 344 rats by sodium chloride (NaCl), which is a tumor promoter in the glandular stomach. Administration of 1 ml of 3.3 M NaCl by gastric intubation induced a maximal 15-fold increase in RDS in the pyloric mucosa by 17 h; this had returned to the control level by 48 h. Administration of 1 ml of 20-400 mM CaCl2 1 h before administration of NaCl resulted in a 60-100% inhibition of the increase in RDS within 4-48 h; the inhibition was dose-dependent. The 400 mM level of CaCl2 also decreased the histological damage to surface epithelial cells induced by NaCl. These results suggest that calcium ion acts as an anti-tumor promoter in stomach carcinogenesis.
Carcinogenesis 1989 Nov
PMID:Calcium chloride inhibits stimulation of replicative DNA synthesis by sodium chloride in the pyloric mucosa of rat stomach. 280 33

Ethanol, potassium metabisulfite, formaldehyde and hydrogen peroxide were tested for tumor-promoting activity in a two-stage stomach carcinogenesis experiment. Male outbred Wistar rats were given N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) in the drinking water (100 mg/liter) and a diet supplemented with 10% sodium chloride for 8 weeks. Thereafter, they were maintained on drinking water containing either 10% ethanol, 1% potassium metabisulfite, 0.5% formalin (formaldehyde) or 1% hydrogen peroxide for 32 weeks and then sacrificed for necropsy and histological examination. In the pylorus of the glandular stomach, potassium metabisulfite and formaldehyde significantly increased the incidence of adenocarcinoma after initiation with MNNG and sodium chloride. Hydrogen peroxide did not enhance the tumor yield, and ethanol showed a tendency to decrease neoplastic development. In the forestomach the incidence of squamous cell papilloma was significantly increased in the groups given hydrogen peroxide or formaldehyde, irrespective of prior initiation. Duodenal adenocarcinoma was induced by the initiation alone (10%) and the incidence was not affected by the subsequent treatments. The results indicate that potassium metabisulfite and formaldehyde both exert tumor-promoting activity in the rat glandular stomach.
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PMID:Effects of ethanol, potassium metabisulfite, formaldehyde and hydrogen peroxide on gastric carcinogenesis in rats after initiation with N-methyl-N'-nitro-N-nitrosoguanidine. 308 23


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