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Query: UMLS:C0596263 (carcinogenesis)
 64,820 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Combined effects of catechol, sodium chloride (NaCl) and ethanol on the post-initiation stage of gastric carcinogenesis were examined in rats pretreated with N-methyl-N'-nitro-N-nitrosoguanidine (MNNG). F344 male rats were given a single intragastric dose of 150 mg/kg b.w. MNNG at 6 weeks of age. Starting 1 week thereafter, groups of 15 rats were administered 0.8% catechol, 5% NaCl and 10% ethanol either individually or in combination, or basal diet alone for 51 weeks. Further groups of animals were similarly treated with these chemicals without the MNNG pretreatment. All rats were killed at the end of week 52 for histopathological examination. In the forestomach, treatment with catechol alone after MNNG initiation caused a 100% incidence of papillomas (versus 67% in the controls) as well as carcinomas (versus 0% in the controls). On the other hand, the treatment with ethanol alone significantly lowered the incidence of papillomas (13 versus 67% in the controls). The combined treatment with catechol, NaCl and ethanol significantly lowered the incidence of squamous cell carcinomas (57%) as compared to the catechol alone group value (100%). In the glandular stomach, catechol enhanced the development of adenocarcinomas (73 versus 0% in the controls), but this was decreased to 29% by the combined treatment with ethanol and NaCl. NaCl without MNNG pretreatment slightly enhanced epithelial cell proliferation in the forestomach. These results indicate that combined treatment with NaCl and ethanol exerts protective effects against catechol-induced forestomach and glandular stomach carcinogenesis, this apparently being largely due to the ethanol.
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PMID:Effects of catechol, sodium chloride and ethanol either alone or in combination on gastric carcinogenesis in rats pretreated with N-methyl-N'-nitro-N-nitrosoguanidine. 948 78

The modifying effects of alpha-difluoromethylomithine (DFMO) on glandular stomach carcinogenesis after initiation with N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) and sodium chloride were investigated in male outbred Wistar rats. Animals were simultaneously given MNNG solution (100 ppm) as their drinking water and diet supplemented with 10% sodium chloride for 8 weeks, and administered DFMO (dietary levels of 2000 ppm or 500 ppm) and tap water for the following 70 weeks. The DFMO treatment did not show any tendency to inhibit the development of gastric adenocarcinomas. The incidences and multiplicities of atypical hyperplasias in the glandular stomachs were also comparable in all groups of rats given MNNG/sodium chloride. Neither gastric carcinomas nor atypical hyperplasias were observed without the carcinogen treatment. Thus, DFMO did not exert any inhibitory effects when given during the post-initiation phase of two-stage glandular stomach carcinogenesis in rats initiated with MNNG and sodium chloride for 8 weeks.
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PMID:Failure of dietary alpha-difluoromethylornithine to inhibit gastric carcinogenesis in rats after 8 weeks of treatment with N-methyl-N'-nitro-N-nitrosoguanidine and sodium chloride. 957 Mar 91

The effects of prolonged administration of genistein, a tyrosine-kinase inhibitor, on sodium-chloride-enhanced induction of gastric carcinogenesis induced by N-methyl-N'-nitro-N-nitrosoguanidine, and the labeling and apoptotic indices and vessel counts in the gastric mucosa and gastric cancers, were investigated in Wistar rats. After 25 weeks of the carcinogen treatment, rats were fed chow pellets containing 10% sodium chloride and were given s.c. injections of genistein at dosages of 15 mg/kg or 30 mg/kg body weight every other day. In week 52, the incidence of gastric cancers was significantly greater in rats fed sodium chloride than in untreated control rats. Prolonged administration of genistein at a dosage of 30 mg/kg, but not 15 mg/kg, body weight significantly reduced the incidence of gastric cancers, which was increased by oral treatment with sodium chloride. Genistein at the higher dose significantly decreased the labeling index and vessel counts of the antral mucosa and the gastric cancers (which were increased by treatment with sodium chloride) and significantly increased the apoptotic index of the antral mucosa and the cancers (which was lowered by the treatment with sodium chloride). These findings suggest that genistein attenuates gastric carcinogenesis promoted by sodium chloride, by inducing increased apoptosis and lower cell proliferation and angiogenesis of antral mucosa and gastric cancers.
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PMID:Attenuation by genistein of sodium-chloride-enhanced gastric carcinogenesis induced by N-methyl-N'-nitro-N-nitrosoguanidine in Wistar rats. 993 80

The effect of prolonged administration of all-trans-retinoic acid (RA) on sodium chloride-enhanced gastric carcinogenesis induced by N-methyl-N'-nitro-N-nitrosoguanidine, and the labelling and apoptotic indices and immunoreactivity of transforming growth factor (TGF) alpha in the gastric cancers was investigated in Wistar rats. After 25 weeks of carcinogen treatment, the rats were given chow pellets containing 10% sodium chloride and subcutaneous injections of RA at doses of 0.75 or 1.5 mg kg(-1) body weight every other day. In week 52, oral supplementation with sodium chloride significantly increased the incidence of gastric cancers compared with the untreated controls. Long-term administration of RA at both doses significantly reduced the incidence of gastric cancers, which was enhanced by oral administration of sodium chloride. RA at both doses significantly decreased the labelling index and TGF-alpha immunoreactivity of gastric cancers, which were enhanced by administration of sodium chloride, and significantly increased the apoptotic index of cancers, which was lowered by administration of sodium chloride. These findings suggest that RA attenuates gastric carcinogenesis, enhanced by sodium chloride, by increasing apoptosis, decreasing DNA synthesis, and reducing TGF-alpha expression in gastric cancers.
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PMID:Attenuation by all-trans-retinoic acid of sodium chloride-enhanced gastric carcinogenesis induced by N-methyl-N'-nitro-N-nitrosoguanidine in Wistar rats. 1007 Aug 61

The modifying effect of diethyl maleate (DEM) on gastric tumor development was studied in rats initially given N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) and hypertonic sodium chloride (H-NaCl 10% or 5%). Groups of animals were maintained with or without a 0.2% DEM dietary supplement after treatment with MNNG and H-NaCl and sacrificed at week 20. Forestomachs and livers cytosolic NAD(P)H:quinone-acceptor oxidoreductase (QR) activity was also analyzed. The incidences of forestomach severe hyperplasias in the MNNG + H-NaCl --> DEM groups were also significantly higher than in the MNNG + H-NaCl alone group (P < 0.01 and P < 0.05 for 5% and 10% groups, respectively). Similarly, in the glandular stomach, the numbers of preneoplastic pepsinogen 1 altered pyloric glands (PAPGs) in the MNNG + H-NaCl --> DEM groups were significantly increased (P < 0.01 for both concentrations). The QR activities in the groups treated with DEM showed 2- to 3-fold increases as compared with the control level. The results indicate that treatment with 0.2% DEM after MNNG initiation exerts enhancing effects on both forestomach and glandular stomach carcinogenesis. Induction of QR, a Phase II enzyme, activity in the rat stomach by DEM may be associated with promotion of stomach carcinogenesis rather than inhibition.
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PMID:Enhanced quinone reductase (QR) activity correlates with promotion potential of diethyl maleate (DEM) in rat forestomach and glandular stomach carcinogenesis initiated with N-methyl-N'-nitrosoguanidine (MNNG). 1037 41

The effects of prolonged administration of d-limonene, a monocyclic monoterpene, on sodium chloride-enhanced induction of gastric carcinogenesis by N-methyl-N'-nitro-N-nitrosoguanidine, the labeling and apoptotic indices, and ornithine decarboxylase (ODC) activity of gastric cancers were investigated in Wistar rats. After 25 weeks of carcinogen treatment, rats were given chow pellets containing 10% sodium chloride and 1% limonene ad libitum. In week 52, the incidence of gastric cancers, the labeling index and ODC activity were significantly higher and the apoptotic index was significantly lower in rats given sodium chlolide than in untreated control rats. However, in rats given both sodium chloride and d-limonene, the incidence of gastric cancers, the labeling index and ODC activity were significantly lower and the apoptotic index was significantly higher than in rats given sodium chloride alone. Our findings suggest that limonene attenuates the gastric carcinogenesis enhanced by sodium chloride via increased apoptosis and decreased ODC activity in gastric cancers.
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PMID:Attenuation by d-limonene of sodium chloride-enhanced gastric carcinogenesis induced by N-methyl-N'-nitro-N-nitrosoguanidine in Wistar rats. 1041 63

Three major factors for human carcinogenesis are (i) cigarette smoking, (ii) infection and inflammation and (iii) nutrition and dietary factors. Nutrition and dietary factors include two categories, namely genotoxic agents and constituents including tumor promotion-associated phenomena. This article first describes the genotoxic agents as microcomponents. These are mutagens/carcinogens in cooked food, fungal products, plant and mushroom substance, and nitrite-related materials, polycyclic aromatic hydrocarbons and oxidative agents. Emphasis has been given to heterocyclic amines (HCAs) to which humans are continuously exposed in an ordinary lifestyle. HCAs in food are mainly produced from creatin(in)e, sugar and from amino acids in meat (upon heating). They are imidazoquinoline and imidazoquinoxaline derivatives and phenylimidazopyridine. HCAs are pluripotent in producing cancers in various organs including breast, colon and prostate. Discussion is also given to plant flavonoids which are mutagenic but not carcinogenic. As a macrocomponent, overintake of total calories, fat and sodium chloride is discussed from the viewpoint of the increase of genetic alterations in tissues and of tumor promotion-associated issues. Studies of nutrition and dietary condition will eventually lead us to cancer prevention, namely delay of onset of cancer to the late phase of human life, which is called 'natural-end cancer' (Tenju-gann).
Carcinogenesis 2000 Mar
PMID:Nutrition and dietary carcinogens. 1068 59

The modifying effects of pure curcumin on glandular stomach carcinogenesis were investigated during the post-initiation phase in male Wistar rats treated with N-methyl-N'-nitro-N-nitrosoguanisine (MNNG) and sodium chloride. A total of 110 male 6-week-old rats were divided into four groups. Groups 1-3 (consisting of 30 rats/group) were given MNNG in their drinking water at a concentration of 100 ppm and simultaneously fed a diet supplemented with 5% NaCl for 8 weeks. They were then fed a diet containing either 0.2% (group 1) or 0.05% (group 2) pure curcumin or kept on a basal diet alone (group 3) for 55 weeks. The rats of the curcumin-treated groups (groups 1 and 2) were then switched to the basal diet for the following 4 weeks before sacrifice. Group 4 (20 rats) served as a non-treatment control. The total incidence of combined atypical hyperplasias and adenocarcinomas in the glandular stomachs was rather lower in groups 1 (93%) and 2 (90%) than in group 3 (100%), albeit without statistical significance. However, the mean number of atypical hyperplasias or adenocarcinomas of the glandular stomachs in group 1 (4.70) was significantly less than the value of group 3 (7.17) (p<0.05). Thus, the development of cancerous and precancerous lesions in the glandular stomach was decreased by exposure to pure curcumin. The present results indicate that the compound exerts chemopreventive effects, when given during the post-initiation phase of glandular stomach carcinogenesis in rats.
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PMID:Chemopreventive effects of curcumin on glandular stomach carcinogenesis induced by N-methyl-N'-nitro-N-nitrosoguanidine and sodium chloride in rats. 1184 1

We investigated "the "chemopreventive potential of lycopene against gastric carcinogenesis induced in male Wistar rats by N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) and saturated sodium chloride (S-NaCl). Administration of lycopene inhibited MNNG+S-NaCl-induced gastric carcinogenesis as revealed by the absence of carcinomas. Lipid peroxidation, reduced glutathione (GSH), glutathione peroxidase (GPx), glutathione S-transferase (GST) and glutathione reductase (GR) were used to monitor the chemopreventive potential of lycopene. The extent of lipid peroxidation was significantly lower, whereas GSH, GPx, GST and GR were markedly enhanced in the gastric mucosa of tumour-bearing animals. Our data suggest that lycopene may exert its inhibitory effects by modulating the oxidant and antioxidant status in the gastric mucosa.
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PMID:Prevention of N-methyl-N'-nitro-N-nitrosoguanidine and saturated sodium chloride-induced gastric carcinogenesis in Wistar rats by lycopene. 1191 5

Female transgenic FVB mice transfected with the mammary erbB-2/neu oncogene were injected 0.1 ml 0.9% solution of sodium chloride (control), 1 meg Vilon peptide (Lys-Glu) or Epitalon peptide (Ala-Glu-Asp-Glu), s.c., 5 days in succession once a month, beginning from the age of 2 months. The characteristics of mammary tumor induction in the control and experimental groups did not differ until the age of 9 months. Later on, Epitalon-treated mice revealed distinct inhibition of carcinogenesis. One tumor per animal was detected in 7% (control), 4% (Vilon) and 16% (Epitalon) (p < 0.05). Two or more tumors per animal were in 75%, 95% and 56%, respectively (p < 0.05). Largest diameter of mammary adenocarcinoma in the Epitalon group was smaller than in controls by 33% (p < 0.05). Although the number of mice with metastases to the lung in all three groups was practically identical, their incidence in the Vilon group was 2.6 times higher than in Epitalon-treated animals (p < 0.05). Largest diameter of metastasis in the Epitalon group was the smallest, too. Our data point to inhibition of mammary carcinogenesis by Epitalon in transgenic erbB-2/neu mice.
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PMID:[Effect of Epitalon and Vilon treatment on mammary carcinogenesis in transgenic erbB-2/NEU mice]. 1210 68


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