Disease relevance of N-benzyl-N-methyl-nitrous amide

• Zinc deficiency and methylbenzylnitrosamine-induced esophageal cancer in rats [1].
• Rapid induction of carcinomas and gamma-glutamyl transpeptidase-rich clones in N-methyl-N-benzylnitrosamine-treated hamster buccal pouch [2].
• Multiple squamous cell neoplasms of the esophagus were induced in 24 inbred F344 rats by sc injection of N-methyl-N-benzylnitrosamine at a dose level of 2.5 mg/kg weekly for 20 weeks [3].
• Mutational activation of the cellular Harvey ras oncogene in rat esophageal papillomas induced by methylbenzylnitrosamine [4].
• N-Nitrosomethylbenzylamine (NMBA)-induced tumorigenesis in the rat esophagus is a model of human esophageal squamous cell carcinoma used for investigations of chemical carcinogenesis and for the evaluation of putative chemopreventive agents [5].

Psychiatry related information on N-benzyl-N-methyl-nitrous amide

• The role of alcohol abuse in the carcinogenic action of N-nitrosomethylbenzylamine, which induces tumors in the esophagus, has been evaluated [6].

High impact information on N-benzyl-N-methyl-nitrous amide

• We tested the inhibitory activity of these retinoids against N-nitrosomethylbenzylamine (NMBA)-induced tumorigenesis in the rat esophagus [7].
• BACKGROUND: Nutritional zinc deficiency in rats increases esophageal cell proliferation and the incidence of N-nitrosomethylbenzylamine (NMBA)-induced esophageal tumors [8].
• For examination of the role of zinc deficiency in esophageal carcinogenesis, methylbenzylnitrosamine [(MBN) CAS: 937-40-6] was used to induce esophageal carcinoma in rats fed either a zinc-deficient or control diet [9].
• Topical application of N-methyl-N-benzylnitrosamine [(MBN) CAS: 937-40-6] to Syrian hamster buccal pouch epithelia resulted within 4 days in the induction of epithelial cell foci with histochemical gamma-glutamyl transpeptidase (GGTase) activity [2].
• Induction and suppression of N-nitrosomethylbenzylamine activation by microsomes from rat liver and esophagus [10].

Chemical compound and disease context of N-benzyl-N-methyl-nitrous amide

• This study investigated the contribution that retroviral immunosuppression has on esophageal cancer induced by the carcinogen N-nitrosomethylbenzylamine (NMBzA), and the response that increased levels of dietary vitamin E has on this induced carcinogenesis [11].

Biological context of N-benzyl-N-methyl-nitrous amide

• Alpha-difluoromethylornithine inhibits N-nitrosomethylbenzylamine-induced esophageal carcinogenesis in zinc-deficient rats: effects on esophageal cell proliferation and apoptosis [12].
• Organ specificity in the microsomal activation and toxicity of N-nitrosomethylbenzylamine in various species [13].
• The zinc-deficient (ZD), N-nitrosomethylbenzylamine (NMBA)-induced rat esophageal cancer model provides a tool to study cell proliferation and cell cycle control in cancer initiation [14].
• Chemopreventive properties of black raspberries in N-nitrosomethylbenzylamine-induced rat esophageal tumorigenesis: down-regulation of cyclooxygenase-2, inducible nitric oxide synthase, and c-Jun [15].
• DNA methylation by N-nitrosomethylbenzylamine in target and non-target tissues of NMRI mice [16].

Anatomical context of N-benzyl-N-methyl-nitrous amide

• Transgenic mice with AZ expression targeted to the basal cell layer of the forestomach epithelium by the keratin 5 promoter were used to investigate whether AZ overexpression inhibited uncontrolled cell proliferation in zinc-deficient (ZD) mice and reduced their susceptibility to forestomach carcinogenesis by N-nitrosomethylbenzylamine (NMBA) [17].
• The metabolism of the rat esophageal carcinogen N-nitrosomethylbenzylamine (NMBzA) was studied using microsomes prepared from liver and esophageal mucosa of untreated male Sprague-Dawley rats [18].
• The metabolism of N-nitrosodimethylamine (NDMA), N-nitrosodiethylamine, N-nitrosobenzylmethylamine, and N-nitrosobutylmethylamine was investigated in incubations with human liver microsomes [19].
• In the present study, rat esophageal tumors induced by methylbenzylnitrosamine (MBNA) and MBNA-transformed esophageal cell lines were analyzed for activated protooncogenes [4].
• The effect of in vivo carcinogen exposure on colony formation and growth of hamster buccal pouch keratinocytes in culture was evaluated at various times after exposing the mucosal surfaces of buccal pouches to initiating regimens of 7,12-dimethylbenz(a)anthracene (DMBA) or N-methyl-N-benzylnitrosamine (MBN) [20].

Associations of N-benzyl-N-methyl-nitrous amide with other chemical compounds

• Inhibitory effects of phenethyl isothiocyanate on N-nitrosobenzylmethylamine carcinogenesis in the rat esophagus [21].
• Piroxicam is an ineffective inhibitor of N-nitrosomethylbenzylamine-induced tumorigenesis in the rat esophagus [5].
• Given the evidence for an interplay between environmental and genetic factors in esophageal squamous carcinogenesis, the aim of this study was to determine the potential cooperation of the nitrosamine compound N-nitrosomethylbenzylamine (NMBA), an esophageal specific carcinogen, in the cyclin D1 transgenic mice [22].
• Effects of ethanol and various alcoholic beverages on the formation of O6-methyldeoxyguanosine from concurrently administered N-nitrosomethylbenzylamine in rats: a dose-response study [23].
• O6-methylguanine levels and histopathological changes in the rat esophagus and liver following single and repeated administration of N-nitrosomethylbenzylamine [24].

Gene context of N-benzyl-N-methyl-nitrous amide

• In the current study a single N-nitrosomethylbenzylamine dose was administered to Fhit +/+, +/-, and -/- mice to compare carcinogen susceptibility in +/- and -/- Fhit-deficient mice [25].
• Both PKCI+/+ and PKCI-/- mice were treated with the chemical carcinogen N-nitrosomethylbenzylamine (NMBA) by intragastric administration and killed 12 weeks later [26].
• The effects of L-748706, a selective cyclooxygenase-2 inhibitor, on N-nitrosomethylbenzylamine-induced rat esophageal tumorigenesis [27].
• Furthermore, carcinogenicity study using N-nitrosomethylbenzylamine demonstrated that, compared to wild-type mice, fore-stomach tumors in E2F-1-deficient mice expressed an increased amount of cyclin E2, but not cyclin E1 [28].
• Thus, kinetic parameters were determined for the hydroxylation of five substrates of diverse chemical structures known to be selective for cytochrome P450 2A6: methyl tert-butyl ether (MTBE), nicotine, coumarin, N-nitrosobenzylmethylamine (NBzMA), and N-nitrosodiethylamine (NDEA) [29].

Analytical, diagnostic and therapeutic context of N-benzyl-N-methyl-nitrous amide

• Distribution of N-nitrosomethylbenzylamine evaluated by whole-body radioautography and densitometry [30].
• Since both tissues develop a high tumour incidence after oral administration of N-nitrosomethylbenzylamine (MBN), this observation suggests that despite their anatomical similarities the level of DNA modification required for malignant transformation differs considerably in these tissue [16].
• Previous work has shown that sustained increased and decreased cell proliferation, induced by dietary zinc deficiency and caloric restriction respectively, influence the course of N-nitrosomethylbenzylamine (NMBA)-induced esophageal carcinogenesis in rats [31].
• To further investigate the role of G1 cyclins in chemical carcinogenesis, the expression of cyclin D1 and cyclin E was analyzed by RT-PCR and immunohistochemical studies in N-nitrosomethylbenzylamine (NMBA)-induced rat esophageal tumorigenesis [32].
• In initial bioassays, freeze-dried STRW, BRB, and BB powders were mixed into AIN-76A synthetic diet at concentrations of 5% and 10% and fed to Fischer 344 rats before, during, and after treatment with the esophageal carcinogen N-nitrosomethylbenzylamine (NMBA) [33].

References