[Prevalence of adenocarcinoma of the esophagus and esophagogastric junction in a 10 year period at a cancer referral center in southern Brazil]. / Prevalência de adenocarcinoma do esôfago e da junção esofagogástrica durante 10 anos num centro de referência para câncer no sul do Brasil.

UNLABELLED: There is increasing incidence of adenocarcinoma of the esophagus and esophagogastric junction in the USA and Europe, however, data in Brazil are scanty. OBJECTIVE AND METHODS: We reviewed all histology confirmed esophageal and esophagogastric junction cancer reports during a 10-year period (1987-1996) obtained by upper digestive endoscopy biopsies at a cancer referral center in Southern Brazil. Cancer cases were classified in three categories: adenocarcinoma, squamous cell carcinoma, and others. RESULTS: Among 349 cases, adenocarcinoma was found in 53 (15.2%), squamous cell carcinoma in 283 (81.1%) and others in 13 (3.7%). CONCLUSIONS: In this study, the prevalence of adenocarcinoma was 15%.

Induction of esophageal carcinogenesis by diethylnitrosamine and assessment of the promoting effect of ethanol and N-nitrosonornicotine: experimental model in mice.

It is known that some nitrosamines preferably affect particular organs because of their organospecificity. Diethylnitrosamine (DEN) is one of the most powerful nitrosamines for experimentally inducing esophagus cancer. The present study aimed to evaluate the rate and type of epithelial lesions induced by DEN in mice. We also assessed the role of alcohol and N-nitrosonornicotine (NNN) as promoters of this carcinogenesis. A total of 208 female mice (Mus musculus) were allocated to five experimental groups: group 1, water only (controls); group 2, DEN + water; group 3, DEN + NNN; group 4, DEN + 6% alcohol solution; group 5, DEN + NNN + 6% alcohol solution. Animals in groups 2, 3, 4 and 5 received DEN (0.04 ml/l) three times per week, and during the following 4 days they received the other solutions. NNN was provided at a final concentration of 30 mg/l. The overall experimental period was 180 days. At the end of this time, the animals were killed and their esophagus was dissected for macro- and microscopic analysis. There was no significant difference in relation to the size of the esophagus and to the average DEN intake by the animals (p > 0.05). A statistically significant difference (p < 0.0001) was observed between controls and all other experimental groups. There was no significant difference among experimental groups treated with carcinogens (p > 0.05). The average incidence of cancer was 85.4%. The experimental model used in the present study is a very potent indicator of esophagus cancer. Owing to the high incidence for cancer observed in the present study, it was not possible to assess the effect of alcohol and NNN as inducers for the development of esophageal cancer.

GMP protects against quinolinic acid-induced loss of NADPH-diaphorase-positive cells in the rat striatum.

When injected into the rat striatum, quinolinic acid causes dose-dependent widespread cell death. All cell types, including the NADPH-diaphorase-positive neurons appear to be sensitive to the toxin. The latter cells are destroyed by quinolinic acid injections of 180 nmol per striatum, this effect being blocked by the concomitant administration of 5 mg/kg of the non-competitive N-methyl-D-aspartate antagonist MK-801. We report that guanosine-5'-monophosphate (GMP), at a dose of 360 nmol, is equally effective in protecting the diaphorase-positive cells against quinolinate toxicity.