The incidence of human carcinoma of the esophagus is increased in association with environmental nitrosamines and dietary zinc deficiency. 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. Histologic examination of the MBN-treated Sprague-Dawley rat esophagi revealed a significantly higher incidence of esophageal carcinoma in the zinc-deficient rats vs. controls (62 vs. 33%). In addition, three distinct cytologic and histologic patterns were observed in the animals with esophageal carcinoma: pattern I - basal cell hyperplasia, atypical basal cells, few dyskeratotic cells: pattern II - basal cell hyperplasia, atypical basal cells, many dyskeratotic cells; and pattern III - many dyskeratotic cells without basal cell hyperplasia. These three patterns did not occur simultaneously in the same esophagi; and zinc deficiency did not alter the appearance of these patterns. A strong correlation between the appearance of moderate or severe dysplasia cytologically and microinvasive carcinoma histologically was demonstrated. In those animals with histologically evident microinvasive carcinoma, there was no cytologic evidence of carcinoma in situ or invasive carcinoma. Cytology of these esophageal carcinomas revealed only moderate or severe dysplasia. To the extent that the rat model represents the evolution of esophageal carcinoma in humans, the results presented here suggest that the cytologic appearance of moderate or severe dysplasia indicates the need for further evaluation of patients at risk for esophageal carcinoma.
|Original language||English (US)|
|Number of pages||9|
|Journal||Journal of the National Cancer Institute|
|State||Published - 1986|
ASJC Scopus subject areas
- Cancer Research