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The influence of S. mansoni infections on the occurrence of liver tumors initiated by N-2-fluorenylacetamide was investigated. Four-week-old female ddY mice were treated as follows; mice exposed to 20 cercariae of S. mansoni (schistosomiasis group); mice given perorally a carcinogen (carcinogen group); and mice receiving both a carcinogen and S. mansoni (schistosomiasis carcinogen group). The first observation of liver tumors in one of the schistosomiasis carcinogen animals was made during the 21 st week and in two of the carcinogen animals during the 40th week. The incidence of liver tumors by 40 weeks was 21 of 45 mice (46.7 %)in the schistosomiasis carcinogen group and 2 of 32 mice (6.3 %) in the carcinogen group. This difference was significant (p<0.005). None of the animals in the schistosomiasis group developed a liver tumor. Microscopic examination of the liver tumors disclosed hyperplastic nodules Type 1 and 2, and hepatocellular carcinoma. The mice in the schisto-somiasis carcinogen group had a significantly higher incidence of both Type 1 nodules (13.3 % compared to 0 % in the carcinogen group) and hepatocellular carcinomas (26.7 % compared to 0 % in the carcinogen group). The schistosomiasis carcinogen treatment resulted in early and marked production of liver tumors.

The influence of Schistosoma mansoni infection on carcinogenesis of mouse livers initiated by N-2-fluorenylacetamide.