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Enhanced Liver Metastatic Potential of Alpha‐fetoprotein‐producing Human Gastric Carcinoma after Carbon Tetrachloride‐induced Liver Damage in Nude Mice
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Enhanced Liver Metastatic Potential of Alpha‐fetoprotein‐producing Human Gastric Carcinoma after Carbon Tetrachloride‐induced Liver Damage in Nude Mice
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Enhanced Liver Metastatic Potential of Alpha‐fetoprotein‐producing Human Gastric Carcinoma after Carbon Tetrachloride‐induced Liver Damage in Nude Mice
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Journal Article
Enhanced Liver Metastatic Potential of Alpha‐fetoprotein‐producing Human Gastric Carcinoma after Carbon Tetrachloride‐induced Liver Damage in Nude Mice
1989
Overview
The liver metastatic potential of alpha‐fetoprotein (AFP)‐producing human gastric carcinoma (NSC‐3) was examined in male, BALB/c, nude mice. Metastatic nodules in the liver were produced by intrasplenic (IS) injection of tumor cell suspension prepared by trypsinization from subcutaneous NSC‐3 tumor. The serum AFP level increased exponentially after IS injection along with the growth of metastatic nodules in the liver, and a positive correlation was observed between the estimated weight of metastatic nodules and serum AFP level. To investigate the effect of liver damage by carbon tetrachloride (CCI4) on the metastatic potential of NSC‐3 cells injected intrasplenlcally, the mice were divided into 4 groups: Group 1 received IS injection of 1×106 of NSC‐3 cells without CCI4, treatment; Groups 2, 3 and 4 received IS injection 7 days, 2 days and 1 day after CCI4 treatment, respectively. All mice were killed 64 days after IS injection. The incidence of liver metastasis was 80% in Group 1, but 100% in Groups 2, 3 and 4. The mean numbers of metastatic nodules per liver were 4.2 in Group 1, 16.8 in Group 2, 18.0 in Group 3 and 44.5 in Group 4. Significant differences in the mean numbers of metastatic nodules were observed between Group 4 and the other groups. It was clearly demonstrated that the metastatic potential of AFP‐producing human gastric carcinoma cells (NSC‐3) is enhanced in the situation prevailing after liver parenchymal cells are damaged by CCI4.
Publisher
Blackwell Publishing Ltd,John Wiley & Sons, Inc
Subject
