Effects of Specific Active Immunization on Tumor Recurrence Following Primary Tumor Resection in WF Rats With 1,2-Dimethylhydrazine-Induced Bowel Cancer&lt;xref ref-type="fn" rid="FN2"&gt;2&lt;/xref&gt;

Although numerous animal tumor models have been used to study colon carcinoma, few display metastatic properties. We have characterized an animal tumor model that has 3 properties essential for the study of metastasis of colon carcinoma cells: epithelial cell origin; a reproducible pattern of metastatic behavior and the ability to be propagated both in vitro and in vivo to facilitate identification of biochemical correlates of metastasis. The K12/TR cell line was derived from a transplantable colon carcinoma induced by dimethylhydrazine in the BD-1X rat strain. Transmission electron microscopy of K12/TR cells demonstrated junctional complexes, desmosomes and surface microvilli characteristic of gastrointestinal epithelial cells. The epithelial cell origin of K12/TR was confirmed by demonstrating the presence of keratin, a marker of epithelial cells, but not vimentin, a constituent of mesenchymal cells. Secretion of CEA and Ca19-9 antigens by K12/TR cells in vitro was below the sensitivity of the assays (1 ng/ml and 6 U/ml respectively). K12/TR cells produced tumors following s.c. injection into syngeneic BD-1X rats, allogeneic RNU/rnuDF rats and xenogeneic CRL:nu/nuBR mice. Macroscopic lung metastases were observed in animals from all 3 groups. Distal lymph node metastases were more frequent in BD-1X rats than in nude rats or mice. The histological appearances of all tumors and metastases were similar, showing a moderate to poorly differentiated glandular carcinoma. Intrasplenic injections of K12/TR cells in nude mice resulted in liver colonization. Preferential growth of tumor cells at sites of trauma was also observed. The results show that the K12/TR system can be used as a model to study metastasis of colon carcinoma cells and may find utility in the testing of chemotherapeutic agents against metastatic lesions.

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The therapeutic effects of an immunopotentiator, PS-K, on 3-methylcholanthrene-induced autochthonous tumors in C57BL/6 mice in combination with the surgical removal of primary sites

Hosokawa

Mizukoshi

Morikawa

et al. 1986

Cancer Immunol Immunother

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We investigated the therapeutic effects of an immunopotentiator PS-K on recurrent or metastatic tumors observed after the surgical removal of MCA-induced primary tumors in autochthonous C57BL/6 mice and on the survival time of treated mice. The MST of mice treated with PS-K at various times (59.8-63.4 days) was prolonged as compared with that of mice treated by surgery alone (48.6 days). Local recurrence of tumors was found in 36 of 66 mice (54.6%) treated by surgery alone, whereas it was inhibited significantly (P less than 0.05) when treatment with PS-K was started 1 day after the surgery and occurred in 22 of 64 mice (34.4%) when PS-K was given for 5 days in 1 week, or in 22 of 66 mice (33.3%) when PS-K was administered twice a week for 7 weeks. The MSTs of mice with local recurrence were also found to be prolonged as compared with those of mice treated by surgery alone (54.8-67.5 days vs 49.8 days). The MSTs of mice without tumor recurrence were also prolonged significantly (P less than 0.05-0.001) by combinations of PS-K at various times, although most of the mice died of metastatic tumors even in the groups of mice where a combined treatment with PS-K had been administered. The above findings suggest that the administration of PS-K inhibits the growth of recurrent or metastatic tumor cells in autochthonous mice after the surgical removal of the primary tumors.

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Effects of Specific Active Immunization on Tumor Recurrence Following Primary Tumor Resection in WF Rats With 1,2-Dimethylhydrazine-Induced Bowel Cancer<xref ref-type="fn" rid="FN2">2</xref>

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Experimental Liver Metastasis

Experimental Liver Metastasis

Characterization of an animal model of metastatic colon carcinoma

The therapeutic effects of an immunopotentiator, PS-K, on 3-methylcholanthrene-induced autochthonous tumors in C57BL/6 mice in combination with the surgical removal of primary sites

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