Mechanism of Enhancement of Metastasis After Resection of Primary Tumor and its Immunotherapy

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The anti-tumor immunity of tumor-bearing host in the regulation of metastasis was assessed using methylchorsanthrene (MCA)-induced tumors in C3H/HeJ or C57B L/6 mice. A variety of metastatic models were used in this investigation, namely pulmonary metastasis of MCA-F, MCA-2A, or MCA-D tumors in C3E/HeJ mice, lymphnode metastasis of MCA-SP in C3H/HeJ, liver metastasis of MC-38 tumor in C57BL/6 mice, peritoneal metastasis, or local recurrent tumor of MCA tumors. Pulmonary or hepatic metastases after resection of primary tumors displayed enhanced outgrowth of metastatic tumors, while metastasis of lymph-node or local recurrent tumor did not be affected by resection of primary tumors. The enhancement of metastatic growth appeared after resection of a larger burden of primary tumor or resection of tumors borne for a longer period. Furthermore, resection of a higher immunogenic tumors enhanced more than resection of poor immunogenic tumors. The progressive outgrowth of primary tumor induced concomitant antimetastatic immunity, which consists of tumor specific immunity in earlier period of tumor growth and non-specific immunity with large tumor burden. The concomitant immunity disappeared after resection of primary tumors. Thereafter metastatic disease increased the size of tumors. Sinecomitant postsurgical immunity showed as tumor specific cytotoxic activity in the spleen of hosts after resection of primary tumor. The post excision immunity, however, was limited to inhibition against growth of metastatic tumor after resection of primary tumor. The results documented by immunotherapy experiments indicated that a combination of tumor specific and non-specific immuno-therapy may potent both concomitant and sinecomitant anti-tumor resistance, thereby reducing metastatic tumor of resection of primary tumor.