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[Cancer Research 34, 61-71, January 1, 1974]
© 1974 American Association for Cancer Research

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Immunological Resistance to Pulmonary Metastases in C3Hf/Bu Mice Bearing Syngeneic Fibrosarcoma of Different Sizes1

Luka Milas2, Nancy Hunter, Kathy Mason and H. Rodney Withers

Section of Experimental Radiotherapy, The University of Texas M.D. Anderson Hospital and Tumor Institute at Houston, Houston, Texas 77025

Immunological resistance to pulmonary metastases of a syngeneic methylcholanthrene-induced fibrosarcoma (FSA) was studied in C3Hf/Bu mice that were actively immunized against or that had borne that tumor for varying times. Tumor metastases were induced by i.v. inoculation of FSA cells, and their number was determined 14 to 17 days later. The number of metastases was greatly reduced in mice that previously had been immunized against the same tumor but not in those immunized against syngeneic mammary carcinoma. This reduction was mediated through the activity of immune spleen and lymph node cells and was related to the number of immune cells transferred into the recipient mice. Spleen cells were found to be more effective than lymph node cells.

The presence of the s.c.-growing tumor reduced the number of pulmonary metastases. This was noted when s.c. implantation of FSA preceded the i.v. inoculation of the tumor cells by 3 hr and 3, 7, and particularly 14 days. Spleen cells from mice bearing s.c.-growing FSA for 3, 8, 12, 20, and 27 days were able to transfer immunity to pulmonary metastases of FSA in sublethally irradiated syngeneic recipients. Immunity was transferred most effectively by spleen cells from mice bearing the tumor for 12 days; this activity of the spleen cells markedly decreased in mice bearing the tumor for 27 days. Lymph node cells, however, were able to transfer antitumor immunity only if taken from mice bearing the tumors for 12 or 20 days. Serum from mice bearing FSA given i.v. to the tumor cell recipient mice as a single injection or in multiple doses did not prevent the reduction of pulmonary metastases by immune spleen and lymph node cells.

1 This investigation was supported by NIH Research Grants CA 6294 and CA 11138 from the National Cancer Institute and Institutional Research Grant RR 5511-11, Allotment IN-19.

2 On leave of absence from Laboratory for Tumor and Transplantation Immunology Department of Experimental Biology and Medicine, Institute Rudjer Boskovic, Zagreb, Croatia, Yugoslavia.

Received 6/ 1/73. Accepted 9/26/73.




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Cancer Research Clinical Cancer Research
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Cancer Prevention Journals Portal Cancer Reviews Online
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Copyright © 1974 by the American Association for Cancer Research.