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Role of Cellular and Humoral Factors in the Destruction of Nascent Plasma Cell Tumors^1,2,

Research Institute for Skeletomuscular Diseases of the Hospital for Joint Diseases & Medical Center, and The Mount Sinai School of Medicine, New York, New York 10035

Previous work from this laboratory established that chronic administration of glycoprotein pituitary hormones to mineral oil-injected BALB/c mice almost completely prevented development of the expected plasma cell tumors in the peritoneal cavity. Tumor prevention was accompanied by the intraperitoneal proliferation of mast-like cells (granulated macrophage in the present study) which, in a few mice, contained phagocytosed myeloma cells. In the present study, cytotoxic antibodies reactive to six lines of transplantable oil-induced plasma cell tumors were sought in the sera of these mice by a fluorochromatic test for immunocytotoxicity in agarose gel of Celada and Rotman; and phagocytic activity of the peritoneal granulated macrophages from individual mice for four lines of plasma cell tumor and two primary plasma cell tumors was studied by in vitro incubation of these cells. Specific phagocytosis of myeloma cells by the granulated macrophage was demonstrated in certain combinations of tumor lines and macrophage donors. Peritoneal macrophages from mice treated with oil alone failed to ingest myeloma cells. Antibodies cytotoxic to myeloma cells were demonstrated in the sera in certain combinations between tumor lines and sera. However, these antibodies were also found in some mice treated with oil alone. Antibodies to the tumor lines derived from primary tumors of short latent periods were found more frequently than to those with a long latent period. The presence of cytotoxic antibodies in the sera of granulated macrophage-bearing mice did not coincide with phagocytosis of tumor cells.

¹ This work was supported by Grant #P397 from the American Cancer Society.

² Presented in part at the Annual Meeting of the American Association for Cancer Research, San Francisco, Calif., March 1969 (Proc. Amer. Assoc. Cancer Res., 10: 101, 1969).

Received 11/19/68. Accepted 2/14/69.