A number of studies have demonstrated that inoculation of certain types of
cancer cells engineered for expression of the
interleukin-2 (IL-2) gene results in reduced tumorigenicity and/or protection from subsequent challenge with a tumorigenic dose of wild-type cells. In the current studies, we have employed murine
plasma cell tumors to examine IL-2-mediated
tumor rejection as a possible model for therapeutic approaches to human myeloma or
plasma cell leukemia. Two murine
plasma cell tumor lines, S107 and X24, were infected with a retroviral vector expressing the human
IL-2 gene, and the antitumor potential of IL-2-expressing infectants was characterized in syngeneic BALB/c and BALB/c nu/nu mice. Results demonstrate that tumorigenicity of both lines correlates inversely with the amount of
IL-2 produced by the
tumor cells. However, there are clear differences between the two lines in terms of reduced tumorigenicity and the ability to protect against co-injected parental
tumor cells that appear unrelated to
IL-2 levels. More importantly, intravenous immunization of animals with irradiated,
IL-2 secreting cells from either line leads to significant protection from challenge with highly metastatic parental cells. These results suggest that such an approach may warrant consideration in the treatment of human
plasma cell dyscrasias.