Abstract
Antisense-mediated downregulation of the insulin-like growth factor I receptor results in massive apoptosis of tumor cells in vivo, leading to abrogation of tumorigenesis. In addition to the apoptotic effect, antitumor responses are elicited in syngeneic immunocompetent animals, protecting them from subsequent tumor challenge and causing regression of established tumors with no further recurrence. The mechanisms involved in the antitumor responses elicited in the animals following exposure to antisense cells are discussed, focusing on the immunogenicity of the antisense cells as well as the effectors that participate in these responses.
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