Abstract

With the use of the DBA/2 mammary adenocarcinoma (T1699), the early events that occurred after a single sc injection of untreated or inactivated tumor cells in the syngeneic host were investigated. Examination of the vascularization of the site of sensitization revealed that by day 3, injection of irradiated T1699 tumor cells (XR-T1699) induced the same high level of blood vessel formation as did untreated T1699 tumor cells (T1699u). Whereas the former then decreased, the latter peaked at day 5 and gradually tapered off. Inoculation sites of mitomycin C-treated T1699 tumor cells (T1699m) were poorly vascularized at all times and stimulated a predominantly granulocyte host cell response that peaked at day 1. XR-T1699 caused a peak granulomatous response at day 5, which was distinguished by increased levels of mononuclear cell infiltration. XR-T1699 showed much longer survival and replicating potential than did T1699m in vivo. However, an increased dose of radiation to 30 krads did not significantly reduce the ability of the XR-T1699 immunization to induce anti-T1699 antibody synthesis and protection against subsequent tumor cell challenge. Surgical excision of the XR-T1699 granuloma at day 3 prevented immunization as indicated by the lack of significant antibody-dependent cellular cytotoxicity (ADCC) activity in the sera of these mice and by their inability to reject a subsequent challenge with T1699u However, removal at day 5 did not decrease the ADCC titer below levels seen in XR-T1699-sensitized mice that were not surgically treated and did not alter the ability of those mice to reject a T1699u challenge.

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