Cancer Research Infection and Cancer: Biology, Therapeutics, and Prevention  AACR Conference on Molecular Diagnostics - 2008
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[Cancer Research 36, 1384-1391, April 1, 1976]
© 1976 American Association for Cancer Research

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Specific Enhancement of Tumor Growth and Depression of Cell-mediated Immunity following Sensitization to Soluble Tumor Antigens1

V. Srinivasa Rao and Benjamin Bonavida

Department of Microbiology and Immunology, School of Medicine, University of California at Los Angeles, Los Angeles, California 90024

W/Fu rats inoculated s.c. with ≤5 x 107 syngeneic (C58NT)D (Gross virus-positive) lymphoma tumor cells normally develop a palpable tumor which reaches its maximum size (12 to 14 mm) at 6 to 8 days and is subsequently rejected by 10 to 12 days. However, rats previously sensitized with soluble tumor antigens from (C58NT)D cells prior to (C58NT)D tumor inoculation demonstrate a significant enhancement of tumor growth (the tumor reaches up to 26 mm and is rejected by 16 to 18 days). This enhancement persisted in antigen-treated rats that continued to receive soluble antigen after tumor inoculation. The in vivo enhancement coincided with a significant in vitro depression of cell-mediated cytotoxicity [assessed with 51Cr-labeled (C58NT)D target cells and peripheral blood leukocytes]. The observed tumor enhancement was specific, inasmuch as presensitization to either soluble tumor antigens from WR6 (Gross virus-negative) tumor, syngeneic to W/Fu rats, or to soluble antigen from W/Fu spleen cells had no enhancing effect on (C58NT)D tumor growth. Interestingly, sensitization to soluble tumor antigen alone did not elicit detectable cell-mediated immunity, cytotoxic antibody, or serum-blocking activity to the (C58NT)D tumor.

We conclude that sensitization to soluble tumor antigens specifically impairs the immune apparatus normally acting in tumor rejection. This impairment appears to act primarily at the induction phase of the immune response.

1 Supported by Grant CA 12800 from the National Cancer Institute, NIH, Bethesda, Md. Part of this work was presented at the 66th Annual Meeting of the American Association for Cancer Research (25).

Received 9/30/75. Accepted 12/ 9/75.







HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Cancer Research Clinical Cancer Research
Cancer Epidemiology Biomarkers & Prevention Molecular Cancer Therapeutics
Molecular Cancer Research Cancer Prevention Research
Cancer Prevention Journals Portal Cancer Reviews Online
Annual Meeting Education Book Meeting Abstracts Online
Copyright © 1976 by the American Association for Cancer Research.