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Augmentation of Natural Immunity and Regulation of Tumor Growth by Conditioning

We have reported the effect of classical (Pavlovian) conditioning of natural immunity on survival of tumor-bearing mice. In the first study, we have observed that mice conditioned, transplanted with tumor, and re-exposed to conditioned stimulus (camphor odor) had an increase in median survival (day...

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Bibliographic Details
Published in:Annals of the New York Academy of Sciences 1988, Vol.521 (1), p.29-42
Main Authors: GHANTA, VITHAL K., MIURA, TAKAJI, HIRAMOTO, NANCY S., HIRAMOTO, RAYMOND N.
Format: Article
Language:English
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Summary:We have reported the effect of classical (Pavlovian) conditioning of natural immunity on survival of tumor-bearing mice. In the first study, we have observed that mice conditioned, transplanted with tumor, and re-exposed to conditioned stimulus (camphor odor) had an increase in median survival (day 43, as compared to days 34, 38, and 37 of various control groups). Two of these conditioned mice lived more than 120 days and showed early tumor growth, but were free of disease at day 97. We report the observations of a repeat study. Two groups of conditioned mice were used for these studies. One group was re-exposed to the conditioning stimulus following transplantation with tumor (CND) and the second group was not re-exposed to odor of camphor (CNDo). Statistically significant delay in growth of MOPC 104E in the CND group was observed when compared with the CNDo group. The survival data supports the observations of tumor IgM values. In an independent study, we investigated the possible mechanisms of MOPC 104E regulation in vitro. Plastic adherent spleen cells (macrophage cells) from mice primed in vivo with MOPC 104E tumor cells suppressed tumor IgM production by MOPC cells by 98% and also reduced colony formation by MOPC cells. The possible mechanism(s) of regulation of tumor growth in conditioned mice might be mediated by plastic adherent activated macrophages.
ISSN:0077-8923
1749-6632
DOI:10.1111/j.1749-6632.1988.tb35263.x