Abstract
In this report, normal lymphocytes from bovine lymph nodes have been used to study the metabolic interactions of tumor promoting phorbol esters and antitumor-promoting retinoids. As shown earlier with this model system, 12-0-tetradecanoylphorbol-13-acetate (TPA) and related tumor-promoting phorbol esters act as co-mitogens in cells treated with a suboptimal level of phytohemagglutinin (PHA) or concanavalin A (con A) (1,2). This mitogenic response, as measured by an increase in the level of DNA synthesis in cultures 48 hours after the initiation of TPA-PHA treatment, is prevented when the cultures are treated simultaneously with retinoic acid (RA) or a related retinoid with anti-tumor promoting activity in mouse skin. This antagonism by RA was also seen in the case of the co-induction of ornithine decarboxylase (ODC) activity by the combination of PHA and TPA during the first 18 hours in such cultures (3).
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Mueller, G.C., Wertz, P.W., Kwong, C.H., Anderson, K., Wrighton, S.A. (1980). Dissection of the Early Molecular Events in the Activation of Lymphocytes by 12-0-Tetradecanoylphorbol-13-Acetate. In: Pullman, B., Ts’o, P.O.P., Gelboin, H. (eds) Carcinogenesis: Fundamental Mechanisms and Environmental Effects. The Jerusalem Symposia on Quantum Chemistry and Biochemistry, vol 13. Springer, Dordrecht. https://doi.org/10.1007/978-94-009-9104-0_26
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DOI: https://doi.org/10.1007/978-94-009-9104-0_26
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