Abstract
Tumor cells can replicate under conditions when normal cells cannot, because to varying degrees depending on the tumor, their replication is not inhibited by controls that inhibit the replication of normal cells. The basic process responsible for the change of a normal cell into a tumor cell is thus a change in the control mechanism for cell replication. The mechanisms that control the replication of normal cells can be divided into 2 types; those in which circulating substances produced by one cell control the growth of another cell, and those that appear to be mediated by cell surface interactions. This second type of control will be referred to as contact inhibition1. The experiments to be presented are concerned with our in vitro studies on the mechanism of the change in the contact inhibition control for cell replication that is induced by carcinogenic agents. Carcinogenesis can be induced by viruses, non-viral chemicals, and physical agents. The present experiments will therefore be concerned with the change in this control induced by small DNA tumor viruses with particular reference to polyoma virus, carcinogenic hydrocarbons, and x-irradiation. The change in control resulting in a change of a normal cell into a tumor cell will be referred to as transformation.
Supported by Research Grant CA 05266 from the National Cancer Institure, US. Public Health Service.
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Sachs, L. (1966). An Analysis of the Mechanism of Carcinogenesis by Polyoma Virus, Hydrocarbons, and X-Irradiation. In: Holzer, H., Holldorf, A.W. (eds) Molekulare Biologie des Malignen Wachstums. Colloquium der Gesellschaft für Physiologische Chemie am 21./23. April 1966 in Mosbach/Baden, vol 17. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-87539-7_23
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