This section is from the book "Symposium Phenomena Of The Tumor Viruses", by U.S. Dept. of Health. Also available from Amazon: Tumor Suppressing Viruses, Genes, and Drugs: Innovative Cancer Therapy Approaches.
Dr. Andervont (National Cancer Institute): It was not clear to me whether Dr. Dawe implied that an important aspect of cancer is that the infected cell can supply something which will produce malignancy in an accompanying cell or whether the accompanying cell controls the activity of the infected cell.
Dr. Dawe: The concept is simply that the mesenchymal cell, as long as it remains in normal relationship with the epithelial cell, continues to exert its supportive influence on this cell and permits it to compete successfully with the virus, and even to proliferate. Perhaps proliferation becomes a necessity for survival under these circumstances. In an indirect way the mesenchymal cells would thus contribute to tumor development.
If this concept is correct, in order to provide conditions that would favor viral proliferation it would only be necessary to separate the previously infected epithelium from the mesenchyme. Under these conditions, the virus should then gain the "upper hand" and proliferate or perhaps complete itself, add a coat, and be released to infect other cells.
Dr. J. T. Syverton (University of Minnesota): We are indebted to Dr. Dawe for his careful guidance through the maize of polyoma-virus trophisms. Dr. Dawe has presented clearly his interesting findings. Two questions concern many of us: (a) What determines transition from tumor to cancer, and (b) what determines whether a virus results in proliferation or necrosis? Dr. Dawe, by using the submandibular gland as an organ culture to observe response to polyoma virus, has demonstrated that epithelial as well as mesenchymal cells respond to infection by hyperplasia. I interpreted the findings of Stanton and his associates, and those of Leuchtenberger, to indicate that polyoma virus exerts a necrotizing effect on epithelial cells and that the virus in turn either directly or quite indirectly provokes the mesenchymal cells to proliferate. Have you found by use of organ culture that you can separate proliferation of epithelial cells from cytolysis? Is mesenchymal proliferation independent of, or secondary to, epithelial proliferation? Do you find by use of organ culture natural attrition or loss of the mesenchymal etfeet?
Dr. Dawe: My impression is that the mesenchyme is not the proliferative part of this process, but the epithelium. The mesenchyme is the supporting element and must, according to this concept, be present or have exerted its influence possibly at some time prior to infection of the epithelial cell in order to make it capable of reacting with the proliferative type of response.
I am unable to interpret any of the proliferative response as being mesenchymal. When one deals with the hamster and other species, the question is entirely different, and I would not suggest that any such sort of concept that I have proposed could apply to the mesenchymal cells in the hamster, which apparently are the cells that respond. There are apparently some very different host-virus relationships concerned with the mesenchymal cells in that animal.