In discussing the area of cell biology in relation to the topic of Dr. Fraumeni's presentation and in relation to the Conference as a whole, I decided to describe two current hypotheses of carcinogenesis-first, the viral oncogene hypothesis proposed by Drs. Huebner and Todaro and, second, the protovirus hypothesis proposed by Dr. Howard Temin. These two hypotheses tend to reconcile the position of the two schools of thought about cancer etiology, namely, the environmentalists and the virologists. Both hypotheses are derived from observations of the RNA tumor viruses, namely, type B virus associated with mammary tumors in mice and the type C viruses associated with leukemia, lymphoma, and sarcoma in a number of animals; with autoimmune diseases in mice; and with a neurologic disease of mice.
VIRAL ONCOGENE HYPOTHESIS
This hypothesis, proposed first by Huebner and Todaro,1 is similar to that stated by Payne and Chubb2 and by Bentvelzen and Daams.3 The hypothesis states that most or all vertebrates contain the genetic information for producing a type C RNA virus in their somatic as well as in their germ cells. This information has been part of the genetic makeup of vertebrates since early in evolution and can persist for many generations in cell culture without overt production of virus. The virogenes (genes for production of type C viruses) and the oncogenes (that portion of the virogene responsible for transforming a normal cell into a tumor cell) are maintained in unexpressed form by repressors in normal cells. Various agents, including physical and chemical carcinogens, may transform cells by switching on the endogenous oncogenic information.
Membrane properties of the gag gene-coded p15 protein of mouse type-C RNA tumor viruses.
