By Bohnenblust H.F.
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In the females, the excessive growth has untoward physiological effects, since breeding females are unable to deliver milk to their offspring. ) The hyperplasia is presumed to be an initial step in mammary tumorigenesis because the transgenic mice, unlike their non-transgenic littermates, frequently develop mammary cancers, with an 80% incidence of at least one tumour in female mice by the age of six months. Thus far, only one mammary tumour has arisen in the few male mice that have been kept for eight months.
I favour the idea that one needs at least two types of physiological changes in the cell in order to get transformation. The paradigm for me is always ras and myc. src is in the ras class and I suggest Rb is in the rnyc class. If one accepts provisionally, independent of the identities of the particular genes involved, that two types of physiological changes are required to get full transformation, one might get reversion from tumorigenicity by two kinds of genetic change. On the one hand, there are downstream targets in the cytoplasm that serve as targets of rus and src and similarly acting genes.
However, there may be a small but significant change of a subset of these phosphoproteins. Varmus: In that situation you might expect the rus gene t o be able t o transform cells, since it's generally thought that rus acts downstream of src. Balmain: It's obvious that there are a number of secondary events involved in generating the tumours. Have you looked for any of these secondary events. for example, ras activation, in a transgenic mouse turnour that was not induced by ras, o r activation of neu in the mammary gland tumours?