Abstract
Our work has suggested that a high-frequency event is involved in the initiation phase of malignant transformation in vitro; a later, mutationlike event appears to be involved in the later stages of transformation. There may be no specific "target gene" which directly interacts with carcinogens. It is hypothesized that nonspecific types of DNA damage are involved in the induction of an ongoing process we know as carcinogenesis. Several genes could be involved in maintaining this process. Our recent results suggest that c-myc and c-fos could be involved in the early stages of carcinogenesis, as they are affected by anticarcinogenic protease inhibitors in a manner that corresponds to the way in which protease inhibitors suppress malignant transformation.
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