Chromosome Break-Points, Somatic Mutation and Oncogene Activation: Some Comments
In previous publications (3, 8) we have attempted to associate the DNA double strand break with the induction of malignancy by making use of the “somatic mutation ” theory of malignancy. In particular, we tried to align our ideas on chromosome aberrations with the then current ideas on the nature of malignancy which suggested that the factor governing malignancy behaved as a recessive gene. This idea had been developed from cell fusion experiments between malignant and non-malignant cells where it was found that the malignant factor was suppressed in the hybrids initially, but returned eventually with the loss of chromosomes from the hybrid cell (6) (see Figure 1). These results in mouse-mouse and mouse-human hybrids which were not very chromosome stable were supported by work with human-human hybrids which were much more chromosomally stable (12). When we developed these ideas we suggested that with the further development of the analysis of malignancy, we would probably have to revise our ideas, although we were convinced that radiation induced cancer and somatic mutation were directly related. However, at that time we did not anticipate the tremendous development in the investigation of the role of oncogenes in malignancy which has occurred during the past few years. In this paper we review the ideas we developed on the basis of the cell fusion-hybrid experiments and discuss some of the more recent developments in the molecular biology of malignancy with respect to the role of chromosome aberrations in the induction of malignancy.
KeywordsChromosome Aberration Viral Oncogene Cellular Oncogene Hamster Embryo Cell Chromosome Banding Technique
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