Abstract

There is increasing evidence in support of the somatic mutation theory of carcinogenesis (2,6,8,12–15,21,36,49,50,56,57,60,70). The recent demonstrations of the involvement of point mutations in the activation of the ras oncogenes (49,60), the associations of chromosomal rearrangements with proto-oncogenes (50,70), and the amplification of oncogenes (36,56,57) in certain tumors add to other lines of evidence, such as the demonstration of DNA as a critical target in neoplastic transformation (6,8) and the correlation between mutagenesis and carcinogenesis (2,8,12,13) with most chemicals (see Ref. 8, 41, and 51 for discussion of the arguments against the somatic mutation theory).

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