Report on NCI symposium: comparison of mechanisms of carcinogenesis by radiation and chemical agents. II. Cellular and animal models
The point at which the common final pathway for induction of cancer by chemical carcinogens and ionizing radiation has not been identified. Although common molecular targets are suggested by recent findings about the role of oncogenes, the mechanism by which the deposition of radiation energy and the formation of adducts or other DNA lesions induced by chemicals affects the changes in the relevant targets may be quite different. The damage to DNA that plays no part in the transformation events, but that influences the stability of the genome, and therefore, the probability of subsequent changes that influence tumorigenesis may be more readily induced by some agents than others. Similarly, the degree of cytotoxic effects that disrupt tissue integrity and increase the probability of expression of initiated cells may be dependent on the type of carcinogen. Also, evidence was presented that repair of the initial lesions could be demonstrated after exposure to low-LET radiation but not after exposure to chemical carcinogens.
- Research Organization:
- Oak Ridge National Lab., TN (USA)
- DOE Contract Number:
- AC05-84OR21400
- OSTI ID:
- 6408396
- Report Number(s):
- CONF-8405207-2; ON: DE85001867
- Resource Relation:
- Conference: Symposium on assessment of risk from low level exposure to radiation and chemicals, Upton, NY, USA, 20 May 1984; Other Information: Portions are illegible in microfiche products
- Country of Publication:
- United States
- Language:
- English
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