Radiation is the most thoroughly studied environmental carcinogenic agent and cancer induction is the most significant late effect of radiation. Ionizing radiation creates a number of lesions in DNA including base modification, single and double strand breaks, and sugar damage. A significant proportion of the radiation-induced mutations in somatic cells are associated with chromosomal deletions and gene rearrangements. These alterations are the result of breakage of the chromosomes followed by loss of genetic material (deletions) or rejoining of broken chromosomes (rearrangements) (l). Radiation has also been found to be a point mutagen in certain model assay systems. The relationship of these geno-toxic effects of radiation to molecular mechanisms of radiation carcinogenesis is not yet understood. We have decided to address this issue using current molecular concepts involving oncogene activation applied to the biologically well-defined experimental model of rat skin carcinogenesis by ionizing radiation. Several types of tumors develop in rat skin following localized exposure to single or fractionated doses of ionizing radiation (2) which include squamous cell carcinomas, basal cell carcinomas, sarcomas, clear cell carcinomas, and sebaceous cell tumors. The histologic type of the tumor presumably reflects the cell type of origin.
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- Multiple Oncogene Activation in a Radiation Carcinogenesis Model
Seymour J. Garte
Mary Jean Sawey
Fredric J. Burns
- Springer US