All rights reserved. Our understanding of the risks of combined exposure to chemicals, drugs and radiation is poor. It is important to determine if the biologic responses from these combined exposures can be predicted. Genetic Variability and Risk of Radiation-Induced Cancer Emphasis should be placed on the identification of traits other than AT, XP, Bloom's syndrome, Fanconi's anemia and Cockayne's syndrome, which are indicators of increased susceptibility to cancer. Although there are far more individuals who are heterozygous for the above recessive inherited traits when compared with those with overt disease, less is known about their susceptibility to radiation-induced neoplasia.
Little information is known about proteins involved in acute radiation response.
Identification of these proteins may lead to the development of therapeutic strategies to limit radiation-induced necrosis following acute exposures. Studies are required to identify the DNA repair enzymes involved in the cellular response to ionizing radiation injury. Experimental evidence indicates that low doses of low-LET radiation reduce the responsiveness of blood lymphocytes and some fibroblasts to acute high doses of radiation. It is important to determine if the proteins responsible for this reduced radiosensitivity are repair proteins and whether they can be induced in epithelial cells, since these cells are so critical in carcinogenesis. Studies are needed to describe the risk of radiation-induced alteration of genetic markers which have already been associated with cancer.