The use of biochemical modifiers of nucleotidc metabolism as clinical radiosensitizers holds renewed interest in the oncology community in light of the recently reported positive clinical trials cited in this article. In general, this approach to radiosensitization attempts to limit the effect of tumor repopulation and to reduce the efficiency of radiation damage repair in tumors during treatment. Since these drug-radiation interactions lack tumor specificity, further improvements in the therapeutic gain can only result by identifying exploitable differecnces in the biologic properties of tumors and dose-limiting normal tissues. The rapid evolution of our understanding of differences in cell cycle regulation in rumors and normal tissues is clearly one area that will likely provide new strategies for these combined modality approaches.