We studied whether cellular sensitivity to anticancer agents was correlated with a repair deficiency in three yeast epistasis groups of radiation sensitive mutants. All these mutants were hypersensitive to cisplatin and mitomycin C. By contrast, both rad51 and rad52 mutants deficient in double-strand breaks repair were hypersensitive to adriamycin and bleomycin, but the rad1 and rad10 mutants deficient in nucleotide excision repair were not. These results were confirmed by examining the cellular sensitivity of either revertants or strains carrying wild RAD+ protein expression plasmids to various drugs. Cellular damage by the above anticancer agents is discussed in relation to the DNA repair mechanisms.