Non-small cell lung cancers have a high incidence of somatic mutations of the beta-tubulin (class I) gene, suggesting involvement in the acquisition of resistance to taxanes, which exert their effects through binding to beta-tubulin. Since taxanes are often used in the treatment of breast cancer, we carried out a mutational analysis of the class I beta-tubulin (GenBank accession AF070600) gene in breast cancer. We paid special attention to the primer design so as not to amplify the pseudogenes. We identified 1 somatic mutation, codon 306 [Arg (CGC) to Cys (TGC)], and 2 genetic polymorphisms, codon 217 [Leu (CTG) to Leu (CTA)] and (C to T) at 57 bases downstream from exon 4. Our results suggest that acquisition of resistance to taxanes is unlikely to be explained by somatic mutations of the class I beta-tubulin gene in most breast cancers. In addition, the overestimation of the incidence of somatic mutations of the class I beta-tubulin gene due to the pseudogenes is discussed.