We studied the relevance of adenomatous polyposis coli (APC)/β-catenin signalling in the development of breast cancer by analysing the expression of β-catenin in 54 primary breast tumours (34 ductal and 20 lobular). We showed that 13% of the tumours exhibited upregulated levels of β-catenin in the cytosol suggesting that defects in APC/β-catenin signalling components had lowered the rate of β-catenin degradation. No mutations were observed in the amino-terminal region of β-catenin, which comprises conserved serine residues important for phosphorylation-dependent degradation of the protein, but the APC protein was altered in 6% of the tumours. Tyrosine phosphorylation of β-catenin was detected in only one tumour and could, therefore, not have been responsible for the observed increased levels of this protein. Although 9% of the tumours displayed upregulation of c-MYC protein, there was no correlation with β-catenin overexpression, suggesting that increased β-catenin expression is not the major cause of c-myc gene activation in breast cancer. It is imperative that elements that selectively drive the oncogenic activity of β-catenin in breast cancer be identified.