This study examines the expression of the cell-cell adhesion molecules E-cadherin and its associated proteins, the catenins and the matrix-cell adhesion molecules 1-and 2-integrins, in primary invasive breast carcinoma. Expression was assessed immunohistochemically on frozen sections by semi-quantitative scoring of the intensity and proportion of immunoreactivity in 55 cases. Associations with each other and with other histological and prognostic features and survival were sought. There was a significant association between loss of E-cadherin expression and loss of -and / -catenin immunostaining. In 20 per cent of cases, membranous immunoreactivity with E-cadherin antibody was absent. Absent cytoplasmic expression of -and / -catenins was seen in 24 and 22 per cent of breast cancers, respectively. The intensity of reactivity with E-cadherin showed a significant association with histological grade (p=0β’002) and tumour type (p<0β’001). Lobular carcinomas frequently showed loss of expression of E-cadherin, as reported elsewhere; loss of catenin expression was also found in these tumours. -Catenin intensity also showed a relationship with grade (p=0β’008) and with oestrogen receptor (ER) status (p=0β’006). / -Catenin expression was not associated with other known prognostic factors. Forty-nine per cent and 42 per cent of cases showed no membrane immunostaining with 1-and 2-integrin, respectively, and co-ordinated loss of 1-and 2-integrin expression was found. Both 1-and 2-integrin expression were associated with histological grade (p=0β’003 and p=0β’031, respectively) and 1 immunoreactivity with tumour type (p=0β’010). None of the variables examined showed a statistically significant association with tumour size or lymph node stage, or with overall survival, although a trend was seen (p=0β’087) towards poorer survival of patients with tumours with absent or weak expression of 1-integrin. The expression of these markers is of biological interest, but appears to be of little additional use in predicting clinical behaviour.