Summary We examined the reactivity of four p53-specific monoclonal antibodies -PAb 1801, p53-BP-12, D07 and CMI -on sections of formalin-fixed tissue collected from 245 breast carcinomas. Immunodetection of p53 varied between 37.6% and 46.6%. The greatest variation was observed among lobular carcinomas and low-grade tumours in which immunodetection varied between 8.3% and 27.3%. In contrast, immunodetection of p53 in invasive ductal carcinomas was subject to a lower degree of variability with between 40.6% and 49.7% of these tumours proving to be positive. In general, we found antibodies PAb 1801 and D07 to be the most effective in immunolocalising p53. Immunodetection of p53 with each of the four antibodies was found to correlate strongly with tumour grade. In survival analysis, the results gained using antibody PAb 1801 proved to be of greatest statistical significance and to provide the strongest index of prognosis. A significant relationship was observed between immunodetection of p53 with each of the four antibodies and poor responsiveness to endocrine therapy. In addition, relationships were also observed between p53 immunostaining and tumour oestrogen receptor (ER) (Iwaya et al., 1991; Sawan et al., 1992;Barnes et al., 1993; Yamashita et al., 1993).The p53 gene is located on the short arm of chromosome 17 and it encodes a 53 kDa nuclear phosphoprotein involved in the control of cell proliferation (Baker et al., 1989). The exact function of the p53 protein is not fully understood but it may play a role in DNA replication and regulation of transcription (Levine et al., 1991). Recent studies have shown that p53 in its 'wild' form may act as a tumour-suppressor gene (Lane and Benchimol, 1990). The precise mechanism of p53 tumour suppression is not known. Recent evidence suggests that p53 indirectly inhibits cell proliferation by regulating the transcription of other unidentified genes (Kern et al., 1992). The p53 gene has been found mutated and/or deleted in a wide range of tumours (Mulligan et al., 1990;Levine et at., 1991). Functional inactivation of the p53 gene by mutation or allelic loss appears to be one of the commonest genetic abnormalities in human cancer (Lane, 1992