Sub‐units and regulators of the activating protein‐1(AP‐1) complex have been implicated in breast‐cancer biology, therapeutic response and prognosis. This study has immunocytochemically examined the impact of c‐jun‐protein activation on biological and clinical parameters in human primary breast cancers, employing an antibody specific for the serine 63‐phosphorylated c‐jun protein. Substantial nuclear immunostaining was commonly apparent, indicative of an activated c‐jun pool, with associations with MAP‐kinase‐signalling elements, e.g., transforming growth factor‐α (p = 0.04), epidermal growth factor receptor (p = 0.08), phosphorylated erk 1/2 MAP kinase (p = 0.001) and phosphorylated jun kinase (p = 0.05) Little association was noted with c‐fos protein, perhaps indicating alternative AP‐1 partners for c‐jun with a diversity of cellular end‐points. This may explain the lack of relationship with proliferation and grade, the imperfect association between increased c‐jun activation and poorer survival (p = 0.061), and the apparent relationship with distant metastasis (p = 0.05). While increased c‐jun activation related to poorer quality (p = 0.09) and shortened duration of endocrine response in oestrogen‐receptor‐positive patients (p = 0.018), no generalized effects on oestrogen‐regulated gene products were noted, indicating that AP‐1 influences on oestrogen‐receptor/oestrogen‐response element transactivation are unlikely to explain endocrine insensitivity. These data reinforce our belief that elevated AP‐1 signalling influences aspects of the breast‐cancer phenotype. Int. J. Cancer (Pred. Oncol.) 89:177–186, 2000. © 2000 Wiley‐Liss, Inc.