a similar version of which was recently published in the Lancet'. While the identification of epidermal growth factor receptors (EGF-r) in breast tumours may prove to be a useful prognostic tool, the authors' statement that 'EGF may be a growth factor for oestrogen receptor negative patients and may selectively permit growth of cells with metastatic potential' must remain pure speculation at present. It would be more reasonable to suggest that the finding of a higher proportion of EGF-r positive tumours in lymph node secondaries compared with primary tumours results from the poorer histological grade that EGF-r positive tumours exhibit.
As many tumour cell lines exhibit EGF receptors in larger numbers than normal cell lines, EGF-r expression may only be a marker for dedifferentiation. The evidence that EGF is associated with malignant transformation of cells is based on the finding of similar but not as stated 'identical' protein sequences coded for by the v-erb-B-oncogene and the EGF receptor. As this oncogene does not code for the EGF binding domain of the receptor, it is difficult to see how EGF itselfmay transform cells expressing this oncogene.
EGF receptors are not restricted to epithelial cells but have been identified on fibroblasts. Do the authors have any information as to whether it is the epithelial or the stromal component of the tumour that is expressing the EGF receptor? Oestrogen receptor positive tumours are in general less cellular. These tumours may be EGF-r positive as a result of an increase in the proportion of stromal cells which express the EGF receptor.