BREAST-CANCER, DESMOID TUMORS, AND FAMILIAL ADENOMATOUS POLYPOSIS - AUNIFYING HYPOTHESIS

There is widespread agreement that epithelial tumours develop as a con sequence of primary events within epithelial cells. According to the m onoclonal theory, a tumour is caused by genetic change within a single cell, which imparts a selective growth advantage. This simple theory fails to take into account two important concepts. First, tumour gener ation is likely to involve multiple genetic events, some of which init iate a tumour, and others promote its growth.1 Second, tumours are usu ally composed of several tissue components, although they are known by the dominant proliferative cell type. This convention has tended to o bscure the importance of ''secondary'' tissue components in carcinogen esis, despite evidence for the involvement of mesenchymal elements bot h in the induction and maintenance of transformation. To shift emphasi s from the monoclonal theory, we propose a unifying hypothesis account ing for the effect of adjuvant tamoxifen in early breast cancer and th e association between gastrointestinal polyps and desmoid tumours.