Breast cancer, desmoid tumours, and familial adenomatous polyposis--a unifying hypothesis.
There is widespread agreement that epithelial tumours develop as a consequence of primary events within epithelial cells. According to the monoclonal 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 generation is likely to involve multiple genetic events, some of which initiate a tumour, and others promote its growth. Second, tumours are usually composed of several tissue components, although they are known by the dominant proliferative cell type. This convention has tended to obscure the importance of "secondary" tissue components in carcinogenesis, despite evidence for the involvement of mesenchymal elements both in the induction and maintenance of transformation. To shift emphasis from the monoclonal theory, we propose a unifying hypothesis accounting for the effect of adjuvant tamoxifen in early breast cancer and the association between gastrointestinal polyps and desmoid tumours.
Benson
J R
JR
Hartwell Laboratory, Academic Section of Surgery, Institute of Cancer Research, London, UK.
Baum
M
M
D011125:Adenomatous Polyposis Coli / Q000209:etiology* / Q000235:genetics / Q000473:pathology; D001943:Breast Neoplasms / Q000209:etiology* / Q000235:genetics / Q000473:pathology; D002471:Cell Transformation, Neoplastic / Q000235:genetics; D005260:Female; D005350:Fibroma / Q000209:etiology* / Q000235:genetics / Q000473:pathology; D006801:Humans; D008648:Mesoderm / Q000473:pathology*