Molecular basis of epithelial tumorigenesis: the thyroid model.
Although a minor cause of cancer mortality, thyroid tumors represent a simple and hence powerful experimental model for studying the cell and molecular biology of tumorigenesis in human epithelial cells. This review uses current knowledge of the physiology of growth control in the thyroid as a framework for discussing the somatic genetic abnormalities responsible for follicular cell tumors. Specific emphasis is placed on the predictable involvement of the G-protein oncogene gsp, the key early role of the ras oncogene family, and the apparent rarity of mutations in the p53 tumor-suppressor gene. Potential contributions of the thyroid model to our understanding of interactions between growth regulatory genes are discussed, particularly the relationships between ras and IGF-1 and between p53 and TGF-beta. Throughout, thyroid tumor data are related to that from other tumor types and interpreted in the context of a general model of cell proliferation.
Wynford-Thomas
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Department of Pathology, University of Wales College of Medicine Heath Park, Cardiff, U.K.
D000230:Adenocarcinoma / Q000473:pathology / Q000503:physiopathology*; D002291:Carcinoma, Papillary / Q000503:physiopathology*; D002455:Cell Division / Q000502:physiology; D004848:Epithelium / Q000473:pathology; D006801:Humans; D008954:Models, Biological; D009857:Oncogenes / Q000235:genetics; D013964:Thyroid Neoplasms / Q000473:pathology / Q000503:physiopathology*