Wynford-Thomas D
Department of Pathology, University of Wales College of Medicine Heath Park, Cardiff, U.K.
Crit Rev Oncog. 1993;4(1):1-23.
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.
尽管甲状腺肿瘤导致的癌症死亡率较低，但它是研究人类上皮细胞肿瘤发生的细胞和分子生物学的一个简单且有力的实验模型。本综述以目前对甲状腺生长控制生理学的认识为框架，讨论导致滤泡细胞肿瘤的体细胞遗传异常。特别强调了G蛋白癌基因gsp的可预测参与、ras癌基因家族的关键早期作用以及p53肿瘤抑制基因突变的明显罕见性。讨论了甲状腺模型对我们理解生长调节基因之间相互作用的潜在贡献，特别是ras与IGF-1之间以及p53与TGF-β之间的关系。在整个过程中，甲状腺肿瘤数据与其他肿瘤类型的数据相关，并在细胞增殖的一般模型背景下进行解释。
