Abstract
Few oncogenes have been found consistently activated in the DNA from human naturally occurring carcinomas of the thyroid gland: ras (Ki-, Ha-, N-ras), trk and ret/PTC (1–4). Among them the trk and ret/PTC oncogenes are found activated exclusively in the papillary histotype (4). In contrast ras oncogenes are frequently found activated in all thyroid carcinoma histotypes ranging from the benign adenoma to the clear malignant adenocarcinoma, thus suggesting that ras activation is an early step in thyroid tumorigenesis (5,6). Different experimental models of thyroid neoplasias have been obtained with ras oncogenes, either by transforming thyroid epithelial cells in vitro or by directly injecting the Kirsten murine sarcoma virus (KiMSV) into the rat thyroid gland (7–10). It has been demonstrated that the Ha-ras is not able to fully transform human thyroid epithelial cells (10), and we have previously demonstrated that ras oncogenes are able to transform the thyroid epithelial cell line PC cl3, only in the presence of another cooperating oncogene (8). To further characterize the role of ras oncogenes in the development of thyroid carcinomas we have generated transgenic mice in which the expression of the Ki-ras oncogene is specifically addressed to the thyroid gland. For this purpose transgenic animals carrying constructs composed by segments of the rat thyroglobulin (TG) (11) gene promoter and by a human mutated Ki-ras oncogene cDNA (12) have been obtained. One thyroid adenoma with multiple foci has appeared after a long latency period in one transgenic mouse. This indicates that the ras oncogene is not able by itself to induce a full malignant transformation of the mouse thyroid.KeywordsThyroid CarcinomaThyroid GlandPapillary Thyroid CarcinomaHuman ThyroidFollicular Thyroid CarcinomaThese keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.
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