Intranuclear Oncogenes

Nuclear protooncogenes involved in thyroid growth are c-myc, c-jurt, and c-fos. They were characterized by their similarity to viral oncogenes. Unlike most oncogenes encoding cell surface receptors or signal-transducing proteins, nuclear protooncogenes function by means of gene amplification.

Because external stimulation of cells by growth factors activates cellular receptors, signal-transducing proteins, second messengers, and nuclear protooncogenes by means of increased gene expression, it is difficult to determine whether alterations in nuclear protooncogenes are primary or secondary cellular phenomena. For example, it is difficult to know whether increased staining for c-myc in thyroid adenomas and thyroid carcinomas, as demonstrated by Auguste and associates,58 is a primary or secondary phenomenon.

In general, c-myc and c-fos protooncogenes are expressed after stimulation of the thyroid by TSH and cAMP, which increase thyroid growth and differentiation. EGF and TPA cause thyroid growth and dedifferentiation mainly by enhancing c-jun protooncogene expression. C-fos and c-jun expression can inhibit the thyroid hormone receptor. The thyroid hormone receptor, however, may inhibit the induction of c-/as73'74 and thus play the role of an antagonist to cell-specific protooncogenes. Understanding this direct regulatory loop of tissue-specific and growth-inhibiting intranuclear hormone receptors with intranuclear protooncogenes may increase our knowledge of thyroid growth and tumor development in low-iodine areas. In 1991, Heldin and Westermark75 demonstrated the loss of a specific tumor suppressor gene, which coded for a nuclear thyroid-specific transcription factor (TTF1), in anaplastic thyroid carcinomas.

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