Malignant tumours specific for the thyroid gland originate from either the follicular cells (papillary, follicular undifferentiated carcinomas) or the parafollicular C-cell system (medullary carcinomas). Regarding the follicle derived carcinomas, various types of data indicate that radiation exposure, for example therapeutic radiation given to children for benign disorders in the head and neck area, is an important risk factor. Dietary components may also be relevant. The marked female predominance. which is not specific for malignant tumours, is probably the result of hormonal cofactors and differences in growth promotion of early lesions (microcarcinomas). Further development of follicle derived tumours is characterized by decreasing tumour cell dependence of TSH, along with the introduction of autocrine loops, e.g. expression of the TGF alpha/EGF-receptor system. and such mechanisms may in part explain the development of autonomous growth. In parallel with these phenotypic changes, several alterations have also been described in various thyroid tumours, including the medullary carcinomas, for example in the ras and ret genes. Activation of some oncogenes, like the EGF-receptor system, may also be relevant for late tumor progression and hence of prognostic value. to-ether with other factors like p53 and nm23. In addition to classical clinocopathological features, molecular data are of increasing importance in biological grading of thyroid tumours.

Related Articles