Polyclonal and monoclonal thyroid nodules coexist within human multinodular goiters.

Although somatic mutations have been identified in a subset of thyroid nodules, the pathogenesis of nodules in multinodular goiters remains unclear. Clonal analysis indicates whether a nodule arises from the polyclonal proliferation of a group of cells or forms a clone from a genetically altered cell. Individual thyroid nodules have been shown to be of polyclonal or monoclonal origin.

The degree of inhibition of thyroid follicular cell proliferation by iodide is a highly individual characteristic of each cell and differs profoundly in vitro and in vivo.

Pharmacological concentrations of iodide (> 1 x 10(-6) mol/l) are known to inhibit thyroid follicular cell growth in vitro. However, the inhibitory effect varies widely, depending on experimental conditions, and usually does not exceed 50%. We demonstrate that iodide (10(-4) mol/l) inhibits the growth of FRTL-5 cells in different passages by 11-67%.

Low intrathyroidal iodine concentration in non-endemic human goitres: a consequence rather than a cause of autonomous goitre growth.

Iodine may have an inhibitory and, in some circumstances, a stimulatory effect on thyroid follicular cell growth. Exogenous iodine deficiency causes the growth of endemic goitres and it has been claimed that low intrathyroidal iodine stores stimulate growth. On the other hand, the role of iodine, if any, in regulating the growth of human nodular goitres exposed to an ample supply of iodine has not been studied systematically.

Morphological and functional polymorphism within clonal thyroid nodules.

Thirty-nine thyroid nodules, removed because of recent growth, were analyzed morphologically by serial histological sections for the classical histomorphological hallmarks of follicular cell replication and for immunohistochemically demonstrable overexpression of the growth-associated ras-gene product p21ras. Clonal analysis was performed using the highly informative probe M27 beta that detects polymorphisms on the locus DXS255 of the X-chromosome. Twenty-four nodules were of clonal and 15 nodules were of poly-clonal origin.

Malignant transformation of rat thyroid cells transfected with the human TSH receptor cDNA.

Growth and function of well differentiated FRTL-5 thyroid cells depend on thyrotropin as its main regulatory hormone. We demonstrate here that stable transfection of FRTL-5 cells with the human thyrotropin receptor cDNA results in cellular transformation of these cells with altered cell shape and loss of contact inhibition. The transformed cells replicate in soft agar and form invasive tumors when cell suspensions are implanted onto nude mice.