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Submitted on June 25, 2003
Accepted on September 26, 2003
1 IRIBHM, Faculté de Médecine de l'ULB, 808 route de Lennik, 1070 Bruxelles; Microarray Facility, Katholiek Universiteit van Leuven; Department of Endocrinology, Hôpital Universiaitre Erasme, 808 route de Lennik, 1070 Bruxelles; Research fellow of the Fonds National de la Recherche Scientifique
* To whom correspondence should be addressed. E-mail: jcgoffar{at}ulb.ac.be.
Mutations of the thyrotropin receptor leading to constitutive activation of the cAMP cascade are responsible for the development of hot nodules, if arising in a somatic cell, and non-auto-immune hyperthyroidism, when occurring in a germinal cell. An animal model of constitutive activation of the thyroid cAMP cascade has been obtained by generating transgenic mice expressing the adenosine receptor (Tg-A2aR) under the control of the thyroglobulin promoter. These mice develop huge goiters and die prematurely due to hyperthyroidism induced cardiac failure. To identify new genes involved in the tumorigenic pathway of the thyroid, we designed a protocol using microarray technology to study the differential expression, between normal and transgenic thyroid, of +/- 13.000 genes. 360 genes or EST showed a strong modulation with background corrected values of fluorescence superior to 2 fold change. The modulated genes were classified according to their proposed gene ontology functions. Approximately half of them were upregulated. The function of the majority of these genes in thyroid physiology is still to be determined. Some of them, like IGF-I, IGF-BP3, IGF-BP5, may play an important role in the development of thyroid nodules through paracrine mechanisms. This study demonstrates the feasibility of sequentially after the cascade of events leading to the formation of benign tumors such as hot thyroid nodule or hyperfunctional goitre.
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