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Submitted on June 29, 2004
Accepted on October 25, 2004
UTER, III. Medical Department, University of Leipzig, Ph.-Rosenthal-Str. 27, D-04103 Leipzig, Germany; Interdisciplinary Center for Clinical Research Leipzig; Institute of Biometrics and Medical Informatics, University of Magdeburg; Interdisciplinary Center for Bioinformatics Leipzig
* To whom correspondence should be addressed.
RALF PASCHKE, E-mail: pasr{at}medizin.uni-leipzig.de
In contrast to the molecular etiology of autonomously functioning thyroid nodules the molecular cause of cold thyroid nodules, their benign, functional inactive counterparts is so far largely unknown. Because of the partially dedifferentiated phenotype of cold thyroid nodules alterations in signaling cascades that favor proliferation but not differentiation are likely candidates for tumor induction and progression. The importance of ras mutations for the development of benign nodules with follicular histology is still in question. However, differentially expressed genes in the context of their signaling cascades could define aberrant signaling in cold thyroid nodules. Therefore, we investigated gene expression in 22 cold thyroid nodules and their normal surrounding tissue using Affymetrix GeneChips. Most prominently, data analysis revealed an increased expression of cell cycle associated genes and a special relevance of protein kinase C signaling, whereas no evidence of ras-MAPK signaling in cold thyroid nodules was found. Moreover, we determined 31 differentially regulated genes in cold thyroid nodules including several histone mRNAs. Taken together, these results explain recent findings showing an increased proliferation in cold thyroid nodules and draw attention to protein kinase C signaling but away from ras MAPK signaling as being involved in the etiology of CTNs.
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