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Bioinformatics Unit, § the Commissariat à l’Energie Atomique LRC-29V, † and the Departments of Clinical Biology, � Nuclear

By Ludovic Lacroix, Vladimir Lazar, Stefan Michiels, Hugues Ripoche, Monique Talbot, Bernard Caillou, Jean-pierre Levillain, Martin Schlumberger and Jean-michel Bidart


Follicular thyroid carcinomas (FTC) arise through oncogenic pathways distinct from those involved in the papillary histotype. Recently, a t(2;3)(q13;p25) rearrangement, which juxtaposes the thyroid transcription factor PAX8 to the peroxisome proliferator-activated receptor (PPAR) �1, was described in FTCs. In this report, we describe gene expression in 11 normal tissues, 4 adenomas, and 8 FTCs, with or without the PAX8-PPAR�1 translocation, using custom 60-mer oligonucleotide microarrays. Results were confirmed by quantitative real-time polymerase chain reaction of 65 thyroid tissues and by immunohistochemistry. Statistical analysis revealed a pattern of 93 genes discriminating FTCs, with or without the translocation, that were morphologically undistinguishable. Although the expression of thyroid-specific genes was detectable, none appeared to be differentially regulated between tumors with or without the translocation. Differentially expressed genes included genes related to lipid/glucose/amino acid metabolism, tumorigenesis, and angiogenesis. Surprisingly, several PPAR � target genes were up-regulated in PAX8-PPAR�-positive FTCs such as angiopoietin-like 4 and aquaporin 7. Moreover many genes involved in PAX8-PPAR � expression profile presented a putative PPAR�-promoter site, compatible with a direct activity of the fusion product. These data identify several differentially expressed genes, such as FGD3, that may serve as potential targets of PPAR � and as members of novel molecular pathways involved in th

Year: 2009
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