Gene expression profiling in sinonasal adenocarcinoma
- Equal contributors
1 Inserm, UMR 892, Nantes, F-44007, France; Université de Nantes, UFR Médecine et Techniques Médicales, Nantes, F-44000, France
2 Service de Médecine du Travail et des Risques Professionnels, CHU de Nantes, Nantes, F-44093, France
3 Service d'Anatomie Pathologique, CHU de Nantes, Nantes, F-44093, France
4 Université de Nantes, UFR Médecine et Techniques Médicales, EA Biométadys, Nantes, F-44093, France
5 Service ORL, CHU de Nantes, Nantes, F-44093, France
6 Université de Nantes, UFR Médecine et Techniques Médicales, Plateforme Puces à ADN-OGP, Nantes, F-44000, France
7 Université de Nantes, UFR Médecine et Techniques Médicales, Laboratoire de Biomathématiques-Biostatistiques, Nantes, F-44000, France
8 Consultation des Pathologies Professionnelles, CH Hôtel-Dieu, Rennes, F-35000, France
9 Service de Biochimie, CHU de Nantes, Nantes, F-44093, France
BMC Medical Genomics 2009, 2:65 doi:10.1186/1755-8794-2-65Published: 10 November 2009
Sinonasal adenocarcinomas are uncommon tumors which develop in the ethmoid sinus after exposure to wood dust. Although the etiology of these tumors is well defined, very little is known about their molecular basis and no diagnostic tool exists for their early detection in high-risk workers.
To identify genes involved in this disease, we performed gene expression profiling using cancer-dedicated microarrays, on nine matched samples of sinonasal adenocarcinomas and non-tumor sinusal tissue. Microarray results were validated by quantitative RT-PCR and immunohistochemistry on two additional sets of tumors.
Among the genes with significant differential expression we selected LGALS4, ACS5, CLU, SRI and CCT5 for further exploration. The overexpression of LGALS4, ACS5, SRI, CCT5 and the downregulation of CLU were confirmed by quantitative RT-PCR. Immunohistochemistry was performed for LGALS4 (Galectin 4), ACS5 (Acyl-CoA synthetase) and CLU (Clusterin) proteins: LGALS4 was highly up-regulated, particularly in the most differentiated tumors, while CLU was lost in all tumors. The expression of ACS5, was more heterogeneous and no correlation was observed with the tumor type.
Within our microarray study in sinonasal adenocarcinoma we identified two proteins, LGALS4 and CLU, that were significantly differentially expressed in tumors compared to normal tissue. A further evaluation on a new set of tissues, including precancerous stages and low grade tumors, is necessary to evaluate the possibility of using them as diagnostic markers.