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J Dent Res. 2015 Jan;94(1):101-11. doi: 10.1177/0022034514556815. Epub 2014 Nov 14.

Early dental epithelial transcription factors distinguish ameloblastoma from keratocystic odontogenic tumor.

Author information

1
Department of Oral and Maxillofacial Surgery, Institute of Dentistry, University of Turku, Turku, Finland Turku University Hospital, Turku, Finland Department of Oral Diagnostic Sciences, Institute of Dentistry, University of Eastern Finland, Kuopio, Finland Department of Oral and Maxillofacial Diseases, Kuopio University Hospital, Kuopio, Finland krihei@utu.fi.
2
Department of Medical Biochemistry and Genetics, University of Turku, Turku, Finland Turku Doctoral Programme of Molecular Medicine, Turku, Finland.
3
Microarray and Sequencing Centre, Turku Centre for Biotechnology, University of Turku, Turku, Finland Åbo Akademi University, Turku, Finland.
4
Turku University Hospital, Turku, Finland Department of Dermatology, University of Turku, Turku, Finland.
5
Molecular Oral Pathophysiology, INSERM UMRS 872, Cordeliers Biomedical Institute, Paris 7 University, Paris, France.
6
Department of Maxillofacial Surgery and Stomatology, André Grégoire Hospital, Paris, France.
7
Molecular Oral Pathophysiology, INSERM UMRS 872, Cordeliers Biomedical Institute, Paris 7 University, Paris, France Assistance Publique-Hôpitaux de Paris, Pitié-Salpêtrière Hospital, Department of Maxillofacial Surgery and Stomatology, Paris, France.
8
Head and Neck/Oral Pathology, Dental Institute, King's College London, London, UK.
9
Institute of Biotechnology, University of Helsinki, Helsinki, Finland.
10
Turku University Hospital, Turku, Finland Department of Pathology, University of Turku, Turku, Finland.

Abstract

The aim of the study was to characterize the molecular relationship between ameloblastoma and keratocystic odontogenic tumor (KCOT) by means of a genome-wide expression analysis. Total RNA from 27 fresh tumor samples of 15 solid/multicystic intraosseous ameloblastomas and 12 sporadic KCOTs was hybridized on Affymetrix whole genome arrays. Hierarchical clustering separated ameloblastomas and KCOTs into 2 distinct groups. The gene set enrichment analysis based on 303 dental genes showed a similar separation of ameloblastomas and KCOTs. Early dental epithelial markers PITX2, MSX2, DLX2, RUNX1, and ISL1 were differentially overexpressed in ameloblastoma, indicating its dental identity. Also, PTHLH, a hormone involved in tooth eruption and invasive growth, was one of the most differentially upregulated genes in ameloblastoma. The most differentially overexpressed genes in KCOT were squamous epithelial differentiation markers SPRR1A, KRTDAP, and KRT4, as well as DSG1, a component of desmosomal cell-cell junctions. Additonally, the epithelial stem cell marker SOX2 was significantly upregulated in KCOT when compared with ameloblastoma. Taken together, the gene expression profile of ameloblastoma reflects differentiation from dental lamina toward the cap/bell stage of tooth development, as indicated by dental epithelium-specific transcription factors. In contrast, gene expression of KCOT indicates differentiation toward keratinocytes.

KEYWORDS:

dental lamina; epithelial stem cell; gene expression; keratocystic odontogenic tumor; tooth germ; tumor bioinformatics

PMID:
25398365
DOI:
10.1177/0022034514556815
[Indexed for MEDLINE]

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