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Genetic Changes in Sporadic Keratocystic Odontogenic Tumors (Odontogenic Keratocysts)

K. Heikinheimo^1,2,,*, K.J. Jee^3,, P.R. Morgan⁴, B. Nagy⁵, S. Knuutila³, and I. Leivo³

¹ Department of Oral and Maxillofacial Surgery, Institute of Dentistry, University of Turku, Lemminkäisenkatu 2, FIN-20520 Turku, Finland;
² Department of Oral Diseases, Turku University Hospital, Lemminkäisenkatu 2, FIN-20500 Turku, Finland;
³ Haartman Institute, Department of Pathology, FIN-00014 University of Helsinki, Finland;
⁴ Department of Oral Pathology, GKT Dental Institute, King’s College London, United Kingdom; and
⁵ Genetic Laboratory, 1st Department of Obstetrics and Gynecology, Semmelweis University, Budapest, Hungary

^* corresponding author, heikinhe{at}netlife.fi

Little is known about the genetic background of keratocystic odontogenic tumors (KCOT, odontogenic keratocysts). Our aim was to characterize genomic aberrations in sporadic KCOT using cDNA-expression arrays and array-comparative genomic hybridization. For cDNA-expression arrays, 10 KCOT specimens and 20 fetal tooth germs were studied. Quantitative real-time reverse-transcription/polymerase chain-reaction and immunohistochemical studies were also undertaken. Several genes were over-expressed in 12q13, including cytokeratin 6B (KRT6B) ( 10-fold), epidermal growth factor receptor ERBB3 (~ 4.7-fold), and glioma-associated oncogene homologue 1 (GLI1) (~ 5- to 12-fold). One amplicon (~ 0.7 Mega base pairs [Mbp]), covering several genes involved in the regulation of cell growth, was found in 12q13.2. Deletions were found in 3q13.1, 5p14.3, and 7q31.3, including the cell-adhesion-related gene cadherin 18 (CDH18) and leukocyte cell adhesion molecule (ALCAM, MEMD). Over-expressed and amplified genes in 12q13, also reported in several other tumors and cell lines, may contribute to the persistent growth characteristics of KCOT.

KEY WORDS: genomic aberrations • gene expression • keratocystic odontogenic tumor • odontogenic keratocyst