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Genetic Changes in Sporadic Keratocystic Odontogenic Tumors (Odontogenic Keratocysts)
K. Heikinheimo1,2, ,*,
K.J. Jee3, ,
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, Kings College London, United Kingdom; and
5 Genetic Laboratory, 1st Department of Obstetrics and Gynecology, Semmelweis University, Budapest, Hungary
Correspondence: * 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
Journal of Dental Research, Vol. 86, No. 6,
544-549 (2007)
DOI: 10.1177/154405910708600611

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