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pubmed-article:17525355pubmed:abstractTextLittle 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) ( approximately 10-fold), epidermal growth factor receptor ERBB3 (approximately 4.7-fold), and glioma-associated oncogene homologue 1 (GLI1) (approximately 5- to 12-fold). One amplicon (approximately 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.lld:pubmed
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pubmed-article:17525355pubmed:pagination544-9lld:pubmed
pubmed-article:17525355pubmed:dateRevised2007-7-21lld:pubmed
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pubmed-article:17525355pubmed:articleTitleGenetic changes in sporadic keratocystic odontogenic tumors (odontogenic keratocysts).lld:pubmed
pubmed-article:17525355pubmed:affiliationDepartment of Oral and Maxillofacial Surgery, Institute of Dentistry, University of Turku, Lemminkäisenkatu 2, FIN-20520 Turku, Finland. heikinhe@netlife.filld:pubmed
pubmed-article:17525355pubmed:publicationTypeJournal Articlelld:pubmed
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pubmed-article:17525355pubmed:publicationTypeResearch Support, Non-U.S. Gov'tlld:pubmed