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Alterations of FHIT and P53 genes in keratocystic odontogenic tumor, dentigerous and radicular cyst
Author(s) -
Malčić Ana,
Jukić Silvana,
Anić Ivica,
Pavelić Božidar,
Kapitanović Sanja,
Krušlin Božo,
Pavelić Krešimir
Publication year - 2008
Publication title -
journal of oral pathology and medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.887
H-Index - 83
eISSN - 1600-0714
pISSN - 0904-2512
DOI - 10.1111/j.1600-0714.2007.00622.x
Subject(s) - fhit , loss of heterozygosity , locus (genetics) , keratocystic odontogenic tumor , biology , gene , dentigerous cyst , gene mutation , ameloblastoma , exon , immunohistochemistry , pathology , cancer research , microbiology and biotechnology , tumor suppressor gene , mutation , genetics , carcinogenesis , cyst , medicine , odontogenic , allele , anatomy , immunology , maxilla
Background: The purpose of this study was to determine fragile histidine triad (FHIT) and p53 protein expression, and to analyze FHIT and p53 gene status in keratocystic odontogenic tumor (KOT), dentigerous cysts (DC) and radicular cysts (RC). Methods: The methods used were immunohistochemistry and molecular genetic methods including loss of heterozygosity (LOH) and gene sequencing. Results: FHIT protein expression was different among groups. Aberrant expression was the highest in KOT, then in RC and DC. p53 protein expression was different among groups. LOH in paraffin‐embedded specimens was detected in 22.6% and 12.9% for FHIT and p53 respectively. Mutation of p53 gene at codon 237 was observed in only two specimens (one KOT and one DC). Of the six frozen specimens, three exhibited FHIT gene LOH (two RC and one KOT). KOT showed loss of exons 6–7 at FHIT locus and mutation at codon 237 at p53 locus, but this could be a chance result. Conclusion: Aberrations of FHIT and p53 genes/proteins could be considered markers responsible for the development of odontogenic lesions.