Alterations of FHIT and P53 genes in keratocystic odontogenic tumor, dentigerous and radicular cyst

• Published in: Journal of oral pathology & medicine Vol. 37; no. 5; pp. 294 - 301
• Main Authors: MALCIC, Ana, JUKIC, Silvana, ANIC, Ivica, PAVELIC, Bozidar, KAPITANOVIC, Sanja, KRUSLIN, Bozo, PAVELIC, Kresimir
• Format: Journal Article
• Language: English
• Published: Oxford, UK Blackwell Publishing Ltd 01.05.2008; Blackwell
• Subjects: Acid Anhydride Hydrolases - genetics; Adolescent; Adult; Aged; Apoptosis; Biological and medical sciences; Cell Proliferation; Dentigerous Cyst - genetics; Dentigerous Cyst - metabolism; Dentistry; DNA Mutational Analysis; DNA, Neoplasm - analysis; Facial bones, jaws, teeth, parodontium: diseases, semeiology; Female; FHIT; Genes, p53 - genetics; Genes, Tumor Suppressor; Humans; Immunohistochemistry; Jaw Cysts - genetics; Jaw Cysts - metabolism; Jaw Neoplasms - genetics; Jaw Neoplasms - metabolism; keratocystic odontogenic tumor; Loss of Heterozygosity; Male; Medical sciences; Middle Aged; Neoplasm Proteins - genetics; Non tumoral diseases; odontogenic cyst; Odontogenic Tumors - genetics; Odontogenic Tumors - metabolism; Otorhinolaryngology. Stomatology; p53; Radicular Cyst - genetics; Radicular Cyst - metabolism; Stomatology; Dental disease; Diseases of the osteoarticular system; Fragile Histidine Triad gene; Odontogenic cyst; ENT; FHIT; Dental root cyst; p53; TP53 Gene; Odontogenic tumor; keratocystic odontogenic tumor; Benign neoplasm; Maxillary disease; Tumor suppressor gene
• ISSN: 0904-2512; 1600-0714
• DOI: 10.1111/j.1600-0714.2007.00622.x

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.