Malcić Ana, Jukić Silvana, Anić Ivica, Pavelić Bozidar, Kapitanović Sanja, Kruslin Bozo, Pavelić Kresimir
Department of Endodontics and Restorative Dentistry, School of Dental Medicine, University of Zagreb, Zagreb, Croatia.
J Oral Pathol Med. 2008 May;37(5):294-301. doi: 10.1111/j.1600-0714.2007.00622.x. Epub 2008 Jan 19.
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).
The methods used were immunohistochemistry and molecular genetic methods including loss of heterozygosity (LOH) and gene sequencing.
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.
Aberrations of FHIT and p53 genes/proteins could be considered markers responsible for the development of odontogenic lesions.
本研究旨在确定脆性组氨酸三联体（FHIT）和p53蛋白的表达情况，并分析牙源性角化囊肿（KOT）、含牙囊肿（DC）和根尖囊肿（RC）中FHIT和p53基因的状态。
采用的方法包括免疫组织化学以及分子遗传学方法，如杂合性缺失（LOH）和基因测序。
FHIT蛋白表达在各组间存在差异。异常表达在KOT中最高，其次是RC和DC。p53蛋白表达在各组间也存在差异。石蜡包埋标本中FHIT和p53的杂合性缺失分别为22.6%和12.9%。仅在两个标本（一个KOT和一个DC）中观察到p53基因第237密码子的突变。在六个冷冻标本中，三个出现了FHIT基因杂合性缺失（两个RC和一个KOT）。KOT在FHIT基因座处显示外显子6 - 7缺失，在p53基因座处显示第237密码子突变，但这可能是偶然结果。
FHIT和p53基因/蛋白的异常可被视为牙源性病变发生的标志物。
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