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.
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http://dx.doi.org/10.1111/j.1600-0714.2007.00622.x | DOI Listing |
Phytomedicine
December 2022
School of Pharmacy, Jiangxi University of Traditional Chinese Medicine, Nanchang 330006, PR China; National Pharmaceutical Engineering Center for Solid Preparation of Chinese Herbal Medicine, Jiangxi University of Traditional Chinese Medicine, Nanchang 330006, PR China; Key Laboratory for evaluation on Anti-tumor Effect of Chinese Medicine by Strengthening Body Resistance to Eliminate Pathogenic Factors, Nanchang 330006, PR China.
Cancer Treat Res Commun
December 2021
Department of Urology. Hospital Clínico Universitario de Valencia, Av. Blasco Ibáñez, 17, 46010. Valencia- España. Electronic address:
Introduction: Renal cell carcinoma (RCC) accounts for 2-3% of all tumors being the most frequent solid lesion in the kidney.
Objective: To determine what genetic alterations and immunohistochemical (IHC) of clear cell renal carcinoma (ccRCC) are associated with prognosis and tumor aggressiveness.
Patients And Methods: Experimental analytical study with 57 patients who underwent radical and partial nephrectomy between 2005 and 2011, all with diagnosis of ccRCC and minimum post-operative follow-up of 36 months.
Iran J Pharm Res
January 2019
Department of Toxicology and Pharmacology, Faculty of Pharmacy, Tehran University of Medical Sciences, Tehran, Iran.
Fragile histidine triad (FHIT) serves a critical function as a tumor suppressor that inhibits p53 degradation by mouse double minute 2 (MDM2). The functional domains of FHIT involved in tumor inhibition was interpreted. screening data were employed to construct truncated forms of FHIT to assess their cytotoxic effects on the HT1080 cell line.
View Article and Find Full Text PDFInt J Cancer
November 2019
Department of Pathology and Cell Biology, Columbia University Irving Medical Center (CUIMC), New York, NY.
The main risk factor for esophageal dysplasia and adenocarcinoma (DAC) is Barrett's esophagus (BE), characterized by intestinal metaplasia. The critical genomic mechanisms that lead to progression of nondysplastic BE to DAC remain poorly understood and require analyses of longitudinal patient cohorts and high-resolution assays. We tested BE tissues from 74 patients, including 42 nonprogressors from two separate groups of 21 patients each and 32 progressors (16 in a longitudinal cohort before DAC/preprogression-BE and 16 with temporally concurrent but spatially separate DAC/concurrent-BE).
View Article and Find Full Text PDFJ Cell Biochem
June 2019
Department of Toxicology Pharmacology, Faculty of Pharmacy, Tehran University of Medical Sciences, Tehran, Iran.
Fragile histidine trail (FHIT) is a tumor suppressor in response to DNA damage which has been deleted in various tumors. However, the signaling mechanisms and interactions of FHIT with regard to apoptotic proteins including p53 and p38 in the DNA damage-induced apoptosis are not well described. In the present study, we used etoposide-induced DNA damage in MCF-7 as a model to address these crosstalks.
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