Catalogo Articoli (Spogli Riviste)

OPAC HELP

Titolo:
The FHIT gene in oral squamous cell carcinoma: allelic imbalance is frequent but cDNA aberrations are uncommon
Autore:
Pateromichelakis, S; Lee, G; Langdon, JD; Partridge, M;
Indirizzi:
Guys Kings & St Thomas Sch Dent, Dept Oral & Maxillofacial Surg Mol Oncol,London SE5 9RW, England Guys Kings & St Thomas Sch Dent London England SE5 9RW SE5 9RW, England
Titolo Testata:
ORAL ONCOLOGY
fascicolo: 2, volume: 36, anno: 2000,
pagine: 180 - 188
SICI:
1368-8375(200003)36:2<180:TFGIOS>2.0.ZU;2-G
Fonte:
ISI
Lingua:
ENG
Soggetto:
3P14.2 FRAGILE SITE; HOMOZYGOUS DELETIONS; TUMOR-SUPPRESSOR; LUNG-CANCER; CIGARETTE-SMOKING; FRA3B; LINES; EXPRESSION; LESIONS; ALCOHOL;
Keywords:
oral cancer; FHIT gene; microsatellite markers; allelic imbalance; tumour suppressor;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Citazioni:
32
Recensione:
Indirizzi per estratti:
Indirizzo: Pateromichelakis, S Rayne Inst, 123 Coldharbour Lane, London SE5 9NU, England Rayne Inst 123 Coldharbour Lane London England SE5 9NU
Citazione:
S. Pateromichelakis et al., "The FHIT gene in oral squamous cell carcinoma: allelic imbalance is frequent but cDNA aberrations are uncommon", ORAL ONCOL, 36(2), 2000, pp. 180-188

Abstract

The FHIT (fragile histidine triad) gene at chromosome 3p14.2 spans the FRA3B fragile site and encodes for a diadenosine triphosphate hydrolase-type protein. FHIT is frequently abnormal in solid tumours including those of theupper aerodigestive tract (UAT) and has therefore been proposed as a tumour-suppressor gene. This proposition was evaluated hers for oral squamous cell carcinoma (SCC) using microsatellite analysis, reverse transcription-polymerase chain reaction (RT-PCR), FHIT exon 5 PCR and direct sequencing. Fifty-eight primary oral SCCs were examined with two FHIT gene microsatellite markers (D3S4103 and D3S1300) and two markers flanking FHIT. Allelic imbalance (AI) occurred in 28 of 52 informative cases (54%) at one or both FHIT markers (D3S4103: 53%; D3S1300: 42%). A significant association was noted between frequency of At and advanced stage rumours for D3S4103 but not between AI frequency and smoking. Al frequency at D3S1300 and at a flanking marker correlated with low survival. Of eight oral/UAT SCC cell lines examined, six produced abundant wild-type transcript and one yielded mostly truncatedtranscripts, the most abundant of which lacked exons 5-7. A double deletion was also detected in one of 11 primary oral SCCs. Our microsatellite assay results show that the FHIT gene is frequently disrupted in oral SCC. However, as FHIT was shows to be expressed normally in the great majority of oral/UAT SCCs studied, its likely involvement in the molecular pathogenesis of the disease as a tumour suppressor remains doubtful. (C) 2000 Elsevier Science Ltd. All rights reserved.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 04/07/20 alle ore 15:01:57