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Titolo:
Inactivation of the p16(INK4A) gene by methylation is not a frequent eventin sporadic ovarian carcinoma
Autore:
Brown, I; Milner, BJ; Rooney, PH; Haites, NE;
Indirizzi:
Univ Aberdeen, Dept Med Genet, Aberdeen AB25 2ZD, Scotland Univ Aberdeen Aberdeen Scotland AB25 2ZD et, Aberdeen AB25 2ZD, Scotland Univ Aberdeen, Inst Med Sci, Dept Mol & Cell Biol, Aberdeen AB25 2ZD, Scotland Univ Aberdeen Aberdeen Scotland AB25 2ZD ol, Aberdeen AB25 2ZD, Scotland
Titolo Testata:
ONCOLOGY REPORTS
fascicolo: 6, volume: 8, anno: 2001,
pagine: 1359 - 1362
SICI:
1021-335X(200111/12)8:6<1359:IOTPGB>2.0.ZU;2-C
Fonte:
ISI
Lingua:
ENG
Soggetto:
HUMAN CANCERS; DNA METHYLATION; P16 GENE; MUTATIONS; TUMORS; HETEROZYGOSITY; EXPRESSION; MTS1; CHROMOSOME-9; P16/MTS1;
Keywords:
ovarian cancer; tumour suppressor gene; p16; methylation;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Citazioni:
28
Recensione:
Indirizzi per estratti:
Indirizzo: Brown, I Univ Aberdeen, Dept Med Genet, Med Sch Bldg, Aberdeen AB25 2ZD, Scotland Univ Aberdeen Med Sch Bldg Aberdeen Scotland AB25 2ZD , Scotland
Citazione:
I. Brown et al., "Inactivation of the p16(INK4A) gene by methylation is not a frequent eventin sporadic ovarian carcinoma", ONCOL REP, 8(6), 2001, pp. 1359-1362

Abstract

The p16(INK4A) tumour suppressor gene (p16) encodes for a cyclin-dependantkinase inhibitor which plays a role in the phosphorylation of the retinoblastoma protein (pRb) during regulation of the GI-S phase of the cell cycle. Loss of heterozygosity at 9p21, the chromosomal location of the p16 gene, has been reported in a broad range of tumours. and this is usually indicative of the presence of a tumour suppressor gene, the second allele being frequently inactivated by mutation or deletion. The p16 gene, however, is often found not be mutated or deleted and it has been suggested that hypermethylation of the CpG islands of the gene may be an alternative mechanism of gene inactivation. We sought to determine the levels of p16 abnormality in a series of epithelial ovarian carcinomas in an attempt to clarify the presently conflicting evidence of whether or not hypermethylation of the p16 geneplays a role in ovarian carcinogenesis. We analysed 57 primary ovarian tumours and their corresponding blood DNA using SSCP analysis, sequencing and the methylation specific PCR (MSP) technique. We found low levels of mutation (6.7% of malignant tumours) and no evidence of methylation in any of oursamples, suggesting that neither mutation or hypermethylation of the CpG islands of the p16 gene play an important role in ovarian carcinogenesis.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 28/03/20 alle ore 13:18:48