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Titolo:
Increased frequency of TP53 mutations in BRCA1 and BRCA2 ovarian tumours
Autore:
Ramus, SJ; Bobrow, LG; Pharoah, PDP; Finnigan, DS; Fishman, A; Altaras, M; Harrington, PA; Gayther, SA; Ponder, BAJ; Friedman, LS;
Indirizzi:
CRC, Human Canc Genet Res Grp, Strangeways Res Lab, Cambridge, England CRC Cambridge England Res Grp, Strangeways Res Lab, Cambridge, England Addenbrookes Hosp, Dept Histopathol, Cambridge CB2 2QQ, England Addenbrookes Hosp Cambridge England CB2 2QQ , Cambridge CB2 2QQ, England Meir Hosp, Sapir Med Ctr, Kfar Saba, Israel Meir Hosp Kfar Saba IsraelMeir Hosp, Sapir Med Ctr, Kfar Saba, Israel
Titolo Testata:
GENES CHROMOSOMES & CANCER
fascicolo: 2, volume: 25, anno: 1999,
pagine: 91 - 96
SICI:
1045-2257(199906)25:2<91:IFOTMI>2.0.ZU;2-O
Fonte:
ISI
Lingua:
ENG
Soggetto:
P53 GENE-MUTATIONS; BREAST-CANCER; PROTEIN ACCUMULATION; EMBRYONIC LETHALITY; GERMLINE MUTATIONS; PROGNOSTIC FACTOR; DNA-REPAIR; MICE; MALIGNANCIES; CARRIERS;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
32
Recensione:
Indirizzi per estratti:
Indirizzo: Ramus, SJ CRC, Human Canc Genet Res Grp, Strangeways Res Lab, Cambridge, England CRC Cambridge England Strangeways Res Lab, Cambridge, England
Citazione:
S.J. Ramus et al., "Increased frequency of TP53 mutations in BRCA1 and BRCA2 ovarian tumours", GENE CHROM, 25(2), 1999, pp. 91-96

Abstract

We screened 81 ovarian tumours (30 BRCAI associated, 18 BRCA2 associated, and 33 sporadic) for somatic TP53 mutations using both DNA analysis and immunostaining. TP53 mutations were significantly more frequent in tumours with mutations in BRCA1 (70% by immunostaining and 60% by DNA analysis) and BRCA2 (67% and 50%) compared to sporadic controls (39% and 30%) (P = 0.009). A higher proportion of tumours with BRCAI and BRCA2 mutations were poorly differentiated, and TP53 mutant tumours in all categories were also more likely to be poorly differentiated. The poor differentiation of tumours with BRCAI and BRCA2 mutations may be directly related to the role of these genesin DNA repair, and the need to overcome cell cycle checkpoints, often through loss of TP53. These results are consistent with the model of BRCA-induced tumorigenesis in which loss of checkpoint control is necessary for tumour development. (C) 1999 Wiley-Liss, Inc.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 22/09/20 alle ore 16:03:10