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Titolo:
ANALYSIS OF LOSS OF HETEROZYGOSITY AND KRAS2 MUTATIONS IN OVARIAN NEOPLASMS - CLINICOPATHOLOGICAL CORRELATIONS
Autore:
CHENEVIXTRENCH G; KERR J; HURST T; SHIH YC; PURDIE D; BERGMAN L; FRIEDLANDER M; SANDERSON B; ZOURNAZI A; COOMBS T; LEARY JA; CRAWFORD E; SHELLING AN; COOKE I; GANESAN TS; SEARLE J; CHOI C; BARRETT JC; KHOO SK; WARD B;
Indirizzi:
QUEENSLAND INST MED RES,ROYAL BRISBANE HOSP PO HERSTON QLD 4029 AUSTRALIA UNIV QUEENSLAND,ROYAL BRISBANE HOSP,DEPT OBSTET & GYNECOL BRISBANE QLD AUSTRALIA PRINCE WALES HOSP,DEPT MED ONCOL RANDWICK NSW 2031 AUSTRALIA UNIV SYDNEY,WESTMEAD HOSP,DEPT MED ONCOL SYDNEY NSW 2006 AUSTRALIA UNIV SYDNEY,WESTMEAD HOSP,DEPT OBSTET & GYNECOL SYDNEY NSW 2006 AUSTRALIA UNIV ALABAMA,MED GENET LAB BIRMINGHAM AL 35294 JOHN RADCLIFFE HOSP,INST MOL MED,IMPERIAL CANC RES FUND OXFORD OX3 9DU ENGLAND ROYAL BRISBANE HOSP,DEPT PATHOL BRISBANE QLD 4029 AUSTRALIA NIEHS,MOL CARCINOGENESIS LAB RALEIGH NC 00000
Titolo Testata:
Genes, chromosomes & cancer
fascicolo: 2, volume: 18, anno: 1997,
pagine: 75 - 83
SICI:
1045-2257(1997)18:2<75:AOLOHA>2.0.ZU;2-H
Fonte:
ISI
Lingua:
ENG
Soggetto:
CHROMOSOME 6Q; FREQUENT LOSS; ALLELIC LOSS; BRCA1 GENE; LATE EVENT; TUMORS; CANCER; CARCINOMA; P53; LOCUS;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Science Citation Index Expanded
Citazioni:
50
Recensione:
Indirizzi per estratti:
Citazione:
G. Chenevixtrench et al., "ANALYSIS OF LOSS OF HETEROZYGOSITY AND KRAS2 MUTATIONS IN OVARIAN NEOPLASMS - CLINICOPATHOLOGICAL CORRELATIONS", Genes, chromosomes & cancer, 18(2), 1997, pp. 75-83

Abstract

The molecular events that give rise to ovarian epithelial neoplasms are not well understood. In particular, it is not known whether adenocarcinomas arise from benign or low malignant potential (LMP) precursors. We have examined a large series of benign (25) and LMP (31) ovarian tumors for loss of heterozygosity (LOH) at multiple loci on 17 chromosomes. LOH was observed in benign tumors on chromosomes 6 (14%) and 9 (5%) and on the X chromosome (33%) only. LOH on these chromosomes was also detected in a small number of LMP neoplasms, suggesting that thesemay derive sometimes from benign precursors. In addition, we examinedLOH in 93 adenocarcinomas. Analysis of associations between LOH events showed that LOH on chromosomes 5 and 17 (P = 0.0002) and on chromosomes 17 and 18 (P = 0.00007) were associated significantly with each other, which suggests that these may represent cooperative, progressive events. No novel significant associations were identified between LOH events and stage, grade, or histology, which would indicate the existence of genetic heterogeneity in ovarian neoplasms. KRAS2 mutations were detected more often in LMP neoplasms than in malignant tumors (P = 0.004) and were detected more often in Stage I/II malignant tumors thanin Stage III/IV malignant tumors (P = 0.033), suggesting that LMP tumors with KRAS2 mutations are unlikely to progress to frank malignancy. Univariate (but not multivariate) survival analysis showed that LOH of chromosomes II (P = 0.039) and 17 (P = 0.04) was associated with a significantly worse prognosis. Replication of these novel findings is necessary, and the identification, isolation, and characterization of the critical genes affected by LOH will determine their importance in the pathogenesis of ovarian malignancies. (C) 1997 Wiley-Liss, Inc.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 29/11/20 alle ore 07:03:34