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Titolo:
DEFICIENCY OF P53 ACCELERATES MAMMARY TUMORIGENESIS IN WNT-1 TRANSGENIC MICE AND PROMOTES CHROMOSOMAL INSTABILITY
Autore:
DONEHOWER LA; GODLEY LA; ALDAZ CM; PYLE R; SHI YP; PINKEL D; GRAY T; BRADLEY A; MEDINA D; VARMUS HE;
Indirizzi:
BAYLOR COLL MED,DIV MOLEC VIROL HOUSTON TX 77030 NCI,VARMUS LAB BETHESDA MD 20892 UNIV CALIF SAN FRANCISCO,DEPT BIOCHEM & BIOPHYS SAN FRANCISCO CA 94143 UNIV TEXAS,MD ANDERSON CANCER CTR,DEPT CARCINOGENESIS SMITHVILLE TX 78957 UNIV CALIF SAN FRANCISCO,DEPT LAB MED,DIV MOLEC CYTOMETRY SAN FRANCISCO CA 94143 BAYLOR COLL MED,HOWARD HUGHES MED INST HOUSTON TX 77030 BAYLOR COLL MED,INST MOLEC GENET HOUSTON TX 77030 BAYLOR COLL MED,DEPT CELL BIOL HOUSTON TX 77030 NIH,OFF DIRECTOR BETHESDA MD 20892 UNIV CALIF SAN FRANCISCO,DEPT MICROBIOL & IMMUNOL SAN FRANCISCO CA 94143
Titolo Testata:
Genes & development
fascicolo: 7, volume: 9, anno: 1995,
pagine: 882 - 895
SICI:
0890-9369(1995)9:7<882:DOPAMT>2.0.ZU;2-8
Fonte:
ISI
Lingua:
ENG
Soggetto:
WILD-TYPE P53; P53-DEFICIENT MICE; BREAST-CANCER; GENE AMPLIFICATION; NEU ONCOGENE; TUMOR VIRUS; INT-2 GENE; FGF GENE; C-MYC; MOUSE;
Keywords:
P53; WNT-1; MAMMARY TUMORS; GENOMIC INSTABILITY; MOUSE; TUMOR MODEL;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Science Citation Index Expanded
Citazioni:
59
Recensione:
Indirizzi per estratti:
Citazione:
L.A. Donehower et al., "DEFICIENCY OF P53 ACCELERATES MAMMARY TUMORIGENESIS IN WNT-1 TRANSGENIC MICE AND PROMOTES CHROMOSOMAL INSTABILITY", Genes & development, 9(7), 1995, pp. 882-895

Abstract

By crossing mice that carry a null allele of p53 with transgenic micethat develop mammary adenocarcinomas under the influence of a Wnt-1 transgene, we have studied the consequences of p53 deficiency in mammary gland neoplasia. In Wnt-1 transgenic mice homozygous for the p53 null allele, tumors appear at an earlier age than in animals heterozygousor wild-type at the p53 locus. About half of the tumors arising in p53 heterozygotes exhibit loss of the normal p53 allele, implying selection for p53-deficient cells. Mammary tumors lacking p53 display less fibrotic histopathology and increased genomic instability with aneuploidy, amplifications, and deletions, as detected by karyotype analysis and comparative genomic hybridization. In one tumor, the amplified region of chromosome 7 had an ectopically expressed int-2/FGF3 proto-oncogene, a gene known to cooperate with Wnt-1 in the production of mammarytumors. These findings favor a model in which p53 deficiency relaxes normal restraints on chromosomal number and organization during tumorigenesis.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 25/11/20 alle ore 10:30:07