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Titolo:
THE HUMAN HOMOLOG FOR THE CAENORHABDITIS-ELEGANS CUL-4 GENE IS AMPLIFIED AND OVEREXPRESSED IN PRIMARY BREAST CANCERS
Autore:
CHEN LC; MANJESHWAR S; LU Y; MOORE D; LJUNG BM; KUO WL; DAIRKEE SH; WERNICK M; COLLINS C; SMITH HS;
Indirizzi:
CALIF PACIFIC MED CTR,GERALDINE BRUSH CANC RES INST,2330 CLAY ST,ROOM100 SAN FRANCISCO CA 94115 UNIV CALIF SAN FRANCISCO,SCH MED SAN FRANCISCO CA 94143 UNIV CALIF SAN FRANCISCO,SCH CANC GENET SAN FRANCISCO CA 94143 LAWRENCE BERKELEY NATL LAB BERKELEY CA 94720
Titolo Testata:
Cancer research
fascicolo: 16, volume: 58, anno: 1998,
pagine: 3677 - 3683
SICI:
0008-5472(1998)58:16<3677:THHFTC>2.0.ZU;2-E
Fonte:
ISI
Lingua:
ENG
Soggetto:
COMPARATIVE GENOMIC HYBRIDIZATION; HOMOGENEOUSLY STAINING REGIONS; IN-SITU HYBRIDIZATION; DIFFERENTIAL DISPLAY; MESSENGER-RNAS; DNA-SEQUENCES; AMPLIFICATION; FAMILY; CARCINOMAS; CLONING;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
32
Recensione:
Indirizzi per estratti:
Citazione:
L.C. Chen et al., "THE HUMAN HOMOLOG FOR THE CAENORHABDITIS-ELEGANS CUL-4 GENE IS AMPLIFIED AND OVEREXPRESSED IN PRIMARY BREAST CANCERS", Cancer research, 58(16), 1998, pp. 3677-3683

Abstract

Amplification is a key mechanism whereby a cancer cell increases the message level of genes that confer a selective advantage when they areoverexpressed. In breast cancer, there are many chromosome regions present in multiple copies relative to overall DNA copy number (amplicons), and their target genes are unknown. Using differential display, wehave cloned and sequenced the full coding region of a candidate amplicon target gene located on chromosome 13, This candidate iri the humanhomologue of the Caenorhabditis elegans cul-4 gene, cul-4A, a member of the novel cullin gene family, which is involved in cell cycle control of C. elegans, cul-4A was amplified and overexpressed in 3 of 14 breast cancer cell lines analyzed, and it was overexpressed in 8 additional cell lines in which it was not amplified. The latter observation, indicating that its overexpression can occur by mechanisms other than gene amplification, suggests that cul-4A plays a key role in carcinogenesis. Moreover, cul-4A was found to be amplified in 17 of 105 (16%) cases of untreated primary breast cancers, and 14 of 30 cases analyzed (47%) were shown by RNA in situ hybridization to overexpress cul-4A. These results suggest that upregulation of cul-4A may play an importantrole in tumor progression.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 20/01/20 alle ore 16:36:05