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Titolo:
MECHANISMS OF INACTIVATION OF E-CADHERIN IN BREAST-CANCER CELL-LINES
Autore:
HIRAGURI S; GODFREY T; NAKAMURA H; GRAFF J; COLLINS C; SHAYESTEH L; DOGGETT N; JOHNSON K; WHEELOCK M; HERMAN J; BAYLIN S; PINKEL D; GRAY J;
Indirizzi:
UNIV CALIF SAN FRANCISCO,CTR CANC,CANC GENET PROGRAM SAN FRANCISCO CA94143 UNIV CALIF SAN FRANCISCO,CTR CANC,CANC GENET PROGRAM SAN FRANCISCO CA94143 JOHNS HOPKINS UNIV,CTR ONCOL BALTIMORE MD 21205 LAWRENCE BERKELEY NATL LAB,DIV LIFE SCI BERKELEY CA 94720 LOS ALAMOS NATL LAB LOS ALAMOS NM 87545 UNIV TOLEDO TOLEDO OH 43606
Titolo Testata:
Cancer research
fascicolo: 9, volume: 58, anno: 1998,
pagine: 1972 - 1977
SICI:
0008-5472(1998)58:9<1972:MOIOEI>2.0.ZU;2-5
Fonte:
ISI
Lingua:
ENG
Soggetto:
FLUORESCENCE INSITU HYBRIDIZATION; MOLECULE E-CADHERIN; PROSTATE-CANCER; GENETIC ALTERATIONS; CARCINOMA-CELLS; EXPRESSION; ADHESION; MUTATIONS; METASTASES; ACID;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
39
Recensione:
Indirizzi per estratti:
Citazione:
S. Hiraguri et al., "MECHANISMS OF INACTIVATION OF E-CADHERIN IN BREAST-CANCER CELL-LINES", Cancer research, 58(9), 1998, pp. 1972-1977

Abstract

Loss of E-cadherin (CDH1) function is thought to contribute to progression in breast cancer and other solid tumors by increasing proliferation, invasion, and/or metastasis. In some cases, the restoration of CDH1 function may be an important therapeutic option. This possibility will depend on the mechanism by which CDH1 is inactivated. Here we present analyses of CDH1 expression, genetic mutation, and promoter methylation in CDH1 in 10 commonly used breast cancer cell lines. Five cell Lines (BT-474, MCF-7, MDA-MB-361, MDA-MB-468, and T-47D) expressed CDH1 and were genetically normal. Five others (SK-BR-3, 600 MPE, MDA-MB-134 IV, CAMA1, and MDA-MB-435) did not express CDH1, Fluorescence in situ hybridization analyses of each of these cell lines showed evidence for the physical deletion of one allele of CDH1, and three cell lines were found to carry homozygous deletions. SK-BR-3 was deleted from exon 12 through the promoter; exon 6 was deleted in MDA-MB-134 TV cells, and 600 MPE cells carried a 21-bp deletion in the splicing acceptor site for exon 9. CAMA1 seemed to have been inactivated through promoter methylation No explanation was found for the inactivation of CDH1 in MDA-MB-435.

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Documento generato il 04/07/20 alle ore 20:31:59