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Titolo:
Genetic changes in paired atypical and usual ductal hyperplasia of the breast by comparative genomic hybridization
Autore:
Gong, G; DeVries, S; Chew, KL; Cha, I; Ljung, BM; Waldman, FM;
Indirizzi:
Univ Calif San Francisco, Ctr Canc, San Francisco, CA 94143 USA Univ CalifSan Francisco San Francisco CA USA 94143 ancisco, CA 94143 USA Univ Calif San Francisco, Dept Pathol, San Francisco, CA 94143 USA Univ Calif San Francisco San Francisco CA USA 94143 ancisco, CA 94143 USA Univ Calif San Francisco, Dept Lab Med, San Francisco, CA 94143 USA Univ Calif San Francisco San Francisco CA USA 94143 ancisco, CA 94143 USA Univ Ulsan, Coll Med, Asan Med Ctr, Dept Pathol, Seoul 138736, South KoreaUniv Ulsan Seoul South Korea 138736 pt Pathol, Seoul 138736, South Korea
Titolo Testata:
CLINICAL CANCER RESEARCH
fascicolo: 8, volume: 7, anno: 2001,
pagine: 2410 - 2414
SICI:
1078-0432(200108)7:8<2410:GCIPAA>2.0.ZU;2-1
Fonte:
ISI
Lingua:
ENG
Soggetto:
CARCINOMA IN-SITU; TERM FOLLOW-UP; MICROSATELLITE ALTERATIONS; CANCER; HETEROZYGOSITY; LOCI; 16Q; PROGRESSION; EXPRESSION; ANOMALIES;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Citazioni:
23
Recensione:
Indirizzi per estratti:
Indirizzo: Waldman, FM Univ Calif San Francisco, Ctr Canc, San Francisco, CA 94143 USA Univ Calif San Francisco San Francisco CA USA 94143 94143 USA
Citazione:
G. Gong et al., "Genetic changes in paired atypical and usual ductal hyperplasia of the breast by comparative genomic hybridization", CLIN CANC R, 7(8), 2001, pp. 2410-2414

Abstract

Purpose: Breast cancer is thought to develop from noninvasive precursor lesions, although the earliest steps of neoplastic transformation are still undefined. Usual ductal hyperplasia (UDH) is considered to represent a benign proliferation of ductal epithelial cells, whereas atypical ductal hyperplasia (ADH) may represent the first clonal neoplastic expansion of these cells. The aim of this study was to examine genetic alterations in UDH and ADHand to determine the relationship between these lesions in the same breastbiopsy. Experimental Design: Comparative genomic hybridization analysis was used to define copy number alterations in DNA extracted from archival sections of18 patients. Nine patients showed ADH with adjacent UDH, and nine showed pure UDH. None showed evidence of invasive cancer or ductal carcinoma in situ. Results: Five of the nine ADH lesions showed chromosome copy number alterations. 16q loss (five cases) and 17p loss (two cases) were the most frequent changes. The associated UDH lesions in these five patients also showed copy number alterations, always a subset of the changes present in the pairedADH. In one other patient, the UDH showed eight chromosomal alterations, whereas the paired ADH showed no changes. Only one of nine cases with pure UDH showed comparative genomic hybridization abnormalities. Conclusions: These data support the likelihood that UDH is a precursor of ADH, at least in some cases representing neoplastic growth. The frequenciesof 16q and 17p losses suggest that alterations of candidate genes located in these chromosomal regions may play a role early in breast carcinogenesis.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 30/03/20 alle ore 19:49:59