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Titolo:
Genome scanning with array CGH delineates regional alterations in mouse islet carcinomas
Autore:
Hodgson, G; Hager, JH; Volik, S; Hariono, S; Wernick, M; Moore, D; Albertson, DG; Pinkel, D; Collins, C; Hanahan, D; Gray, JW;
Indirizzi:
Univ Calif San Francisco, Ctr Canc, Canc Genet Program, San Francisco, CA 94143 USA Univ Calif San Francisco San Francisco CA USA 94143 ancisco, CA 94143 USA Univ Calif San Francisco, Ctr Canc, Breast Oncol Program, 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 Calif San Francisco, Ctr Diabet, Dept Biochem & Biophys, San Francisco, CA 94143 USA Univ Calif San Francisco San Francisco CA USA 94143 ancisco, CA 94143 USA Univ Calif San Francisco, Ctr Comprehens Canc, San Francisco, CA 94143 USAUniv Calif San Francisco San Francisco CA USA 94143 ancisco, CA 94143 USA
Titolo Testata:
NATURE GENETICS
fascicolo: 4, volume: 29, anno: 2001,
pagine: 459 - 464
SICI:
1061-4036(200112)29:4<459:GSWACD>2.0.ZU;2-F
Fonte:
ISI
Lingua:
ENG
Soggetto:
CDNA MICROARRAYS; TRANSGENIC MICE; CELL-LINES; HYBRIDIZATION; DNA; CHROMOSOME-16; AMPLIFICATION; ONCOGENE; CLONING; TUMORS;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
25
Recensione:
Indirizzi per estratti:
Indirizzo: Gray, JW Univ Calif San Francisco, Ctr Canc, Canc Genet Program, Box 0808,San Francisco, CA 94143 USA Univ Calif San Francisco Box 0808 San Francisco CA USA 94143 USA
Citazione:
G. Hodgson et al., "Genome scanning with array CGH delineates regional alterations in mouse islet carcinomas", NAT GENET, 29(4), 2001, pp. 459-464

Abstract

Carcinomas that develop in the pancreatic islets of transgenic mice expressing the SV40 T-antigens (Tag) under transcriptional control of the rat insulin II promoter (RIP) progress through well-characterized stages that are similar to aspects of human tumor progression, including hyperplastic growth, increased angiogenesis and reduced apoptosis'. The latter two stages have been associated with recurrent loss of heterozygosity (LOH)(2) and reduced genome copy number(3) on chromosomes 9 (LOH9) and 16 (LOH16), aberrationswhich we believe contribute to these phenotypes. Earlier analyses localized LOH9 to approximately 3 Mb and LOH16 to approximately 30 Mb (both syntenic with human 3q21-q25) but were limited by low throughput and a lack of informative polymorphic markers. Here we show that comparative genomic hybridization to DNA microarrays (array CGH)(4-7) overcomes these limitations by allowing efficient, genome-wide analyses of relative genome copy number. TheCGH arrays used in these experiments carried BACs distributed at 2-20-MB intervals across the mouse genome and at higher density in regions of interest. Using array CGH, we further narrowed the loci for LOH9 and LOH16 and defined new or previously unappreciated recurrent regions of copy-number decrease on chromosomes 6, 8 and 14 (syntenic with human chromosomes 12p11-p13,16q24.3 and 13q11-q32, respectively) and regions of copy-number increase on chromosomes 2 and 4 (syntenic to human chromosomes 20q13.2 and 1p32-p36, respectively). Our analyses of human genome sequences syntenic to these regions suggest that CYP24, PFDN4, STMN1, CDKN1B, PPP2R3 and FSTL1 are candidate oncogenes or tumor-suppressor genes. We also show that irradiation and genetic background influence the spectrum of aberrations present in these tumors.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 25/01/20 alle ore 19:36:28