Catalogo Articoli (Spogli Riviste)

OPAC HELP

Titolo:
TSLC1 is a tumor-suppressor gene in human non-small-cell lung cancer
Autore:
Kuramochi, M; Fukuhara, H; Nobukuni, T; Kanbe, T; Maruyama, T; Ghosh, HP; Pletcher, M; Isomura, M; Onizuka, M; Kitamura, T; Sekiya, T; Reeves, RH; Murakami, Y;
Indirizzi:
Natl Canc Ctr, Res Inst, Tumor Suppress & Funct Genom Project, Tokyo 104, Japan Natl Canc Ctr Tokyo Japan 104 ss & Funct Genom Project, Tokyo 104, Japan Johns Hopkins Univ, Sch Med, Dept Physiol, Baltimore, MD 21205 USA Johns Hopkins Univ Baltimore MD USA 21205 hysiol, Baltimore, MD 21205 USA Univ Tokyo, Inst Med Sci, Ctr Human Genome, Tokyo, Japan Univ Tokyo Tokyo Japan yo, Inst Med Sci, Ctr Human Genome, Tokyo, Japan Univ Tsukuba, Inst Clin Med, Dept Surg, Ibaraki, Osaka, Japan Univ Tsukuba Ibaraki Osaka Japan n Med, Dept Surg, Ibaraki, Osaka, Japan Univ Tokyo, Fac Med, Dept Urol, Tokyo 113, Japan Univ Tokyo Tokyo Japan 113 v Tokyo, Fac Med, Dept Urol, Tokyo 113, Japan
Titolo Testata:
NATURE GENETICS
fascicolo: 4, volume: 27, anno: 2001,
pagine: 427 - 430
SICI:
1061-4036(200104)27:4<427:TIATGI>2.0.ZU;2-N
Fonte:
ISI
Lingua:
ENG
Soggetto:
NUDE-MICE; LINES; METHYLATION; HMLH1; HETEROZYGOSITY; ADENOCARCINOMA; TUMORIGENICITY; LOCALIZATION; CISPLATIN; FRAGMENTS;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
29
Recensione:
Indirizzi per estratti:
Indirizzo: Murakami, Y Natl Canc Ctr, Res Inst, Tumor Suppress & Funct Genom Project,Tokyo 104, Japan Natl Canc Ctr Tokyo Japan 104 enom Project, Tokyo 104, Japan
Citazione:
M. Kuramochi et al., "TSLC1 is a tumor-suppressor gene in human non-small-cell lung cancer", NAT GENET, 27(4), 2001, pp. 427-430

Abstract

The existence of tumor-suppressor genes was originally demonstrated by functional complementation through whole-cell and microcell fusion(1,2). Transfer of chromosome 11 into a human non-small-cell lung cancer (NSCLC) cell line, A549, suppresses tumorigenicity(3). Loss of heterozygosity (LOH) on the long arm of chromosome 11 has been reported in NSCLC and other cancers(4-6). Several independent studies indicate that multiple tumor-suppressor genes are found in this region, including the gene PPP2R1B at 11q23-24 (ref. 7). Linkage studies of NSCLC are precluded because no hereditary forms are known(8,9). We previously identified a region of 700 kb on 11q23.2 that completely suppresses tumorigenicity of A549 human NSCLC cells(10). Most of this tumor-suppressor activity localizes to a 100-kb segment by functional complementation. Here we report that this region contains a single confirmed gene, TSLC1, whose expression is reduced or absent in A549 and several otherNSCLC, hepatocellular carcinoma (HCC) and pancreatic cancer (PaC) cell lines. TSLC1 expression or suppression is correlated with promoter methylationstate in these cell lines. Restoration of TSLC1 expression to normal or higher levels suppresses tumor formation by A549 cells in nude mice. Only 2 inactivating mutations of TSLC1 were discovered in 161 tumors and tumor celllines, both among the 20 primary tumors with LOH for 11q23.2. Promoter methylation was observed in 15 of the other 18 primary NSCLC, HCC and Pac tumors with LOH for 11q23.2. Thus, attenuation of TSLC1 expression occurred in 85% of primary tumors with LOH. Hypermethylation of the TSLC1 promoter would seem to represent the 'second hit' in NSCLC with LOH.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 06/04/20 alle ore 07:51:45