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Titolo:
Analysis of chromosomal imbalances in sporadic and NFI-associated peripheral nerve sheath tumors by comparative genomic hybridization
Autore:
Mechtersheimer, G; Otano-Joos, M; Ohl, S; Benner, A; Lehnert, T; Willeke, F; Moller, P; Otto, HF; Lichter, P; Joos, S;
Indirizzi:
Deutsch Krebsforschungszentrum, Abt 110700, Abt Org Komplexer Genome, D-69120 Heidelberg, Germany Deutsch Krebsforschungszentrum Heidelberg GermanyD-69120 lberg, Germany Univ Heidelberg, Inst Pathol, D-6900 Heidelberg, Germany Univ Heidelberg Heidelberg Germany D-6900 ol, D-6900 Heidelberg, Germany Univ Heidelberg, Chirurg Klin, D-6900 Heidelberg, Germany Univ HeidelbergHeidelberg Germany D-6900 in, D-6900 Heidelberg, Germany Univ Ulm, Abt Pathol, Ulm, Germany Univ Ulm Ulm GermanyUniv Ulm, Abt Pathol, Ulm, Germany
Titolo Testata:
GENES CHROMOSOMES & CANCER
fascicolo: 4, volume: 25, anno: 1999,
pagine: 362 - 369
SICI:
1045-2257(199908)25:4<362:AOCIIS>2.0.ZU;2-9
Fonte:
ISI
Lingua:
ENG
Soggetto:
NEUROFIBROMATOSIS TYPE-1 GENE; AMPLIFIED DNA-SEQUENCES; SOFT-TISSUE SARCOMAS; CYTOGENETIC ANALYSIS; VONRECKLINGHAUSEN NEUROFIBROMATOSIS; MUTATIONS; NEUROBLASTOMA; DELETION; LOSSES; GAINS;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
43
Recensione:
Indirizzi per estratti:
Indirizzo: Joos, S Deutsch Krebsforschungszentrum, Abt 110700, Abt Org Komplexer Genome, Neuenheimer Feld 280, D-69120 Heidelberg, Germany Deutsch Krebsforschungszentrum Neuenheimer Feld 280 Heidelberg Germany D-69120
Citazione:
G. Mechtersheimer et al., "Analysis of chromosomal imbalances in sporadic and NFI-associated peripheral nerve sheath tumors by comparative genomic hybridization", GENE CHROM, 25(4), 1999, pp. 362-369

Abstract

Peripheral nerve sheath tumors arise either sporadically or in associationwith neurofibromatosis type I (von Recklinghausen's neurofibromatosis, NF1) or type 2. In this study, comprehensive screening for relative chromosomecopy number changes was performed on 10 benign and 19 malignant peripheralnerve sheath tumors (MPNSTs) by applying comparative genomic hybridization(CGH). In benign tumors, no chromosomal imbalances were found by CGH, whereas in MPNSTs chromosomal gains and losses were frequently detected. No differences regarding the frequency and distribution of chromosomal imbalanceswere observed between the 13 sporadic and 6 NF1-associated MPNSTs analyzed. In both, the number of gains was significantly higher than the number of losses, suggesting a predominant role of proto-oncogene activation during MPNST progression. Candidate regions with potentially relevant proto-oncogenes included chromosomal bands 17q24-q25, 7p11-p13, 5p15, 8q22-q24, and 12q21-q24; those with putative tumor suppressor genes were 9p21-p24, 13q14-q22,and Ip. High-level amplifications were restricted to sporadic tumors and affected eight different chromosomal subregions. In three of these MPNSTs, identical subregions on chromosomal arms 5p and 12q were coamplified. This study revealed a number of new characteristic chromosomal imbalances and provides a basis for molecular identification of oncogenes and tumor suppressor genes of pathogenetic relevance in both sporadic and NF1-associated MPNSTs. Genes Chromosomes Cancer 25:362-369, 1999. (C) 1999 Wiley-Liss, Inc.

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Documento generato il 24/09/20 alle ore 22:12:31