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Titolo:
Comparative genomic in situ hybridization discloses recurrent gain of chromosome 4 in experimental gliomas of the rat
Autore:
Kappler, R; Schlegel, J; Kindler-Rohrborn, A; Mennel, HD; Scherthan, H;
Indirizzi:
Univ Kaiserslautern, Dept Human Biol & Human Genet, D-67653 Kaiserslautern, Germany Univ Kaiserslautern Kaiserslautern Germany D-67653 iserslautern, Germany Univ Marburg, Ctr Med, Dept Neuropathol, Marburg, Germany Univ Marburg Marburg Germany tr Med, Dept Neuropathol, Marburg, Germany Univ Essen Gesamthsch, Sch Med, Inst Cell Biol Canc Res, Essen, Germany Univ Essen Gesamthsch Essen Germany Cell Biol Canc Res, Essen, Germany
Titolo Testata:
CYTOGENETICS AND CELL GENETICS
fascicolo: 3-4, volume: 84, anno: 1999,
pagine: 194 - 198
SICI:
0301-0171(1999)84:3-4<194:CGISHD>2.0.ZU;2-H
Fonte:
ISI
Lingua:
ENG
Soggetto:
COPY NUMBER CHANGES; GROWTH-FACTOR HGF; SOLID TUMORS; ALPHA GENE; MET; AMPLIFICATION; NORVEGICUS; EXPRESSION; SEQUENCE; LOSSES;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
30
Recensione:
Indirizzi per estratti:
Indirizzo: Scherthan, H Univ Kaiserslautern, Dept Human Biol & Human Genet, POB 3049,D-67653 Kaiserslautern, Germany Univ Kaiserslautern POB 3049 Kaiserslautern Germany D-67653
Citazione:
R. Kappler et al., "Comparative genomic in situ hybridization discloses recurrent gain of chromosome 4 in experimental gliomas of the rat", CYTOG C GEN, 84(3-4), 1999, pp. 194-198

Abstract

The genetic characterization of experimental tumors is essential in order to evaluate their relevance as appropriate animal models for human neoplasms. We have used flow cytometry and a recently established Comparative Genomic in situ Hybridization (CGH) protocol for the rat (Kappler et al., 1998) to investigate chromosome copy number changes in five ethylnitrosourea induced gliomas of the rat. Flow cytometry showed aneuploid DNA indices in three of the tumors investigated. CGH analysis of primary tumors revealed wholechromosome and subchromosomal gains of rat chromosomes (RNO) 1, 2, 4, 6, 7, 10, 11, 12, and 13. Loss of RNO 5q23 --> q35 was apparent in one tumor. High level copy number gains were not observed using CCH as well as semiquantitative PCR with Tgfa, Met and Hbb primers. Low copy number gain of RNO 4 represents the most common aberration, since it was detected in four of five tumors investigated. Three tumors showed gain of RNO 7, while two tumors showed gains of RNO 10q3 --> qter and RNO 12q. Deletion of RNO 5q23 --> q35and gain of RNO 4 occurred mutually exclusively. Therefore, we conclude that these two alterations may represent different pathways in the pathogenesis of experimental gliomas in the rat. Findings are discussed in analogy tohuman gliomas.

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Documento generato il 23/09/20 alle ore 07:50:21