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  Gene amplification as double minutes or homogeneously staining regions in solid tumors: Origin and structure

Storlazzi, C. T., Lonoce, A., Guastadisegni, M. C., Trombetta, D., D'Addabbo, P., Daniele, G., et al. (2010). Gene amplification as double minutes or homogeneously staining regions in solid tumors: Origin and structure. Genome Research, 20(9), 1198-1206. doi:10.1101/gr.106252.110.

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Genre: Journal Article
Alternative Title : Genome Res.

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 Creators:
Storlazzi, Clelia Tiziana, Author
Lonoce, Angelo, Author
Guastadisegni, Maria C., Author
Trombetta, Domenico, Author
D'Addabbo, Pietro, Author
Daniele, Giulia, Author
L'Abbate, Alberto, Author
Macchia, Gemma, Author
Surace, Cecilia, Author
Kok, Klaas, Author
Ullmann, Reinhard1, Author           
Purgato, Stefania, Author
Palumbo, Orazio, Author
Carella, Massimo, Author
Ambros, Peter F., Author
Rocchi, Mariano, Author
Affiliations:
1Molecular Cytogenetics (Reinhard Ullmann), Dept. of Human Molecular Genetics (Head: Hans-Hilger Ropers), Max Planck Institute for Molecular Genetics, Max Planck Society, ou_1479645              

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 Abstract: Double minutes (dmin) and homogeneously staining regions (hsr) are the cytogenetic hallmarks of genomic amplification in cancer. Different mechanisms have been proposed to explain their genesis. Recently, our group showed that the MYC-containing dmin in leukemia cases arise by excision and amplification (episome model). In the present paper we investigated 10 cell lines from solid tumors showing MYCN amplification as dmin or hsr. Particularly revealing results were provided by the two subclones of the neuroblastoma cell line STA-NB-10, one showing dmin-only and the second hsr-only amplification. Both subclones showed a deletion, at 2p24.3, whose extension matched the amplicon extension. Additionally, the amplicon structure of the dmin and hsr forms was identical. This strongly argues that the episome model, already demonstrated in leukemias, applies to solid tumors as well, and that dmin and hsr are two faces of the same coin. The organization of the duplicated segments varied from very simple (no apparent changes from the normal sequence) to very complex. MYCN was always overexpressed (significantly overexpressed in three cases). The fusion junctions, always mediated by nonhomologous end joining, occasionally juxtaposed truncated genes in the same transcriptional orientation. Fusion transcripts involving NBAS (also known as NAG), FAM49A, BC035112 (also known as NCRNA00276), and SMC6 genes were indeed detected, although their role in the context of the tumor is not clear.

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Language(s): eng - English
 Dates: 2010-07-14
 Publication Status: Published in print
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Title: Genome Research
  Alternative Title : Genome Res.
Source Genre: Journal
 Creator(s):
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Pages: - Volume / Issue: 20 (9) Sequence Number: - Start / End Page: 1198 - 1206 Identifier: ISSN: 1088-9051