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| 001 | 119777 | ||
| 005 | 20240228145440.0 | ||
| 024 | 7 | _ | |a 10.1038/ncomms14257 |2 doi |
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| 041 | _ | _ | |a eng |
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| 100 | 1 | _ | |a Shumilov, Anatoliy |0 P:(DE-He78)6848fb449349189d3fde6a1667392cec |b 0 |e First author |u dkfz |
| 245 | _ | _ | |a Epstein-Barr virus particles induce centrosome amplification and chromosomal instability.060 |
| 260 | _ | _ | |a London |c 2017 |b Nature Publishing Group |
| 336 | 7 | _ | |a article |2 DRIVER |
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| 336 | 7 | _ | |a Journal Article |b journal |m journal |0 PUB:(DE-HGF)16 |s 1511252760_9859 |2 PUB:(DE-HGF) |
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| 520 | _ | _ | |a Infections with Epstein-Barr virus (EBV) are associated with cancer development, and EBV lytic replication (the process that generates virus progeny) is a strong risk factor for some cancer types. Here we report that EBV infection of B-lymphocytes (in vitro and in a mouse model) leads to an increased rate of centrosome amplification, associated with chromosomal instability. This effect can be reproduced with virus-like particles devoid of EBV DNA, but not with defective virus-like particles that cannot infect host cells. Viral protein BNRF1 induces centrosome amplification, and BNRF1-deficient viruses largely lose this property. These findings identify a new mechanism by which EBV particles can induce chromosomal instability without establishing a chronic infection, thereby conferring a risk for development of tumours that do not necessarily carry the viral genome. |
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| 700 | 1 | _ | |a Delecluse, Henri-Jacques |0 P:(DE-He78)25d3c74b949988c637571e696fc04b25 |b 13 |e Last author |u dkfz |
| 773 | _ | _ | |a 10.1038/ncomms14257 |g Vol. 8, p. 14257 - |0 PERI:(DE-600)2553671-0 |p 14257 - |t Nature Communications |v 8 |y 2017 |x 2041-1723 |
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