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EBNA3B-deficient EBV promotes B cell lymphomagenesis in humanized mice and is found in human tumors

Overview of attention for article published in Journal of Clinical Investigation, March 2012
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About this Attention Score

  • In the top 25% of all research outputs scored by Altmetric
  • High Attention Score compared to outputs of the same age (89th percentile)
  • Good Attention Score compared to outputs of the same age and source (78th percentile)

Mentioned by

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1 news outlet
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5 X users

Citations

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138 Dimensions

Readers on

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104 Mendeley
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Title
EBNA3B-deficient EBV promotes B cell lymphomagenesis in humanized mice and is found in human tumors
Published in
Journal of Clinical Investigation, March 2012
DOI 10.1172/jci58092
Pubmed ID
Authors

Robert E. White, Patrick C. Rämer, Kikkeri N. Naresh, Sonja Meixlsperger, Laurie Pinaud, Cliona Rooney, Barbara Savoldo, Rita Coutinho, Csaba Bödör, John Gribben, Hazem A. Ibrahim, Mark Bower, Jamie P. Nourse, Maher K. Gandhi, Jaap Middeldorp, Fathima Z. Cader, Paul Murray, Christian Münz, Martin J. Allday

Abstract

Epstein-Barr virus (EBV) persistently infects more than 90% of the human population and is etiologically linked to several B cell malignancies, including Burkitt lymphoma (BL), Hodgkin lymphoma (HL), and diffuse large B cell lymphoma (DLBCL). Despite its growth transforming properties, most immune-competent individuals control EBV infection throughout their lives. EBV encodes various oncogenes, and of the 6 latency-associated EBV-encoded nuclear antigens, only EBNA3B is completely dispensable for B cell transformation in vitro. Here, we report that infection with EBV lacking EBNA3B leads to aggressive, immune-evading monomorphic DLBCL-like tumors in NOD/SCID/γc-/- mice with reconstituted human immune system components. Infection with EBNA3B-knockout EBV (EBNA3BKO) induced expansion of EBV-specific T cells that failed to infiltrate the tumors. EBNA3BKO-infected B cells expanded more rapidly and secreted less T cell-chemoattractant CXCL10, reducing T cell recruitment in vitro and T cell-mediated killing in vivo. B cell lines from 2 EBV-positive human lymphomas encoding truncated EBNA3B exhibited gene expression profiles and phenotypic characteristics similar to those of tumor-derived lines from the humanized mice, including reduced CXCL10 secretion. Screening EBV-positive DLBCL, HL, and BL human samples identified additional EBNA3B mutations. Thus, EBNA3B is a virus-encoded tumor suppressor whose inactivation promotes immune evasion and virus-driven lymphomagenesis.

X Demographics

X Demographics

The data shown below were collected from the profiles of 5 X users who shared this research output. Click here to find out more about how the information was compiled.
Mendeley readers

Mendeley readers

The data shown below were compiled from readership statistics for 104 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Germany 1 <1%
Unknown 103 99%

Demographic breakdown

Readers by professional status Count As %
Student > Ph. D. Student 24 23%
Student > Bachelor 13 13%
Student > Master 12 12%
Researcher 9 9%
Student > Doctoral Student 4 4%
Other 14 13%
Unknown 28 27%
Readers by discipline Count As %
Medicine and Dentistry 21 20%
Agricultural and Biological Sciences 20 19%
Biochemistry, Genetics and Molecular Biology 19 18%
Immunology and Microbiology 10 10%
Business, Management and Accounting 2 2%
Other 2 2%
Unknown 30 29%
Attention Score in Context

Attention Score in Context

This research output has an Altmetric Attention Score of 12. This is our high-level measure of the quality and quantity of online attention that it has received. This Attention Score, as well as the ranking and number of research outputs shown below, was calculated when the research output was last mentioned on 20 March 2012.
All research outputs
#2,993,525
of 25,436,226 outputs
Outputs from Journal of Clinical Investigation
#3,915
of 17,202 outputs
Outputs of similar age
#17,854
of 168,967 outputs
Outputs of similar age from Journal of Clinical Investigation
#25
of 112 outputs
Altmetric has tracked 25,436,226 research outputs across all sources so far. Compared to these this one has done well and is in the 88th percentile: it's in the top 25% of all research outputs ever tracked by Altmetric.
So far Altmetric has tracked 17,202 research outputs from this source. They typically receive a lot more attention than average, with a mean Attention Score of 16.7. This one has done well, scoring higher than 77% of its peers.
Older research outputs will score higher simply because they've had more time to accumulate mentions. To account for age we can compare this Altmetric Attention Score to the 168,967 tracked outputs that were published within six weeks on either side of this one in any source. This one has done well, scoring higher than 89% of its contemporaries.
We're also able to compare this research output to 112 others from the same source and published within six weeks on either side of this one. This one has done well, scoring higher than 78% of its contemporaries.