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Title: Analysis of mutational signatures in exomes from B-cell lymphoma cell lines suggest APOBEC3 family members to be involved in the pathogenesis of primary effusion lymphoma

Abstract

Here, primary effusion lymphoma (PEL) is a rare large B-cell neoplasm particularly affecting immunodeficient hosts with an increased incidence in young or middle-aged males infected with the HIV.1 The clinical outcome of patients with PEL is unfavorable with a median survival of <6 months.1 PEL has been closely associated with human herpes virus 8 (HHV8, previously called Kaposi sarcoma herpesvirus) infection.1 In some cases a coinfection of HHV8 with the Epstein–Barr Virus (EBV) has been described.1 HHV8 encodes various genes homologous to cellular genes that have proliferative and anti-apoptotic functions.2 Although HHV8 is supposed to be a major driver of PEL, it alone is not sufficient for a full-blown lymphomagenesis.2 PEL usually shows complex karyotypes with many chromosomal aberrations.3 This chromosomal complexity might be driven by the viral infection and lead to genetic alterations cooperating with HHV8 in PEL lymphomagenesis.4

Authors:
 [1];  [2];  [3];  [4];  [1];  [5];  [1];  [6];  [6];  [1]
+ Show Author Affiliations
  1. Univ. Hospital Schleswig-Holstein, Christian-Albrechts-Univ., Kiel (Germany)
  2. Los Alamos National Lab. (LANL), Los Alamos, NM (United States)
  3. Univ. Hospital of Cologne, Cologne (Germany)
  4. Deutsches Krebsforschungszentrum Heidelberg (DKFZ), Heidelberg (Germany)
  5. Leibniz-Institute DSMZ, Braunschweig (Germany)
  6. Wellcome Trust Cancer Sanger Institute, Hinxton (United Kingdom)
Publication Date:
Research Org.:
Los Alamos National Laboratory (LANL), Los Alamos, NM (United States)
Sponsoring Org.:
USDOE
OSTI Identifier:
1248630
Report Number(s):
LA-UR-15-20054
Journal ID: ISSN 0887-6924; leu201522
Grant/Contract Number:  
AC52-06NA25396
Resource Type:
Accepted Manuscript
Journal Name:
Leukemia
Additional Journal Information:
Journal Volume: 29; Journal Issue: 7; Journal ID: ISSN 0887-6924
Publisher:
Nature Publishing Group (NPG)
Country of Publication:
United States
Language:
English
Subject:
59 BASIC BIOLOGICAL SCIENCES

Citation Formats

Wagener, R., Alexandrov, L. B., Montesinos-Rongen, M., Schlesner, M., Haake, A., Drexler, H. G., Richter, J., Bignell, G. R., McDermott, U., and Siebert, R. Analysis of mutational signatures in exomes from B-cell lymphoma cell lines suggest APOBEC3 family members to be involved in the pathogenesis of primary effusion lymphoma. United States: N. p., 2015. Web. doi:10.1038/leu.2015.22.
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Wagener, R., Alexandrov, L. B., Montesinos-Rongen, M., Schlesner, M., Haake, A., Drexler, H. G., Richter, J., Bignell, G. R., McDermott, U., & Siebert, R. Analysis of mutational signatures in exomes from B-cell lymphoma cell lines suggest APOBEC3 family members to be involved in the pathogenesis of primary effusion lymphoma. United States. https://doi.org/10.1038/leu.2015.22
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Wagener, R., Alexandrov, L. B., Montesinos-Rongen, M., Schlesner, M., Haake, A., Drexler, H. G., Richter, J., Bignell, G. R., McDermott, U., and Siebert, R. Wed . "Analysis of mutational signatures in exomes from B-cell lymphoma cell lines suggest APOBEC3 family members to be involved in the pathogenesis of primary effusion lymphoma". United States. https://doi.org/10.1038/leu.2015.22. https://www.osti.gov/servlets/purl/1248630.
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@article{osti_1248630,
title = {Analysis of mutational signatures in exomes from B-cell lymphoma cell lines suggest APOBEC3 family members to be involved in the pathogenesis of primary effusion lymphoma},
author = {Wagener, R. and Alexandrov, L. B. and Montesinos-Rongen, M. and Schlesner, M. and Haake, A. and Drexler, H. G. and Richter, J. and Bignell, G. R. and McDermott, U. and Siebert, R.},
abstractNote = {Here, primary effusion lymphoma (PEL) is a rare large B-cell neoplasm particularly affecting immunodeficient hosts with an increased incidence in young or middle-aged males infected with the HIV.1 The clinical outcome of patients with PEL is unfavorable with a median survival of <6 months.1 PEL has been closely associated with human herpes virus 8 (HHV8, previously called Kaposi sarcoma herpesvirus) infection.1 In some cases a coinfection of HHV8 with the Epstein–Barr Virus (EBV) has been described.1 HHV8 encodes various genes homologous to cellular genes that have proliferative and anti-apoptotic functions.2 Although HHV8 is supposed to be a major driver of PEL, it alone is not sufficient for a full-blown lymphomagenesis.2 PEL usually shows complex karyotypes with many chromosomal aberrations.3 This chromosomal complexity might be driven by the viral infection and lead to genetic alterations cooperating with HHV8 in PEL lymphomagenesis.4},
doi = {10.1038/leu.2015.22},
journal = {Leukemia},
number = 7,
volume = 29,
place = {United States},
year = {Wed Feb 04 00:00:00 EST 2015},
month = {Wed Feb 04 00:00:00 EST 2015}
}
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https://doi.org/10.1038/leu.2015.22
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    Works referencing / citing this record:

    Clock-like mutational processes in human somatic cells
    journal, November 2015

    • Alexandrov, Ludmil B.; Jones, Philip H.; Wedge, David C.
    • Nature Genetics, Vol. 47, Issue 12
    • DOI: 10.1038/ng.3441

    The effects of mutational processes and selection on driver mutations across cancer types
    journal, May 2018

    Discovering novel mutation signatures by latent Dirichlet allocation with variational Bayes inference
    journal, April 2019

    Understanding mutagenesis through delineation of mutational signatures in human cancer
    journal, May 2016

    Mutational signatures associated with tobacco smoking in human cancer
    journal, November 2016

    Biology and management of primary effusion lymphoma
    journal, November 2018

    Mutational signatures associated with tobacco smoking in human cancer
    posted_content, May 2016

    • Alexandrov, Ludmil B.; Ju, Young Seok; Haase, Kerstin
    • bioRxiv
    • DOI: 10.1101/051417

    The effects of mutational processes and selection on driver mutations across cancer types
    posted_content, June 2017

    • Temko, Daniel; Tomlinson, Ian P. M.; Severini, Simone
    • bioRxiv
    • DOI: 10.1101/149096

    Author Correction: The effects of mutational processes and selection on driver mutations across cancer types
    journal, April 2020

    Discovering novel mutation signatures by latent Dirichlet allocation with variational Bayes inference
    journal, April 2019

    The ubiquitous ‘cancer mutational signature’ 5 occurs specifically in cancers with deleted FHIT alleles
    journal, November 2017

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