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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

Journal Article · · Leukemia
DOI:https://doi.org/10.1038/leu.2015.22· OSTI ID:1248630
 [1];  [2];  [3];  [4];  [1];  [5];  [1];  [6];  [6];  [1]
  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)

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

Research Organization:
Los Alamos National Laboratory (LANL), Los Alamos, NM (United States)
Sponsoring Organization:
USDOE
Grant/Contract Number:
AC52-06NA25396
OSTI ID:
1248630
Report Number(s):
LA-UR-15-20054; leu201522
Journal Information:
Leukemia, Vol. 29, Issue 7; ISSN 0887-6924
Publisher:
Nature Publishing Group (NPG)Copyright Statement
Country of Publication:
United States
Language:
English
Citation Metrics:
Cited by: 16 works
Citation information provided by
Web of Science

References (14)

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Distinct Subsets of Primary Effusion Lymphoma Can Be Identified Based on Their Cellular Gene Expression Profile and Viral Association journal December 2004
Gene expression profile analysis of AIDS-related primary effusion lymphoma (PEL) suggests a plasmablastic derivation and identifies PEL-specific transcripts journal January 2003
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Functional Genomic Relationships in HIV‐1 Disease Revealed by Gene‐Expression Profiling of Primary Human Peripheral Blood Mononuclear Cells
  • Ockenhouse, Christian F.; Bernstein, Wendy B.; Wang, Zhining
  • The Journal of Infectious Diseases, Vol. 191, Issue 12 https://doi.org/10.1086/430321
journal June 2005
Microarray Analysis of Lymphatic Tissue Reveals Stage-Specific, Gene Expression Signatures in HIV-1 Infection journal July 2009
Signatures of mutational processes in human cancer. text January 2013

Cited By (11)

Clock-like mutational processes in human somatic cells journal November 2015
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
Genetic heterogeneity and mutational signature in Chinese Epstein-Barr virus-positive diffuse large B-cell lymphoma journal August 2018
Mutational signatures associated with tobacco smoking in human cancer posted_content May 2016
The effects of mutational processes and selection on driver mutations across cancer types posted_content June 2017
Author Correction: The effects of mutational processes and selection on driver mutations across cancer types journal April 2020
The ubiquitous ‘cancer mutational signature’ 5 occurs specifically in cancers with deleted FHIT alleles journal November 2017