View : 17 Download: 0

Integrated Copy Number and Gene Expression Profiling Analysis of Epstein-Barr Virus-Positive Diffuse Large B-Cell Lymphoma

Title
Integrated Copy Number and Gene Expression Profiling Analysis of Epstein-Barr Virus-Positive Diffuse Large B-Cell Lymphoma
Authors
Yoon, HeejeiPark, SanghuiJu, HyunjeongHa, Sang YunSohn, InSukJo, JisukDo, In-GuMin, SookeeKim, Seok JinKim, Won SeogYoo, Hae YongKo, Young Hyeh
Ewha Authors
박상희
SCOPUS Author ID
박상희scopus
Issue Date
2015
Journal Title
GENES CHROMOSOMES & CANCER
ISSN
1045-2257JCR Link1098-2264JCR Link
Citation
vol. 54, no. 6, pp. 383 - 396
Publisher
WILEY-BLACKWELL
Indexed
SCI; SCIE; SCOPUS WOS scopus
Abstract
Viral oncogenes and host immunosenescence have been suggested as causes of Epstein-Barr virus-positive diffuse large B-cell lymphoma (EBV+DLBCL) of the elderly. To investigate the molecular genetic basis of immune evasion and tumor outgrowth, we analyzed copy number alterations (CNAs) and gene expression profiles in EBV+DLBCL samples compared with EBV-DLBCL. There were relatively few genomic alterations in EBV+DLBCL compared with those detected in EBV-negative DLBCL. The most frequent CNAs (>30%) in EBV+DLBCLs were gains at 1q23.2-23.3, 1q23.3, 1q32.1, 5p15.3, 8q22.3, 8q24.1-24.2, and 9p24.1; losses at 6q27, 7q11.2, and 7q36.2-36.3 were also recurrent. A gene expression profile analysis identified the host immune response as a key molecular signature in EBV+DLBCL. Antiviral response genes, proinflammatory cytokines, and chemokines associated with the innate immune response were overexpressed, indicating the presence of a virusinduced inflammatory microenvironment. Genes associated with the B-cell receptor signaling pathway were downregulated. An integrated analysis indicated that SLAMF1 and PDL2 were key targets of the gains detected at 1q23.2-23.3 and 9p24.1. The chromosomal gain at 9p24.1 was associated with poor overall survival. Taken together, our results led to the identification of recurrent copy number alterations and distinct gene expression associated with the host immune response in EBV+DLBCL. We suggest that the upregulation of PDL2 on 9p24.1 promotes immune evasion and is associated with poor prognosis in EBV+DLBCL. (c) 2015 Wiley Periodicals, Inc.
DOI
10.1002/gcc.22249
Appears in Collections:
의학전문대학원 > 의학과 > Journal papers
Files in This Item:
There are no files associated with this item.
Export
RIS (EndNote)
XLS (Excel)
XML


qrcode

Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.

BROWSE