EBV-Positive and EBV-Negative Posttransplant Diffuse Large B Cell Lymphomas Have Distinct Genomic and Transcriptomic Features
The molecular pathogenesis of posttransplant diffuse large B cell lymphoma (PT-DLBCL) is largely unknown. We have recently shown that Epstein-Barr virus–positive (EBV+) and –negative (EBV−) PT-DLBCL have distinct gene expression profiles, and the transcriptomic profile of EBV− PT-DLBCL is similar to...
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| Veröffentlicht in: | American journal of transplantation 2016-02, Vol.16 (2), p.414-425 |
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| creator | Finalet Ferreiro, J. Morscio, J. Dierickx, D. Vandenberghe, P. Gheysens, O. Verhoef, G. Zamani, M. Tousseyn, T. Wlodarska, I. |
| description | The molecular pathogenesis of posttransplant diffuse large B cell lymphoma (PT-DLBCL) is largely unknown. We have recently shown that Epstein-Barr virus–positive (EBV+) and –negative (EBV−) PT-DLBCL have distinct gene expression profiles, and the transcriptomic profile of EBV− PT-DLBCL is similar to that of DLBCL in immunocompetent individuals (IC-DLBCL). To validate these observations at the genomic level, we performed array–comparative genome hybridization (aCGH) analysis of 21 EBV+ PT-DLBCL, 6 EBV− PT-DLBCL, and 11 control IC-DLBCL, and subsequently combined genomic and transcriptomic data. The analysis showed that EBV+ and EBV− PT-DLBCL have distinct aCGH profiles and shared only one recurrent imbalance. EBV− PT-DLBCL, however, displayed at least 10 aberrations recurrent in IC-DLBCL, among which characteristic gain of 3/3q and 18q, and loss of 6q23/TNFAIP3 as well as 9p21/CDKN2A. The most prevalent aberration in EBV+ PT-DLBCL was gain/amplification of 9p24.1 targeting PDCD1LG2/PDL2. Our data indicate that the FOXP1 oncogene and the tumor suppressor CDKNA2 implicated in EBV− DLBCL, do not play a critical role in the pathogenesis of EBV+ PT-DLBCL. Altogether, genomic profiling of PT-/IC-DLBCL confirms that EBV− and EBV+ PT-DLBCL are distinct entities, while EBV− PT-DLBCL has features in common with IC-DLBCL. These findings support the hypothesis that EBV− PT-DLBCL are de novo lymphomas in transplant recipients. |
| doi_str_mv | 10.1111/ajt.13558 |
| format | Article |
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We have recently shown that Epstein-Barr virus–positive (EBV+) and –negative (EBV−) PT-DLBCL have distinct gene expression profiles, and the transcriptomic profile of EBV− PT-DLBCL is similar to that of DLBCL in immunocompetent individuals (IC-DLBCL). To validate these observations at the genomic level, we performed array–comparative genome hybridization (aCGH) analysis of 21 EBV+ PT-DLBCL, 6 EBV− PT-DLBCL, and 11 control IC-DLBCL, and subsequently combined genomic and transcriptomic data. The analysis showed that EBV+ and EBV− PT-DLBCL have distinct aCGH profiles and shared only one recurrent imbalance. EBV− PT-DLBCL, however, displayed at least 10 aberrations recurrent in IC-DLBCL, among which characteristic gain of 3/3q and 18q, and loss of 6q23/TNFAIP3 as well as 9p21/CDKN2A. The most prevalent aberration in EBV+ PT-DLBCL was gain/amplification of 9p24.1 targeting PDCD1LG2/PDL2. Our data indicate that the FOXP1 oncogene and the tumor suppressor CDKNA2 implicated in EBV− DLBCL, do not play a critical role in the pathogenesis of EBV+ PT-DLBCL. Altogether, genomic profiling of PT-/IC-DLBCL confirms that EBV− and EBV+ PT-DLBCL are distinct entities, while EBV− PT-DLBCL has features in common with IC-DLBCL. These findings support the hypothesis that EBV− PT-DLBCL are de novo lymphomas in transplant recipients.</description><identifier>ISSN: 1600-6135</identifier><identifier>EISSN: 1600-6143</identifier><identifier>DOI: 10.1111/ajt.13558</identifier><identifier>PMID: 26780579</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Adolescent ; Adult ; Aged ; Aged, 80 and over ; B-cell lymphoma ; Biomarkers, Tumor - genetics ; Case-Control Studies ; Child ; Child, Preschool ; Comparative Genomic Hybridization ; Epstein-Barr virus ; Epstein-Barr Virus Infections - complications ; Epstein-Barr Virus Infections - genetics ; Epstein-Barr Virus Infections - virology ; Female ; Follow-Up Studies ; Foxp1 protein ; Gene expression ; Gene Expression Profiling ; Genomics ; Genomics - methods ; Graft Rejection ; Graft Survival ; Herpesvirus 4, Human ; Humans ; Hybridization ; Immunoenzyme Techniques ; In Situ Hybridization ; Lymphoma ; Lymphoma, Large B-Cell, Diffuse - genetics ; Lymphoma, Large B-Cell, Diffuse - surgery ; Lymphoma, Large B-Cell, Diffuse - virology ; Male ; Middle Aged ; Pathogenesis ; Postoperative Complications - genetics ; Prognosis ; Real-Time Polymerase Chain Reaction ; Reverse Transcriptase Polymerase Chain Reaction ; RNA, Messenger - genetics ; Transcriptomics ; Transplants & implants ; Tumor suppressor genes ; Young Adult</subject><ispartof>American journal of transplantation, 2016-02, Vol.16 (2), p.414-425</ispartof><rights>2016 American Society of Transplantation & American Society of Transplant Surgeons. Published by Elsevier Inc. All rights reserved.</rights><rights>Copyright 2015 The American Society of Transplantation and the American Society of Transplant Surgeons</rights><rights>Copyright 2015 The American Society of Transplantation and the American Society of Transplant Surgeons.</rights><rights>2016 the American Society of Transplantation and the American Society of Transplant Surgeons</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5268-5dd3b94995ca7c5e761327b15b2513af59e1302399a16c733a8a6319bab3bbbb3</citedby><cites>FETCH-LOGICAL-c5268-5dd3b94995ca7c5e761327b15b2513af59e1302399a16c733a8a6319bab3bbbb3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1111%2Fajt.13558$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1111%2Fajt.13558$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,777,781,1412,27905,27906,45555,45556</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/26780579$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Finalet Ferreiro, J.</creatorcontrib><creatorcontrib>Morscio, J.</creatorcontrib><creatorcontrib>Dierickx, D.</creatorcontrib><creatorcontrib>Vandenberghe, P.</creatorcontrib><creatorcontrib>Gheysens, O.</creatorcontrib><creatorcontrib>Verhoef, G.</creatorcontrib><creatorcontrib>Zamani, M.</creatorcontrib><creatorcontrib>Tousseyn, T.</creatorcontrib><creatorcontrib>Wlodarska, I.</creatorcontrib><title>EBV-Positive and EBV-Negative Posttransplant Diffuse Large B Cell Lymphomas Have Distinct Genomic and Transcriptomic Features</title><title>American journal of transplantation</title><addtitle>Am J Transplant</addtitle><description>The molecular pathogenesis of posttransplant diffuse large B cell lymphoma (PT-DLBCL) is largely unknown. We have recently shown that Epstein-Barr virus–positive (EBV+) and –negative (EBV−) PT-DLBCL have distinct gene expression profiles, and the transcriptomic profile of EBV− PT-DLBCL is similar to that of DLBCL in immunocompetent individuals (IC-DLBCL). To validate these observations at the genomic level, we performed array–comparative genome hybridization (aCGH) analysis of 21 EBV+ PT-DLBCL, 6 EBV− PT-DLBCL, and 11 control IC-DLBCL, and subsequently combined genomic and transcriptomic data. The analysis showed that EBV+ and EBV− PT-DLBCL have distinct aCGH profiles and shared only one recurrent imbalance. EBV− PT-DLBCL, however, displayed at least 10 aberrations recurrent in IC-DLBCL, among which characteristic gain of 3/3q and 18q, and loss of 6q23/TNFAIP3 as well as 9p21/CDKN2A. The most prevalent aberration in EBV+ PT-DLBCL was gain/amplification of 9p24.1 targeting PDCD1LG2/PDL2. Our data indicate that the FOXP1 oncogene and the tumor suppressor CDKNA2 implicated in EBV− DLBCL, do not play a critical role in the pathogenesis of EBV+ PT-DLBCL. Altogether, genomic profiling of PT-/IC-DLBCL confirms that EBV− and EBV+ PT-DLBCL are distinct entities, while EBV− PT-DLBCL has features in common with IC-DLBCL. These findings support the hypothesis that EBV− PT-DLBCL are de novo lymphomas in transplant recipients.</description><subject>Adolescent</subject><subject>Adult</subject><subject>Aged</subject><subject>Aged, 80 and over</subject><subject>B-cell lymphoma</subject><subject>Biomarkers, Tumor - genetics</subject><subject>Case-Control Studies</subject><subject>Child</subject><subject>Child, Preschool</subject><subject>Comparative Genomic Hybridization</subject><subject>Epstein-Barr virus</subject><subject>Epstein-Barr Virus Infections - complications</subject><subject>Epstein-Barr Virus Infections - genetics</subject><subject>Epstein-Barr Virus Infections - virology</subject><subject>Female</subject><subject>Follow-Up Studies</subject><subject>Foxp1 protein</subject><subject>Gene expression</subject><subject>Gene Expression Profiling</subject><subject>Genomics</subject><subject>Genomics - methods</subject><subject>Graft Rejection</subject><subject>Graft Survival</subject><subject>Herpesvirus 4, Human</subject><subject>Humans</subject><subject>Hybridization</subject><subject>Immunoenzyme Techniques</subject><subject>In Situ Hybridization</subject><subject>Lymphoma</subject><subject>Lymphoma, Large B-Cell, Diffuse - genetics</subject><subject>Lymphoma, Large B-Cell, Diffuse - surgery</subject><subject>Lymphoma, Large B-Cell, Diffuse - virology</subject><subject>Male</subject><subject>Middle Aged</subject><subject>Pathogenesis</subject><subject>Postoperative Complications - genetics</subject><subject>Prognosis</subject><subject>Real-Time Polymerase Chain Reaction</subject><subject>Reverse Transcriptase Polymerase Chain Reaction</subject><subject>RNA, Messenger - genetics</subject><subject>Transcriptomics</subject><subject>Transplants & implants</subject><subject>Tumor suppressor genes</subject><subject>Young Adult</subject><issn>1600-6135</issn><issn>1600-6143</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kUtv3CAURlHVqnl10T9QIXXTLpyAMQaWyeTVatRmMckWYXydMvKrgFPNIv-9eCbJomrLBnQ59-jCh9B7So5pWidmHY8p41y-Qvu0JCQracFev5wZ30MHIawJoSKX-Vu0l5dCEi7UPnq8OLvLbobgonsAbPoaz4VvcG-2hXQTozd9GFvTR3zummYKgJfG3wM-wwtoW7zcdOOPoTMBX5vUcu5CdL2N-Ar6oXN2K13NDuvdGLelSzBx8hCO0JvGtAHePe2H6PbyYrW4zpbfr74sTpeZ5XkpM17XrFKFUtwaYTmI9KZcVJRXOafMNFwBZSRnShlaWsGYkaZkVFWmYlVa7BB92nlHP_ycIETduWDT8KaHYQqaJmMhGBFFQj_-ga6HyfdpOp1LKagsuCT_o2YXLQVXs-vzjrJ-CMFDo0fvOuM3mhI9J6dTcnqbXGI_PBmnqoP6hXyOKgEnO-CXa2Hzb5M-_bp6VrJdB6SvfXDgdbAOegu182Cjrgf3l0F-A80ssmI</recordid><startdate>201602</startdate><enddate>201602</enddate><creator>Finalet Ferreiro, J.</creator><creator>Morscio, J.</creator><creator>Dierickx, D.</creator><creator>Vandenberghe, P.</creator><creator>Gheysens, O.</creator><creator>Verhoef, G.</creator><creator>Zamani, M.</creator><creator>Tousseyn, T.</creator><creator>Wlodarska, I.</creator><general>Elsevier Inc</general><general>Elsevier Limited</general><scope>6I.</scope><scope>AAFTH</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7QP</scope><scope>7T5</scope><scope>7U9</scope><scope>H94</scope><scope>K9.</scope><scope>7X8</scope></search><sort><creationdate>201602</creationdate><title>EBV-Positive and EBV-Negative Posttransplant Diffuse Large B Cell Lymphomas Have Distinct Genomic and Transcriptomic Features</title><author>Finalet Ferreiro, J. ; 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We have recently shown that Epstein-Barr virus–positive (EBV+) and –negative (EBV−) PT-DLBCL have distinct gene expression profiles, and the transcriptomic profile of EBV− PT-DLBCL is similar to that of DLBCL in immunocompetent individuals (IC-DLBCL). To validate these observations at the genomic level, we performed array–comparative genome hybridization (aCGH) analysis of 21 EBV+ PT-DLBCL, 6 EBV− PT-DLBCL, and 11 control IC-DLBCL, and subsequently combined genomic and transcriptomic data. The analysis showed that EBV+ and EBV− PT-DLBCL have distinct aCGH profiles and shared only one recurrent imbalance. EBV− PT-DLBCL, however, displayed at least 10 aberrations recurrent in IC-DLBCL, among which characteristic gain of 3/3q and 18q, and loss of 6q23/TNFAIP3 as well as 9p21/CDKN2A. The most prevalent aberration in EBV+ PT-DLBCL was gain/amplification of 9p24.1 targeting PDCD1LG2/PDL2. Our data indicate that the FOXP1 oncogene and the tumor suppressor CDKNA2 implicated in EBV− DLBCL, do not play a critical role in the pathogenesis of EBV+ PT-DLBCL. Altogether, genomic profiling of PT-/IC-DLBCL confirms that EBV− and EBV+ PT-DLBCL are distinct entities, while EBV− PT-DLBCL has features in common with IC-DLBCL. These findings support the hypothesis that EBV− PT-DLBCL are de novo lymphomas in transplant recipients.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>26780579</pmid><doi>10.1111/ajt.13558</doi><tpages>12</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Adolescent Adult Aged Aged, 80 and over B-cell lymphoma Biomarkers, Tumor - genetics Case-Control Studies Child Child, Preschool Comparative Genomic Hybridization Epstein-Barr virus Epstein-Barr Virus Infections - complications Epstein-Barr Virus Infections - genetics Epstein-Barr Virus Infections - virology Female Follow-Up Studies Foxp1 protein Gene expression Gene Expression Profiling Genomics Genomics - methods Graft Rejection Graft Survival Herpesvirus 4, Human Humans Hybridization Immunoenzyme Techniques In Situ Hybridization Lymphoma Lymphoma, Large B-Cell, Diffuse - genetics Lymphoma, Large B-Cell, Diffuse - surgery Lymphoma, Large B-Cell, Diffuse - virology Male Middle Aged Pathogenesis Postoperative Complications - genetics Prognosis Real-Time Polymerase Chain Reaction Reverse Transcriptase Polymerase Chain Reaction RNA, Messenger - genetics Transcriptomics Transplants & implants Tumor suppressor genes Young Adult |
| title | EBV-Positive and EBV-Negative Posttransplant Diffuse Large B Cell Lymphomas Have Distinct Genomic and Transcriptomic Features |
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