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  • 1
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    MHC class II transactivator CIITA is a recurrent gene fusion partner in lymphoid cancers (2011)
    Nature Publishing Group (NPG)
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    Publication Date: 2011-03-04
    Description: Chromosomal translocations are critically involved in the molecular pathogenesis of B-cell lymphomas, and highly recurrent and specific rearrangements have defined distinct molecular subtypes linked to unique clinicopathological features. In contrast, several well-characterized lymphoma entities still lack disease-defining translocation events. To identify novel fusion transcripts resulting from translocations, we investigated two Hodgkin lymphoma cell lines by whole-transcriptome paired-end sequencing (RNA-seq). Here we show a highly expressed gene fusion involving the major histocompatibility complex (MHC) class II transactivator CIITA (MHC2TA) in KM-H2 cells. In a subsequent evaluation of 263 B-cell lymphomas, we also demonstrate that genomic CIITA breaks are highly recurrent in primary mediastinal B-cell lymphoma (38%) and classical Hodgkin lymphoma (cHL) (15%). Furthermore, we find that CIITA is a promiscuous partner of various in-frame gene fusions, and we report that CIITA gene alterations impact survival in primary mediastinal B-cell lymphoma (PMBCL). As functional consequences of CIITA gene fusions, we identify downregulation of surface HLA class II expression and overexpression of ligands of the receptor molecule programmed cell death 1 (CD274/PDL1 and CD273/PDL2). These receptor-ligand interactions have been shown to impact anti-tumour immune responses in several cancers, whereas decreased MHC class II expression has been linked to reduced tumour cell immunogenicity. Thus, our findings suggest that recurrent rearrangements of CIITA may represent a novel genetic mechanism underlying tumour-microenvironment interactions across a spectrum of lymphoid cancers.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3902849/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3902849/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Steidl, Christian -- Shah, Sohrab P -- Woolcock, Bruce W -- Rui, Lixin -- Kawahara, Masahiro -- Farinha, Pedro -- Johnson, Nathalie A -- Zhao, Yongjun -- Telenius, Adele -- Neriah, Susana Ben -- McPherson, Andrew -- Meissner, Barbara -- Okoye, Ujunwa C -- Diepstra, Arjan -- van den Berg, Anke -- Sun, Mark -- Leung, Gillian -- Jones, Steven J -- Connors, Joseph M -- Huntsman, David G -- Savage, Kerry J -- Rimsza, Lisa M -- Horsman, Douglas E -- Staudt, Louis M -- Steidl, Ulrich -- Marra, Marco A -- Gascoyne, Randy D -- 178536/Canadian Institutes of Health Research/Canada -- R00 CA131503/CA/NCI NIH HHS/ -- R00CA131503/CA/NCI NIH HHS/ -- T32 GM007288/GM/NIGMS NIH HHS/ -- England -- Nature. 2011 Mar 17;471(7338):377-81. doi: 10.1038/nature09754. Epub 2011 Mar 2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology and Laboratory Medicine, Centre for Lymphoid Cancers and the Centre for Translational and Applied Genomics, Vancouver, British Columbia, V5Z4E6, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21368758" target="_blank"〉PubMed〈/a〉
    Keywords: Antigens, CD/genetics/metabolism ; Antigens, CD274 ; Antigens, CD80/genetics/metabolism ; Base Sequence ; Cell Line, Tumor ; Chromosome Breakpoints ; Gene Expression Profiling ; Gene Expression Regulation, Neoplastic ; Hodgkin Disease/genetics ; Humans ; In Situ Hybridization, Fluorescence ; Jurkat Cells ; Lymphocyte Activation ; Lymphoma, B-Cell/*genetics ; Molecular Sequence Data ; Nuclear Proteins/*genetics ; Oncogene Proteins, Fusion/*genetics ; Programmed Cell Death 1 Ligand 2 Protein ; RNA, Neoplasm/genetics ; T-Lymphocytes/immunology/metabolism/pathology ; Tissue Array Analysis ; Trans-Activators/*genetics ; Translocation, Genetic/*genetics ; Tumor Microenvironment
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 2
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    Correlation of DNA Copy Number, Gene Expression, Protein Expression and Clinical Outcome in a Group of Patients with Diffuse Large B Cell Lymphoma (DLBCL) Treated with CHOP Plus Rituximab (CHOP-R). (2006)
    American Society of Hematology
    Details
    Publication Date: 2006-11-01
    Description: Background: DLBCL is the most common subtype of Non-Hodgkin lymphoma and has a mortality rate of 40%. It is characterized by marked clinical and biological heterogeneity. Tumors with similar histology have different genetic abnormalities. The influence of many of these genetic changes on clinical outcome is unknown. Furthermore, treatment itself can influence the prognostic significance of certain biomarkers. Exploring the impact of genetic aberrations on gene expression, protein expression and clinical outcome is the focus of this investigation. Understanding the biology of DLBCL from patients treated with CHOP-R may lead to the discovery of novel biomarkers that are relevant in the CHOP-R era. Methods: RNA and DNA were extracted from frozen de novo DLBCL biopsies taken at the time of diagnosis from April 2001 to April 2005. Cases were selected based on their clinical outcome (11 patients with a 〉2 year remission with CHOP-R and 10 patients who progressed or relapsed after CHOP-R). We studied DNA amplifications and deletions using array comparative genomic hybridization (aCGH) comprising of 〉26,000 overlapping bacterial artificial chromosomes. This provides a 〉95% coverage of the human genome and the capability to reproducibly detect amplifications and deletions as small as 120 kb. We performed gene expression profiling (GEP) using the Affymetrix Human Genome U133 Plus 2 array. A tissue microarray was constructed to assess protein expression using paraffin active antibodies. BCL2, BCL6, P53 and MUM1 genes were assessed using all three platforms and results were correlated with clinical outcome. Results: DNA gains and losses were identified in all patients with an average of 19 alterations per tumor with amplifications being more frequent than deletions. GEP revealed a predominance (57%) of Activated B Cell (ABC) type. A supervised analysis identified a list of 471 genes that were differentially expressed (p
    Print ISSN: 0006-4971
    Electronic ISSN: 1528-0020
    Topics: Biology , Medicine
    Published by American Society of Hematology
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  • 3
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    Impact of whole genome amplification on analysis of copy number variants (2008)
    Oxford University Press
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    Publication Date: 2008-06-17
    Print ISSN: 0305-1048
    Electronic ISSN: 1362-4962
    Topics: Biology
    Published by Oxford University Press
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