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Among 31 RT cases classified as diffuse large B\u2010cell lymphoma (DLBCL), seven (23%) showed EBV expression. In contrast to EBV\n                    <jats:sup>\u2013<\/jats:sup>\n                    tumours, EBV\n                    <jats:sup>+<\/jats:sup>\n                    DLBCLs derived predominantly from\n                    <jats:italic>IGVH<\/jats:italic>\n                    \u2010hypermutated CLL, and they also showed CLL\u2010unrelated\n                    <jats:italic>IGVH<\/jats:italic>\n                    sequences more frequently. Intriguingly, despite having different cellular origins, clonally related and unrelated EBV\n                    <jats:sup>+<\/jats:sup>\n                    DLBCLs shared a previous history of immunosuppressive chemo\u2010immunotherapy, a non\u2010germinal centre DLBCL phenotype, EBV latency programme type II or III, and very short survival. These data suggested that EBV reactivation during therapy\u2010related immunosuppression can transform either CLL cells or non\u2010tumoural B lymphocytes into EBV\n                    <jats:sup>+<\/jats:sup>\n                    DLBCL. To investigate this hypothesis, xenogeneic transplantation of blood cells from 31 patients with CLL and monoclonal B\u2010cell lymphocytosis (MBL) was performed in Rag2\n                    <jats:sup>\u2013\/\u2013<\/jats:sup>\n                    IL2\u03b3c\n                    <jats:sup>\u2013\/\u2013<\/jats:sup>\n                    mice. Remarkably, the recipients' impaired immunosurveillance favoured the spontaneous outgrowth of EBV\n                    <jats:sup>+<\/jats:sup>\n                    B\u2010cell clones from 95% of CLL and 64% of MBL patients  samples, but not from healthy donors. Eventually, these cells generated monoclonal tumours (mostly CLL\u2010unrelated but also CLL\u2010related), recapitulating the principal features of EBV\n                    <jats:sup>+<\/jats:sup>\n                    DLBCL in patients. Accordingly, clonally related and unrelated EBV\n                    <jats:sup>+<\/jats:sup>\n                    DLBCL xenografts showed indistinguishable cellular, virological and molecular features, and synergistically responded to combined inhibition of EBV replication with ganciclovir and B\u2010cell receptor signalling with ibrutinib\n                    <jats:italic>in vivo<\/jats:italic>\n                    . Our study underscores the risk of RT driven by EBV in CLL patients receiving immunosuppressive therapies, and provides the scientific rationale for testing ganciclovir and ibrutinib in EBV\n                    <jats:sup>+<\/jats:sup>\n                    DLBCL. Copyright \u00a9 2018 Pathological Society of Great Britain and Ireland. Published by John Wiley &amp; Sons, Ltd.\n                  <\/jats:p>","DOI":"10.1002\/path.5060","type":"journal-article","created":{"date-parts":[[2018,2,21]],"date-time":"2018-02-21T15:28:35Z","timestamp":1519226915000},"page":"61-73","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":31,"title":["Richter transformation driven by Epstein\u2013Barr virus reactivation during therapy\u2010related immunosuppression in chronic lymphocytic leukaemia"],"prefix":"10.1002","volume":"245","author":[{"given":"Maria J","family":"Garc\u00eda\u2010Barchino","sequence":"first","affiliation":[{"name":"Division of Haematological Oncology, Centre for Applied Medical Research (CIMA), CIBERONC University of Navarra  Pamplona Spain"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Maria E","family":"Sarasquete","sequence":"additional","affiliation":[{"name":"Department of Haematology University Hospital, and Institute of Molecular 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