**4. EBV-positive PTLD vs. EBV-negative PTLD**

Epstein-Barr virus-positive (EBV (+)) and EBV-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) and supports the hypothesis that EBV (−) PT-DLBCL are de novo lymphomas. EBV (+) and EBV (−) PT-DLBCL have distinct aCGH profiles and shared only one recurrent imbalance. EBV (−) PT-DLBCL, however, display at least ten 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 is due to gain/amplification of 9p24.1 targeting PDCD1LG2/PDL2. FOXP1 oncogene and the tumor suppressor CDKNA2 implicated in EBV (−) DLBCL do not play a critical role in the pathogenesis of EBV (+) PT-DLBCL [14].
