Objective: E2F-1 is a member of the E2F family group of transcriptional factors that play a major role in cell cycle progression and arrest, as well as in apoptosis. In different tumors E2F1 can demonstrate opposing roles, acting either as an oncogene or as a tumor suppressor gene. Method: We have previously established E2F-1's immunohistochemical expression in Hodgkin lymphoma (HL) and its correlation with p53 expression, although no relationship with either proliferation or apoptosis was demonstrated. A further investigation in a larger series of 100 cases of primary HL with the addition of new apoptotic techniques and the use of p21 expression as an indicator of p53 functional status was undertaken. Results: Following stratification of our cases based on p53 functionality, E2F-1 was inversely correlated with the proliferation marker TopoIIa. Independently of p53, high levels of E2F-1 expression showed a linear trend with apoptosis and an inverse trend with proliferation (borderline p value in both cases). Conclusion: Both E2F-1 and p53 activity is upregulated in HL, however it seems that p53 status is a major regulator of the relationship between E2F-1 expression and tumor growth. Alternatively, E2F-1 may use p53-independent pathways to induce apoptosis. Objective: PTLD represent a spectrum of usually EBV-driven lymphoplasmacytic proliferations in the settings of immunodeficiency associated with allograft. EBV infects cells in latent or lytic forms. Although viral oncogenes are expressed in latency programs, lytic EBV replication is required to develop lymphomas in mouse models. The role of intratumoral EBV replication in PTLD has never been addressed before. Method: A series of 35 PTLD was reviewed and EBV latency genes were explored in all cases and included EBER1-2, LMP1 and EBNA2. Moreover, two early lytic genes involved in EBV replication, BZLF1/ZEBRA and EAD11 were also analyzed. All clinical and pathological data were collected. Results: The median age was 50 years (27-77) with a male predominance (26 M: 9 F). EBV infection was observed in 28 cases (80 %). EBV replication was observed in 40 % of the cases. These were more likely to be polymorphic PTLD with latency III in the context of stem cell transplantation. Moreover these cases had atypical clinical presentations such as brain involvement or disseminated disease with aggressive behavior (OS: 11 months vs. 48 months). Conclusion: EBV replication occurs in tumor cells of PTLD-patients associated with poor outcome and may be share common morphological and phenotypical features. In routine praxis, their differential diagnosis might represent a challenge requiring a specific work-up of immunohistochemical (IHC) and fluorescent in situ hybridization (FISH) analyses. Method: Paraffin sections from 17 CD20+/CD5+ blastic B-NHL were examined for cyclin-D1, CD10, bcl-6 and MUM-1 IHC expression together with FISH method using probes for CCND1 rearrangement and/or IGH/CCND1 translocation. The final diagnosis was established according to the criteria of WHO classification. Results: 11/17 cases were diagnosed as bMCL showing cyclin-D1 positivity and CCND1 rearrangement, other analysed IHC markers were negative. Five of these cases were polyploid. 6/17 cases were diagnosed as CD5+ DLBCL in spite of coexpression of cyclin-D1 in 2 of them, as they showed various CD10, bcl-6 and MUM-1 expressions and missed CCND1 gene rearrangement. Conclusion: Cyclin-D1 positivity may appear in other than MCL lymphomas due to changes at transcriptional or posttranscriptional level. In spite of overlaping phenotypes, FISH analysis of CCND1 represents an effective tool to increase the diagnostic accuracy to distinguish CD5+ DLBCL from bMCL. Supported by VEGA grant Nr. 1/ 0378/12 and projects CEPRII (IMTS: 26220120036) and MDCC (IMTS: 26220220113) co-financed by EU sources.