Diffuse large B-cell lymphoma (DLBCL) constitutes 30%–58% of non-Hodgkin's lymphoma series. The crude incidence in Europe is 3.8/100 000/year [1]. The incidence increases with age and varies considerably across Europe. A family history of lymphoma, autoimmune disease, human immunodeficiency virus (HIV) infection, hepatitis C virus (HCV) seropositivity, a high body mass as a young adult and some occupational exposures have been identified as risk factors of DLBCL [2]. In recent years, there have been important survival improvements for DLBCL in all European regions [3].

Progress in understanding the biology of multiple myeloma (MM), a plasma cell malignancy, has been slow. The discovery of microRNAs (miRNAs), a class of small noncoding RNAs targeting multiple mRNAs, has revealed a new level of gene expression regulation. To determine whether miRNAs play a role in the malignant transformation of plasma cells (PCs), we have used both miRNA microarrays and quantitative real time PCR to profile miRNA expression in MM-derived cell lines (n= 49) and CD138+ bone marrow PCs from subjects with MM (n= 16), monoclonal gammopathy of undetermined significance (MGUS) (n= 6), and normal donors (n= 6). We identified overexpression ofmiR-21,miR-106b∼25cluster,miR-181aandbin MM and MGUS samples with respect to healthy PCs. Selective up-regulation ofmiR-32andmiR-17∼92cluster was identified in MM subjects and cell lines but not in MGUS subjects or healthy PCs. Furthermore, two miRNAs,miR-19aand19b, that are part of themiR-17∼92cluster, were shown to down regulate expression of SOCS-1, a gene frequently silenced in MM that plays a critical role as inhibitor of IL-6 growth signaling. We also identified p300-CBP-associated factor, a gene involved in p53 regulation, as a bona fide target ofthe miR106b∼25cluster,miR-181aandb, andmiR-32. Xenograft studies using human MM cell lines treated withmiR-19aandb, andmiR-181aandbantagonists resulted in significant suppression of tumor growth in nude mice. In summary, we have described a MM miRNA signature, which includes miRNAs that modulate the expression of proteins critical to myeloma pathogenesis.

To complement the existing treatment guidelines for all tumour types, ESMO organizes consensus conferences to focus on specific issues in each type of tumour. In this setting, a consensus conference on the management of lymphoma was held on 18 June 2011 in Lugano, next to the 11th International Conference on Malignant Lymphoma. The conference convened ∼30 experts from all around Europe, and selected six lymphoma entities to be addressed; for each of them, three to five open questions were to be addressed by the experts. For each question, a recommendation should be given by the panel, referring to the strength of the recommendation based on the level of evidence. This consensus report focuses on the three less common lymphoproliferative malignancies: marginal zone lymphoma, mantle cell lymphoma, and peripheral T-cell lymphomas. A first report had focused on diffuse large B-cell lymphoma, follicular lymphoma, and chronic lymphocytic leukaemia.

Mantle cell lymphoma (MCL) is a relatively uncommon subtype of lymphoid malignancy and represents 5%–7% of malignant lymphoma in Western Europe. The annual incidence of this disease has increased during recent decades to 1–2/100 000 recently. MCL is more common in males than in women with a 3 : 1 ratio.

Purpose: We investigated the effect on minimal residual disease, by qualitative and real-time quantitative polymerase chain reaction (RQ-PCR), of a consolidation regimen that included bortezomib, thalidomide, and dexamethasone (VTD) in patients with multiple myeloma (MM) responding to autologous stem-cell transplantation (auto-SCT). Patients and Methods: Patients achieving at least very good partial response who had an available molecular marker based on the immunoglobulin heavy-chain rearrangement received four courses of treatment every month: four infusions per month of bortezomib at 1.6 mg/m², thalidomide at 200 mg/d, and dexamethasone at 20 mg/d on days 1 to 4, 8 to 11, and 15 to 18. Patients were studied with tumor-clone–specific primers by qualitative nested PCR and RQ-PCR. Results: Of 39 patients enrolled, 31 received the four VTD courses. Immunofixation complete responses increased from 15% after auto-SCT to 49% after VTD. Molecular remissions (MRs) were 3% after auto-SCT and 18% after VTD. Median time to maximum response was 3.5 months. So far, no patient in MR has relapsed (median follow-up, 42 months). VTD consolidation induced an additional depletion of 4.14 natural logarithms of tumor burden by RQ-PCR. Patients with a tumor load less than the median value after VTD had outcomes better than those who had tumor loads above the median value after VTD (at median follow-up: progression-free survival, 100% v 57%; P < .001). Conclusion: To the best of our knowledge, this study is the first to document the occurrence of persistent MRs in a proportion of MM patients treated without allogeneic transplantation. Moreover, the major reduction in tumor load recorded by RQ-PCR after VTD suggests that unprecedented levels of tumor cell reduction can be achieved in MM thanks to the new nonchemotherapeutic drugs.