In the last years, several studies of molecular profiling of aggressive lymphomas were performed. In particular, it was shown that DLBCL can be distinguished in two different entities according to GEP. Specifically, ABC and GCB subtypes were characterized by having different pathogenetic and clinical features. In addition, it was demonstrated that DLBCLs are distinct from BL. Indeed, the latter is a unique molecular entity. However, relevant pathological differences emerged among the clinical subtypes. More recently, microRNA profiling provided further information concerning BL-DLBCL distinction as well as for their subclassification. In this paper, the authors based on their own experience and the most updated literature review, the main concept on molecular profiling of aggressive lymphomas. 1. Introduction Burkitt lymphoma (BL) and diffuse large B-cell lymphoma (DLBCL) are the commonest aggressive B-NHL worldwide and represent distinct entities in the World Health Organization (WHO) classification [1, 2]. BL is listed in the WHO classification as a single genetic and morphologic entity with variable clinical presentation. It accounts for 30–50% of lymphomas in children, but only 1-2% in adults. In particular, the WHO classification recognizes 3 clinical subsets of BL: endemic (eBL), sporadic (sBL), and immunodeficiency-associated (ID-BL) [1]. The endemic form is the commonest type, being the most frequent childhood cancer in equatorial Africa [1, 3–5]. eBL is almost invariably associated with Epstein-Barr virus (EBV) infection, although local environmental toxics (i.e., Euphorbia tirucalli) and coinfection with arbovirus or malaria also appear to be important for its pathogenesis [6–8]. sBL is the most commonly recorded form in the USA and Europe. Contrary to eBL, only ~20% of cases are correlated to EBV [9]. Immunodeficiency-associated BL occurs more commonly in patients infected with HIV (HIV-BL). Intriguingly, because HIV-BL can occur in patients with relatively high CD4 counts, immunosuppression per se is not sufficient to explain the relatively high prevalence of BL in this setting [10, 11]. The diagnosis of classical BL rests on the presence of a monotonous infiltrate of medium-sized blastic lymphoid cells that show round nuclei with clumped chromatin and multiple, centrally located nucleoli. The tumor cells have a high proliferation rate and intermingled macrophages containing apoptotic debris lead to the morphological aspect of a “starry sky” pattern [1]. Immunophenotypic features of BL include positivity of tumor cells for CD20 and CD10 (and
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