Hodgkin lymphoma (HL) accounts for approximately 15% to 30% of all malignant lymphomas. According to current diagnostic criteria, approximately 90% to 95% of HLs fall into the Classical Hodgkin lymphoma (CHL) category; the remaining cases are nodular lymphocyte-predominant subtype of Hodgkin’s lymphoma (NLPHL) which is recognized as a separate entity in the World Health Organization (WHO) classification1. WHO classification is based on the fact that there are clear and consistent histologic, epidemiologic, immunologic, and genetic differences between NLPHL and CHL. NLPHL is an indolent germinal center (GC) B-cell malignancy, that represents a nodular proliferation comprised of a minority of large neoplastic centroblasts with multilobated nuclei, the so-called popcorn or lymphocyte-predominant (LP) cells. Immunohistochemically LP cells are CD20+, PAX5+, BCL6+, EBV-LMP1-, CD30- and CD15-. Background inflammatory infiltrate represent mixture of small B and T lymphocytes1. This type of tumour is characterised clinically by a relatively indolent course and a very good response to standard therapy in cases with low stage disease. Unfortunately, the prognosis is unfavourable for advanced stages2. CHL is also a clonal, malignant lymphoproliferation originating from germinal center B cells3. CHL has a bimodal age curve in western countries, showing a peak at 15-35 years of age and a second peak later in life at 45-60 years1. A histopathologic diagnosis of CHL is based on the identification of diagnostic Reed-Sternberg (RS) cells in an appropriate inflammatory background of mixed infiltrate by histiocytes, small lymphocytes, eosinophils, neutrophils, plasma cells, fibroblasts and colagen. Based on characteristics of the reactive infiltrate and the specific features of neoplastic cells, cases may be subclassified into one of four subtypes: nodular sclerosis (NSCHL), lymphocyte-rich (LRCHL), mixed cellularity (MCCHL) and lymphocyte-depleted classical Hodgkin lymphoma (LDCHL)1,4. Although most cases can be diagnosed on the basis of morphology alone, diagnostic criteria include the characteristic immunophenotype of the neoplastic population. RS cells and variants express the CD30 and CD15 antigens in the majority of cases and lack the common leukocyte antigen CD455,6. The LMP-1 protein of EBV is expressed in approximately 25% to 50% of CHLs depending on the histologic subtype and patient age7. The staining is membranous and cytoplasmic, and usually most neoplastic cells are positive. Etiology of CHL is still questionable, but due to the unique epidemiologic and clinical features of the disease, an infectious cause has long been suspected. Currently, immunohistochemistry for the EBV latent membrane protein-1 (LMP-1) and nonradioactive in situ hybridization for EBV-encoded early RNAs (EBERs) are the methods of choice for the detection of EBV in routinely fixed, paraffin-embedded tissues8. Recent data suggest that the EBV status of tumour cells in classical HL could have prognostic significance for patients with this heterogenous disease9.

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