The recently proposed World Health Organization classification of neoplastic diseases of the lymphoid tissues is based on the principles of the Revised European-American Classification of Lymphoid Neoplasms introduced in 1994. Use of these classifications implies a new approach to lymphoma diagnosis, especially because of the inclusion of clinical data among which the site of involvement (nodal v extranodal) is very important. Recent technical advances allowing molecular biological investigations on the single cell level helped gain new insights into the cellular origin of  B-cell lymphomas. Tumor cells of the majority of .B-cell non-Hodgkin’s lymphomas (NHL) harbor somatically mutated immunoglobulin variable region genes, and are therefore derived from germinal center B cells or their descendants. The same is true for Hodgkin’s disease, which (at least in the majority of cases) is a germinal center derived B-cell lymphoma. Significant news on the molecular pathogenesis of NHL include the prognostically relevant dichotomy of B-CLL, the involvement of translocations affecting 3q27 in 20% to 40% of diffuse large B-cell lymphomas (DLBCL), the prognostical implication of the t(2;5) in anaplastic large cell lymphoma, and detection of the t(11 ;18) in gastric mucosa-assoclated lymphoid tissue (MALT)-type lymphoma. A major step forward with regard to gastric MALT-type lymphoma therapy was the discovery of a causal relationship between Helicobacterpyloriinfection and lymphomagenesis. Cyclophosphamide, doxorublcin, vincrisfine, and prednisone (CHOP) chemotherapy remains the golden standard for DLBCL treatment.

This review focuses on the modem approach to lymphoma diagnosis, discusses new insights into lymphoma biology and pathogenesis, and outlines current therapeutic strategies. All of these aspects will mainly deal with the most frequently encountered lymphoid neoplasms, which are of B-cell origin.