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Molecular biology of Hodgkin lymphoma Kuppers RHematology Am Soc Hematol Educ Program 2009[]; ä (ä): 491-6Hodgkin lymphoma (HL) is derived from mature B cells and subdivided into classical HL and nodular lymphocyte predominant HL (NLPHL). HL is unique among human B cell lymphomas because of the rarity of the lymphoma cells, the Hodgkin and Reed-Sternberg (HRS) cells in classical HL and the lymphocyte-predominant (LP) cells in NLPHL, which usually account for 0.1% to 10% of the cells in the affected tissues. Moreover, HRS cells are unique in the extent to which they have lost their B cell-typical gene expression pattern. Deregulation of transcription factor networks plays a key role in this reprogramming process. HRS cells show strong constitutive activity of the transcription factor NF-kappaB. Multiple mechanisms likely contribute to this deregulated activation, including signaling through particular receptors and genetic lesions. Inactivating mutations in the TNFAIP3 tumor suppressor gene, encoding a negative regulator of NF-kappaB activity, were recently identified in about 40% of patients with classical HL. HRS cells are latently infected by Epstein-Barr virus in about 40% of patients, and an important role of this virus in HL pathogenesis-in particular for cases in which HRS cells had lost the capacity to express a B-cell receptor due to destructive somatic mutation-was recently substantiated.|B-Lymphocytes/*pathology/virology[MESH]|Cell Dedifferentiation[MESH]|Cell Transformation, Neoplastic[MESH]|Cell Transformation, Viral[MESH]|DNA-Binding Proteins[MESH]|Epstein-Barr Virus Infections/genetics/pathology[MESH]|Gene Expression Profiling[MESH]|Gene Expression Regulation, Neoplastic[MESH]|Herpesvirus 4, Human/isolation & purification[MESH]|Hodgkin Disease/*genetics/pathology/virology[MESH]|Humans[MESH]|Immunophenotyping[MESH]|Intracellular Signaling Peptides and Proteins/deficiency/genetics[MESH]|NF-kappa B/metabolism[MESH]|Neoplasm Proteins/genetics/metabolism[MESH]|Nuclear Proteins/deficiency/genetics[MESH]|Reed-Sternberg Cells/pathology/virology[MESH]|Transcription Factors/metabolism[MESH]|Transcription, Genetic[MESH]|Tumor Necrosis Factor alpha-Induced Protein 3[MESH] |
