title: Origin and pathogenesis of B cell lymphomas.
abstract: Immunoglobulin (Ig) gene remodeling by V(D)J recombination plays a central role in the generation of normal B cells, and somatic hypermutation and class switching of Ig genes are key processes during antigen-driven B cell differentiation. However, errors of these processes are involved in the development of B cell lymphomas. Ig locus-associated translocations of proto-oncogenes are a hallmark of many B cell malignancies. Additional transforming events include inactivating mutations in various tumor suppressor genes, and also latent infection of B cells with viruses, such as Epstein-Barr virus. Many B cell lymphomas require B cell antigen receptor expression, and in several instances chronic antigenic stimulation plays a role in sustaining tumor growth. Often, survival and proliferation signals provided by other cells in the microenvironment are a further critical factor in lymphoma development and pathophysiology. Many B cell malignancies derive from germinal center B cells, most likely because of the high proliferation rate of these cells and the high activity of mutagenic processes.
authors.affiliation: Institute of Cell Biology (Cancer Research), Medical School, University of Duisburg-Essen, Essen, Germany.
authors.forename: Marc
authors.initials: M
authors.lastname: Seifert
authors.forename: René
authors.initials: R
authors.lastname: Scholtysik
authors.forename: Ralf
authors.initials: R
authors.lastname: Küppers
mesh_terms: D000818:Animals; D001402:B-Lymphocytes / Q000276:immunology / Q000378:metabolism / Q000473:pathology; D006801:Humans; D016393:Lymphoma, B-Cell / Q000209:etiology* / Q000235:genetics / Q000473:pathology* / Q000821:virology; D059016:Tumor Microenvironment