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Origin and Pathogenesis of B Cell Lymphomas

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Lymphoma

Part of the book series: Methods in Molecular Biology ((MIMB,volume 971))

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.

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Acknowledgements

Own work discussed in this review was supported by grants from the Deutsche Forschungsgemeinschaft (TRR60, KU1315/7-1, KU1315/8-1, GK1431), the Deutsche Krebshilfe, the Wilhelm Sander Foundation, the José Carreras Leukemia Foundation, and the BMBF (Haematosys consortium). We thank the other members of our group and Martin-Leo Hansmann for many stimulating discussions.

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Seifert, M., Scholtysik, R., Küppers, R. (2013). Origin and Pathogenesis of B Cell Lymphomas. In: Küppers, R. (eds) Lymphoma. Methods in Molecular Biology, vol 971. Humana Press, Totowa, NJ. https://doi.org/10.1007/978-1-62703-269-8_1

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