Abstract
The demonstration that distinct types of lymphoid neoplasms could be assigned to stages of B or T cell development provided great insights into the biology of these malignancies1,2. Historically this has been approached by utilizing cell surface markers associated with various developmental stages of B or T cell maturation. Despite a large number of lineage-associated cell surface markers, it is still frequently impossible to conclusively classify a lymphoid neoplasm as B or T cell in origin. This is often due to the admixture of large numbers of nonneoplastic cells with the neoplastic cells in a lymphomatous tissue. Alternatively, other malignancies may be at a stage of differentiation prior to the expression of any lineage-restricted cell surface antigen. Moreover, the determination of clonality in lymphoid neoplasms has for all practical purposes been limited to the mature B cell malignancies that display the presence of but one light (L)-chain isotype, κ or λ. The DNA rearrangements which assemble the gene subsegments for antigen-specific receptors in B cells as well as T cells serve as molecular markers which are unique to individual neoplasms. The rearranging determinants have made an enormous contribution to refining the diagnosis and understanding the pathogenesis of lymphoid neoplasms.
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© 1986 Plenum Press, New York
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Korsmeyer, S.J., Bakhshi, A., Wright, J.J., Graninger, W.C., Felix, C., Seto, M. (1986). Molecular Markers of Clonality, Lineage, Differentiation, and Translocation in B Cell Neoplasms. In: Ferrarini, M., Pernis, B. (eds) The Molecular Basis of B-Cell Differentiation and Function. NATO ASI Series, vol 123. Springer, Boston, MA. https://doi.org/10.1007/978-1-4684-7035-2_18
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DOI: https://doi.org/10.1007/978-1-4684-7035-2_18
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