Molecular Markers of Clonality, Lineage, Differentiation, and Translocation in B Cell Neoplasms
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.
KeywordsChronic Lymphocytic Leukemia Lymphoid Neoplasm Breakpoint Cluster Region Diffuse Large Cell Lymphoma Follicular Lymphomas7
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