AI Article Synopsis
- - CD27 is a protein marker that typically indicates normal memory B cells, but its expression can be inconsistent in certain types of cancer, like Waldenström's macroglobulinemia (WM).
- - In WM, somatic hypermutation (SHM) in immunoglobulin genes marks the memory B cell origin, distinguishing between a dominant mutated subset and a lesser unmutated subset.
- - Recent findings suggest that normal memory B cells can exist without CD27, and this raises questions about whether WM originates from typical memory B cells that lose CD27 expression and indicates ongoing changes within the tumor cells.
Article Abstract
CD27 is a tumor necrosis factor receptor family glycoprotein, identified in seminal studies as an apparently robust marker for normal memory B cells. Somatic hypermutation (SHM) in immunoglobulin variable (V) region genes, however, remains the definitive memory imprint. In Waldenström's macroglobulinemia (WM), SHM defines a predominant mutated (MUT) subset and a minor unmutated subset indicative of naive B-cell origin. In MUT-WM, tumor cells can lack CD27 expression, raising suggestions of unusual memory B-cell origins. We recently identified such normal IgM+D+CD27-ve memory B-cells, with low levels of SHM in VH genes. While these could seed WM, the possibility remains that WM could derive from classical memory B cells that shed CD27. The utility of CD27 expression in defining memory in MUT-WM origins, then, is uncertain, but SHM unequivocally defines memory B-cell derivation in most WM. Patterns of SHM and additional IgH locus events furthermore reveal ongoing intra-tumoral diversification in WM.
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| http://dx.doi.org/10.3816/CLM.2009.n.007 | DOI Listing |
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