Variable heavy-chain gene analysis of follicular lymphomas: subclone selection rather than clonal evolution over time

To investigate B-cell receptor evolution in follicular lymphomas (FLs), immunoglobulin variable heavy chain (V(H)) gene regions of 3 FLs were analyzed at different time points. One FL with a high somatic mutation load and intraclonal V(H) gene diversity was investigated in situ. V(H) gene transcripts were amplified and sequenced from samples of approximately 50 tumor cells isolated from frozen tissue sections by laser microdissection. Interestingly, the mutation pattern of the prevalent subclone in the relapse biopsy was virtually identical to that of a subclone isolated by microdissection from the presentation biopsy 9 years earlier. In a second FL, proof was obtained that the subclone that dominated the relapse sample had already been present in the initial biopsy. The finding that subclones found in the relapses of these FLs had not evolved over time but were preexistent, challenges the concept of antigen-driven B-cell receptor evolution during disease cours

The small FOXP1 isoform predominantly expressed in activated B cell-like diffuse large B-cell lymphoma and full-length FOXP1 exert similar oncogenic and transcriptional activity in human B cells

Proteomic

Guidelines for diagnosis and management of Waldenström’s macroglobulinemia

On behalf of the lymphoma and multiple myeloma working parties of the Dutch/Belgian HaematoOncology Foundation for Adults in the Netherlands (HOVON), we present a guideline for diagnosis and management of Waldenström’s macroglobulinemia (WM). Considering the indolent behavior and heterogeneous clinical presentation of WM, it is crucial to determine the right indications for treatment, as well as to individualize therapeutic options. There is a lack of large clinical trials due to the low incidence of WM. Based on the available data, we provide a practical diagnostic classification, as well as recommendations for first line therapy and options for treating relapsed disease