Table 1.
Clinical data of our series of patients (DOD: Dead of disease; DOC: Dead of other cause; CR: Complete response; DLBCL: Diffuse large B-cell-lymphoma; LPL: Lymphoplasmacytic lymphoma).
Fig 1.
Case 1 showing p53 expression in both LPL and DLBCL component.
A-B. H-E staining of the bone marrow biopsy at different magnification showing a diffuse interstitial infiltration of lymphoid and lymphoplasmocytoid cells expressing CD20 (C) and P53 (D). In E (H-E staining) a diffuse proliferation of neoplastic cells effacing the lymph node architecture is seen. At higher magnification (F) these cells showed inmunoblastic or plasmablastic morphology (H-E staining), high proliferation index (G) with KI67 and p53 positivity (H). Scale bars of figures A-E is 10 mm, figures B-F is 500μm and figures D-H is 100μm.
Fig 2.
Another LPL case evolving into DLBCL is shown.
In figure A (H-E) and B (H-E) bone marrow biopsy with lymphoplasmacytic infiltration is seen. Cytoplasmic inmunoglobulins displacing the nuclei to the periphery of the cell are clearly seen (B). In C (H-E), effacement of lymph node architecture by the proliferation of large cells with inmunoblastic morphology is seen (D) (H-E). Scale bars of figures A is 2 mm, figure Bis 100μm, figure C is 1 mm and figure D is 50 μm.
Table 2.
NGS results and IgH rearrangement analysis in all cases.
Fig 3.
Hypothesis of DLBCL development in patients with LPL.
First Hypothesis: Sequential mutation adquisition from LPL to DLBCL. Second hypothesis: Common origin with divergent evolution of either LPL and DLBCL neoplasms. Third hypothesis: A. Different lymphomas from a common stem cell or B. Different lymphomas from different stem cells.