PMC10485152_01
Clinical and Pathological findings (A) Serum protein electrophoresis showed an M-peak (B) Serum protein immunofixation electrophoresis showed an IgM-kappa monoclonal gammopathy. (C, D) Hematoxylin and eosin (H & E) stain. Small-to-medium-sized atypical cells are densely increased in the intratrabecular spaces, and the bone trabecula is compressed. Tumor cells were positive for (E) bcl2, (F) CD20, (G) kappa, (H) lambda with light chain restriction. (I) Flow cytometry analysis in bone marrow mononuclear cells. Tumor cells are positive for CD19, CD20, and SmIgM, with light chain restriction.
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Serum protein electrophoresis showed an M-peak, and serum immunofixation electrophoresis showed an IgM-kappa type M protein (Fig. 1A & B). In situ hybridization (ISH) of kappa and lambda light chains indicated that the increased lymphocytes in the bone marrow were clonal B cells with kappa restriction (Fig. 1C-I).
Cytogenetic analysis (A) Karyotyping of bone marrow shows 46, XX, t(14;18)(q32;q21). (B) 41% of the cells in bone marrow show IgH-MALT1 translocation(t(14;18)(q32;q21)). (C) MYD88L265P mutation is detected in bone marrow mononuclear cells. A total of 40 clones were sequenced.
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In addition, bone marrow chromosome analysis showed that the karyotype was 46, XX, t(14;18)(q32;q21)[1]/46, XX[19] (Fig. 2A). The IgH-MALT1 fusion signal was detected in 41% of the cells, whereas the IgH-Bcl2 signal was undetectable (Fig. 2B). Furthermore, the MYD88 L265P mutation was identified in bone marrow mononuclear cells in 2/40 clones using Sanger sequence analysis (Fig. 2C).