We report, for the first time, the occurrence of a SETBP1 mutation in two cases, as well as changes in G-CSF and IL-6 in SETBP1 wild type vs. mutated patients that are supportive of a hypothesis that neutrophilia associated with plasma cell neoplasms may sometimes be reactive and may sometimes represent a second clonal entity.
The newly developed mouse strains may provide a good preclinical research tool for the design and testing of new approaches to target IL-6 in treatment and prevention of human PCNs.
Tumor suppressor CD99 is downregulated in plasma cell neoplasms lacking CCND1 translocation and distinguishes neoplastic from normal plasma cells and B-cell lymphomas with plasmacytic differentiation from primary plasma cell neoplasms.
The plasma cells from the t(11;14)-positive PCNs were largely CD19-/CD45-, similar to the t(11;14)-negative PCNs and unlike the BCL-PCD plasma cells (p < .0001).
Flow cytometric analysis with a panel of antibodies that includes CD19, CD56, CD138, CD45 and other aberrant markers commonly expressed by PCN will allow identification of clonally unrelated PCN and B-NHL in a composite neoplasm, and distinguish them from B-NHL with plasmacytic differentiation and PCN with lymphoplasmacytic morphology.
Plasma cell immunophenotyping by flow cytometry can aid in this distinction as by this technique the plasma cells of LPL/WM express both CD19 and CD45 whereas primary plasma cell neoplasms are CD19 or CD45 negative.
This report implicates an unidentified role of Bcl-X(L) in bone marrow plasma cell tumor formation, as ABL-MYC retroviral infection only elicits bone marrow plasma cell tumors in mice that ectopically express Bcl-X(L) in their B- and plasma cells.
Our findings demonstrate that the enforced expression of Myc and Bcl-X(L) by Ig enhancers with peak activity in plasma cells generates a mouse model of human PCN that recapitulates some features of human multiple myeloma.
This suggests to us that cyclin D1 deregulation due to the presence of t(11;14) is involved in the early development of plasma cell neoplasms, and that this event alone is not enough for the development of symptomatic myeloma.
We found three polymorphic sequence variants, either alone or in combination, at codons 5 and 8, and in intron 1 at base 58 of the BCL10 gene in 37 patients with plasma cell dyscrasia.
Polyneuropathy, organomegaly, endocrinopathy, M-protein, skin changes (POEMS) syndrome is a paraneoplastic syndrome due to an underlying plasma cell neoplasm.
This study aimed to investigate whether changes in the megakaryocytic expression of GATA-1, pro-inflammatory cytokines (interleukin [IL]-6 and IL-8), and CD9 affect platelet counts and dysmegakaryopoiesis in patients with PCN and MDS.
Vk*MYC mice under glyphosate exposure developed progressive hematological abnormalities and plasma cell neoplasms such as splenomegaly, anemia, and high serum IgG.
This discussion focuses on diagnostic pitfalls related to the use of immunohistochemistry for CD20 and CD3 in hematopathology, and specifically on diagnostic challenges that arise when (1) CD20 is not expressed in B-cell lymphomas, when (2) CD20 is expressed in plasma cell neoplasms and T-cell lymphomas, and when (3) CD3 is expressed in B-cell lymphomas and Hodgkin lymphoma.
This discussion focuses on diagnostic pitfalls related to the use of immunohistochemistry for CD20 and CD3 in hematopathology, and specifically on diagnostic challenges that arise when (1) CD20 is not expressed in B-cell lymphomas, when (2) CD20 is expressed in plasma cell neoplasms and T-cell lymphomas, and when (3) CD3 is expressed in B-cell lymphomas and Hodgkin lymphoma.
We investigated flow cytometric CD19 and CD45 expression, DNA ploidy index and M-protein subtype in 416 t(11;14)-positive PCNs, as well as control groups (88 BCL-PCDs and 81 t(11;14)-negative PCNs).
Flow cytometry displayed atypical plasma cells expressing cluster of differentiation (CD38, CD20, and CD56) with cytoplasm and lambda light chain, approximately 20%, consistent with a plasma cell dyscrasia.
Flow cytometry displayed atypical plasma cells expressing cluster of differentiation (CD38, CD20, and CD56) with cytoplasm and lambda light chain, approximately 20%, consistent with a plasma cell dyscrasia.
Flow cytometry displayed atypical plasma cells expressing cluster of differentiation (CD38, CD20, and CD56) with cytoplasm and lambda light chain, approximately 20%, consistent with a plasma cell dyscrasia.