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At least 217 records · Page 12Linked to original sources
PubMed1987

Plasma cell leukemia.

In summary, plasma cell leukemia is a rare disorder that can develop spontaneously or evolve in patients with multiple myeloma. The diagnosis is based on laboratory features, including a plasmacytosis exceeding 2 X 10(9)/L or 20% of the differential cell count. Primary plasma cell leukemia should also be considered when fewer plasma cells are present provided that a clonal proliferation is documented. Most clinical characteristics are similar in both types of plasma cell leukemia. Lymphadenopathy and hepatosplenomegaly are more common in the primary form, and lytic bone lesions are more frequent in the secondary form. Patients with primary plasma cell leukemia may initially respond better to chemotherapy, including single agent drugs commonly used in multiple myeloma. However, resistant disease is expected, and most data suggest a median survival of less than 6 months in both types of leukemia. Because patients with primary plasma cell leukemia are in better condition, intensive chemotherapy and approaches such as bone marrow transplantation should be considered, especially in younger patients.

Antineoplastic Combined Chemotherapy Protocols↗
PubMed2003

Multiple myeloma presenting as primary non-secretory plasma cell leukemia.

Primary plasma cell leukemia is a rare manifestation of multiple myeloma, whose neoplastic hierarchy in the classification of malignant hematological disorders is not yet very clearly defined. Morphological and immunological criteria indicate that the cells are at end stage of B cell maturation pathway. This unusual disorder is diagnosed by the presence of more than 2 x 10(9) plasma cells per liter of peripheral blood or more than 20% of the leucocytes being plasma cells on differential count. This occurs either denovo or as a terminal event in patients with long standing multiple myeloma. A case report of a young male patient with primary plasma cell leukemia is presented.

Adult↗
PubMed1984

Plasma exchange treatment of peripheral neuropathy associated with plasma cell dyscrasia.

Plasma exchange was used to treat 10 patients with polyneuropathy and a monoclonal antibody (plasma cell dyscrasia). Six patients had improvement of the neuropathy, while three patients had stabilisation of the neuropathy during plasma exchange. The patients who improved maintained a 64% or greater decrease in the monoclonal antibody between exchanges. Patients with axonal polyneuropathy as well as patients with demyelinating polyneuropathy recovered some neurologic function. With cessation of plasma exchanges, the monoclonal antibody titre approached pre-treatment levels and the neuropathy progressed. Plasma exchange was effective in rapidly lowering the level of monoclonal antibody and allowing for some recovery of neurologic function.

Adult↗
PubMed1978

Iron-containing plasma cells.

Iron in plasma cells has been described in patients with diseases characterized by iron overload. We observed iron-containing plasma cells in 21 anemic alcoholic patients admitted to the hospital for treatment of complications of alcoholism. The presence of iron-containing plasma cells is suggestive of alcoholism and its complications, and diseases associated with iron overload or inability of RBCs to utilize iron. The mechanism of entry of iron into plasma cells is unknown.

Anemia↗
PubMed1980

Circulating immunoglobulin-secreting cells in patients with plasma cell dyscrasia.

Immunoglobulin-secreting cells (ISC) in peripheral blood mononuclear cells (PBM) isolated from patients with plasma cell dyscrasia of various stages were studied using reverse hemolytic plaque assay. Normal healthy individuals contained 35 +/- 16 ISC/10(5) PBM. Aleukemic or subleukemic patients with overt myeloma contained 825 +/- 713 ISC, whereas leukemic patients contained 12,675 +/- 2520 ISC. Patients of premyelomatous stage, however, contained ISC/10(5) PBM of normal range. The relationship between ISC and clinical stage or laboratory data is discussed.

Aged↗
PubMed1977

Enhancement by irradiated T cells of human plasma cell production: dissection of helper and suppressor functions in vitro.

The addition of irradiated T-enriched lymphocytes to B cell-enriched fractions of human peripheral blood or to unseparated mononuclear cells stimulated the differentiation of plasmacytoid cells in culture with pokeweek mitogen beyond the synergy obtained by the addition of unirradiated T cells. This stimulation was observed in both the proportion and absolute number of plasmacytoid cells recovered from the cultures, and in the amount of IgM detected in culture supernatants by a hemagglutination inhibition assay. Irradiation-induced enhancement was observed with normal and hypogammaglobulinmic T cells, but not with monoclonal T cells from two patients. Inactivation of T cells by heating or by repeated freezing and thawing did not produce the same effects as did irradiation. These data suggest that cell-mediated suppressor function in man is selectively radiosensitive, while helper activity is not. Irradiation may be a useful method for the functional isolation of helper cells and for the manipulation of the balance between suppressor and helper cell activities.

B-Lymphocytes↗
PubMed2003

Targeted overexpression of Bcl-XL in B-lymphoid cells results in lymphoproliferative disease and plasma cell malignancies.

Multiple myeloma is an incurable malignancy, and there is currently no mouse model that fully recapitulates the development and progression of the disease. We now describe a transgenic mouse that expresses a Bcl-XL transgene under the control of the 3'kappa immunoglobulin light chain enhancer, which is most active in murine B cells in late developmental stages. These mice developed nonmalignant plasma cell foci in the bone marrow and soft tissues and hyaline tubular casts in the kidneys. Median survival of the 3'KE/Bcl-XL mice was similar to littermate controls. When the 3'KE/Bcl-XL mouse was crossed to an Emu/c-Myc transgenic mouse, median survival of double transgenic progeny was 5.5 weeks. Peripheral blood and soft tissues were infiltrated with immature/mature B cells, and plasma cell lesions were identified in the bone marrow of all mice coexpressing Bcl-XL and c-Myc. These B- and plasma cell lesions demonstrated features consistent with malignancy. These results indicate that the 3'kappa immunoglobulin light chain enhancer can effectively target expression of Bcl-XL to B cells in late developmental stages, and they provide direct evidence that Bcl-XL can contribute to plasmacytomagenesis. Furthermore, this murine model serves as an important step in developing a novel genetically induced mouse model of plasma cell malignancies exhibiting bone marrow involvement.

Animals↗
PubMed1999

Characteristics of IgVH genes used by human intestinal plasma cells from childhood.

Plasma cells secreting immunoglobulin M (IgM) and IgA in human intestinal mucosa are the largest antibody-producing population in the human body. Despite this there have been relatively few studies of the characteristics and maturation of the genes which encode the mucosal immunoglobulins. We have previously demonstrated that intestinal plasma cells use highly mutated IgVH genes, likely to reflect germinal centre origin. Here we show that IgVH genes used by intestinal lamina propria plasma cells secreting IgM and IgA are highly mutated from childhood, with no change in the frequency of mutation through to adulthood, though IgVH genes used by IgM are significantly less mutated than those used by IgA. There was no difference between the IgA subclasses in either the frequency or distribution of mutations. The frequency of mutation in IgVH4-34 genes used by IgG was also studied in the adult biopsies, and was found to be of the same order as that observed in IgA and was significantly higher than that observed in IgM. We have identified IgM and IgA sequences which share identical CDR3 and distribution of mutations. Isotype switching may therefore occur after extensive mutation of IgM sequences, and IgM- and IgA-secreting plasma cells with the same specificity may occur within the same microenvironment. IgM should therefore be considered to be a component of secondary immune responses in the gut.

Adolescent↗
PubMed1995

The incidence and epidemiology of plasma cell neoplasms.

Plasma cell neoplasia includes monoclonal gammopathy of undetermined significance (MGUS), multiple myeloma (MM), and Waldenström's macroglobulinemia (WM). In MGUS, a large, stable clone does not cause symptoms; additional change(s) is/are required to convert this clone into a progressively expanding tumor that becomes symptomatic, as in MM or WM. The prevalence of MGUS (i.e., the number of cases in a defined population at a certain time) is 20 times greater than MM. The incidence (i.e., the number of cases developing in a defined population in a defined period) has not been determined for MGUS. Between 1960 and 1969, the average, annual, age-adjusted (1950 standard) incidence of MM in Malmö, Sweden was 3.4/10(5). The incidence of MM is strongly influenced by the age and race of the population, and the diagnostic services available. MM is a disease of old age; it rarely occurs before the age of 40. The incidence of MM increases rapidly with age, is lowest among the Chinese and Japanese, intermediate among Caucasians in America and Europe, and highest among blacks in the USA. The striking differences in the incidence of MM in different countries appears to be due to racial rather than environmental differences, since the low incidence among the Chinese and Japanese in Asia has migrated with them to the Bay area of California and to Hawaii. The high incidence of MM in USA black males (10.8/10(5)) and females (7.2/10(5)) is more than twice the rate for whites in the same regions.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1997

Multiple myeloma: reduced plasma cell contamination in peripheral blood progenitor cell collections performed after repeated high-dose chemotherapy courses.

The possibility of reducing tumour cell contamination by cytotoxic drug courses prior to peripheral blood progenitor cell (PBPC) collection was evaluated in two consecutives groups of multiple myeloma (MM) patient candidates for autograft. All patients were at disease onset and received two VAD (vincristine, doxorubicin and dexamethasone) courses as initial debulking. In the first group (44 patients), mobilization and harvest were performed 'upfront', after a single cyclophosphamide (CY) administration of 4 g/m2; in the second group (17 patients), PBPC were collected at the end of a high-dose sequential chemotherapy programme, including: CY 5 g/m2, etoposide (VP16) 2 g/m2, a chemotherapy-free interval with three courses of high-dose dexamethasone, a final mobilizing CY at 7 g/m2. G-CSF was given following each high-dose cytotoxic drug. Cytofluorimetric analysis was performed to quantify progenitors (CD34+ cells) and plasma cells, identified by the high CD38 expression and/or CD38 and CD138 coexpression. Large amounts of PBPC were collected in either group (median harvested CD34+/kg: 15.8 x 10(6) and 13.4 x 10(6), respectively; P=0.9). Circulating plasma cells were significantly higher in patients mobilized 'upfront' compared to those who received the high-dose sequence (median peak values of CD38bright/microl: 39 and 10, respectively; P=0.02); a similar difference was observed in the amount of contaminating plasma cells in the harvest products (median CD38bright/kg: 7.4 x 10(6) and 1.3 x 10(6), respectively; P=0.02). The results demonstrate that an in vivo purging approach is feasible in myeloma patients through repeated high-dose chemotherapy courses; this may provide less-contaminated material suitable for further in vitro purging procedures.

Adult↗
PubMed2006

Novel analysis of clonal diversification in blood B cell and bone marrow plasma cell clones in immunoglobulin light chain amyloidosis.

Immunoglobulin light chain amyloidosis (AL) is characterized by a limited clonal expansion of plasma cells and amyloid formation. Here, we report restriction in the diversity of VL gene usage with a dominance of clonally related B cells in the peripheral blood (PB) isotype-specific repertoire of AL patients. A rigorous quantification of lineage trees reveals presence of intraclonal variations in the PB clones compared to the bone marrow (BM) clones, which suggests a common precursor that is still subject to somatic mutation. When compared to normal BM and PB B cells, AL clones showed significant but incomplete impairment of antigenic selection, which could not be detected by conventional R and S mutation analysis. Therefore, graphical analysis of B cell lineage trees and mathematical quantification of tree properties provide novel insights into the process of B cell clonal evolution in AL.

Algorithms↗
PubMed2006

ERK signaling is a molecular switch integrating opposing inputs from B cell receptor and T cell cytokines to control TLR4-driven plasma cell differentiation.

Differentiation of B cells into plasma cells represents a critical immunoregulatory checkpoint where neutralizing Abs against infectious agents must be selected whereas self-reactive Abs are suppressed. Bacterial LPS is a uniquely potent bacterial immunogen that can bypass self-tolerance within the T cell repertoire. We show here that during LPS-induced plasma cell differentiation, the ERK intracellular signaling pathway serves as a pivotal switch integrating opposing inputs from Ag via BCR and from the two best characterized B cell differentiation factors made by T cells, IL-2 and IL-5. Continuous Ag receptor signaling through the RAS/MEK/ERK pathway, as occurs in self-reactive B cells, inhibits LPS induction of Blimp-1 and the plasma cell differentiation program. Differentiation resumes after a transient pulse of Ag-ERK signaling, or upon inactivation of ERK by IL-2 and IL-5 through induction of dual-specificity phosphatase 5 (Dusp5). The architecture of this molecular switch provides a framework for understanding the specificity of antibacterial Ab responses and resistance to bacterially induced autoimmune diseases such as Guillain-Barré syndrome.

Animals↗