UMLS:C0079731 - FACTA Search

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Query: UMLS:C0079731 (B-cell lymphoma)
16,671 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In 14 adult patients suffering from lymphoproliferative diseases, the relation between numbers of lymphocytes determined by the rosette test (nSE) with neuraminidase-treated sheep red blood cells and numbers of lymphocytes giving a positive reaction for acid phosphatase was determined. Statistical analysis of multiple test results in the patients (n = 38) showed highly positive correlation between the two markers. A similar positive correlation in the course of cytostatic treatment was observed in selected patients with type T and B cell lymphoma. The results indicate that determination of acid phosphatase activity can serve as an additional marker of T lymphocytes in groups of patients with lymphoproliferative disease.
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PMID:Correlation between the rosette test with neuraminidase-treated sheep red blood cells and acid phosphatase activity in lymphocytes from patients with lymphoproliferative disease. 31 34

The specificity and properties of a novel IgA receptor expressed on the surface of a tissue culture-adapted B cell lymphoma, T560, that originated in murine gut-associated lymphoid tissue, have been explored. Like the IgA receptors of murine T and splenic B cells studied by others, the T560 IgA receptor is trypsin sensitive and neuraminidase resistant and is up-regulated on T560 cells by exposing them overnight to high concentrations of polymeric IgA. Unlike them, the T560 IgA receptor is inhibited by low concentrations of IgM and high concentrations of IgG2a and IgG2b, binds at pH 4.0 but not at pH 8.0, is down-regulated by activation of protein kinase C and is sensitive to phosphatidylinositol-specific phospholipase C, indicating that it is glycosyl phosphatidylinositol-linked to the cell membrane. It is not a cell-bound form of galactosyl transferase, does not appear to bind to Ig through carbohydrate residues and does not react specifically with antibody to secretory component. It may be a completely new, cross-reactive receptor, perhaps related in some way to the polymeric Ig receptor or to the receptor for IgA expressed on the apical surface of Peyer's patch M cells, which is known to cross-react with IgG. Alternatively, it may be homologous to the highly IgA-specific Fc alpha R of T cells but, perhaps because of its glycosyl phosphatidylinositol linker, may have an ability to move and interact with other Ig receptors on the cell surface such that Ig bound to them are cross-inhibitory.
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PMID:A novel IgA receptor expressed on a murine B cell lymphoma. 137 46

This study reports six non-Hodgkin's lymphoma cases that we called histiocyte-rich B-cell lymphoma (BCL) because of the prominent reactive histiocytic infiltrate obscuring the malignant B-cell population. The involved lymph nodes are characterized by a mixed nodular and diffuse infiltrate and occasionally feature prominent sinuses. The infiltrate is composed of reactive lymphocytes and numerous histiocytes obscuring a tumor population composed of variably sized scattered cells with irregular or multilobar vesicular nuclei. Immunostaining of paraffin sections for the B-cell marker recognized by L26 helps in the identification of these neoplastic cells. The clonal nature and further evidence of the B-cell lineage of this condition is shown by immunoglobulin gene rearrangements detected in three cases. The six cases of histiocyte-rich BCL are remarkably similar clinically: all presented with stage IVB disease with splenomegaly and follow an aggressive clinical course. Except for these features, our series show striking similarities to paragranuloma lymphocyte-predominant Hodgkin's disease, including male preponderance (all patients are male), age distribution (mean age, 41 years), propensity to progress to a diffuse, large B-cell lymphoma (two cases), as well as morphology of the neoplastic B-cell population and expression of Hodgkin's cell markers (Leu-M1 positivity after neuraminidase digestion in three cases, Leu-M1 positivity without neuraminidase digestion in one case, and additional epithelial membrane antigen [EMA] positivity in two cases). Both morphologically and clinically, the present series can be differentiated from other types of infiltrate-rich BCL, such as T-cell-rich BCL. Although additional cases will have to be recognized, histiocyte-rich B-cell lymphoma most likely represents a distinct clinicopathological entity. We speculate that it develops from a subset of B cells that also gives rise to the lymphocytic-histiocytic (L/H) cell, the Hodgkin's cell variant of lymphocyte-predominant Hodgkin's disease, paragranuloma subtype.
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PMID:Histiocyte-rich B-cell lymphoma. A distinct clinicopathologic entity possibly related to lymphocyte predominant Hodgkin's disease, paragranuloma subtype. 172 95

The authors report on the extensive characterization, on normal and pathologic tissues, of the T-cell-specific monoclonal antibody (MoAb) A6, which the authors previously found to identify a fixation- and paraffin-embedding-resistant epitope. A6 reacted with most T lymphocytes, macrophages, and Langerhans' cells of normal tissues and with peripheral T-cell lymphomas (31 of 34), Ki-1+ lymphomas (12 of 18), and T-cell leukemias (1 of 5). All cases of X and non-X histiocytosis examined and monocytic leukemias with mature phenotype only were A6 positive. Three of 47 cases of B-cell lymphoma and leukemia were labeled. Hairy cell leukemias, multiple myelomas, and Hodgkin's and Reed-Sternberg cells were negative. The A6 reactivity was preserved with different fixatives (formalin, Bouin's fluid, Carnoy's fixative, and B5) and decalcification procedures and was slightly enhanced by trypsin digestion. The pattern of reactivity of A6 was similar to that obtained with MoAb UCHL-1, recognizing the CD45RO determinant of leukocyte common antigen; however, in pathologic tissues, A6 labeled a higher percentage of cells than UCHL-1. Cross-blocking and enzyme digestion studies (Pronase E [Sigma Chemical, St. Louis, MO] and neuraminidase [Sigma Chemical]) indicated that the two MoAbs may identify close epitopes on the same molecule. In conclusion, the authors' study indicates that A6 is an excellent reagent for detection of the CD45RO molecule on paraffin-embedded normal and pathologic tissues.
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PMID:A6--a new 45RO monoclonal antibody for immunostaining of paraffin-embedded tissues. 182 47

Many reports have suggested a strong correlation between certain lectin-binding patterns and biological behavior in various tumors. To clarify a relationship between lectin-binding reactivity and survival of patients with diffuse large B-cell lymphoma (B-DLCL), 57 cases with B-DLCL were analyzed by lectin histochemistry and lectin blot method with or without treatment of neuraminidase or acidic hydrolytic conditions. B-DLCL cases were grouped into three types based on the data on lectin-binding reactivity under neuraminidase-treated or untreated conditions: (i) Group A (non-reactive type); (ii) Group B (sialylated type); and (iii) Group C (non-sialylated type). Among various lectins, Phaseolus vulgaris-L (L-PHA) binding reactivity showed that the survival of patients with Group A + B or Group B was significantly shorter than that of patients with Group C. Lectin blot analysis revealed failure of L-PHA-binding to 32 kd and 29 kd glycoproteins, which may be attributable to the masking of L-PHA-binding sites by sialylation or the lack of L-PHA-binding sites, leading to the short survival of patients with B-DLCL. L-PHA-binding reactivity may be a useful marker for the evaluation of survival of patients with B-DLCL.
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PMID:Phaseolus vulgaris leukoagglutinating lectin-binding reactivity in human diffuse large B-cell lymphoma and its relevance to the patient's clinical outcome: lectin histochemistry and lectin blot analysis. 1057 20

Alternate splicing of exons of the CD45 molecule generates multiple isoforms differing in their molecular weights (MWs). In B-lymphocytes the CD45RA isoform was previously shown to be expressed on glycoproteins with MWs of 220 and 205 kDa, while the CD45RO isoform was expressed on glycoproteins with MW of 180 kDa. The present study demonstrated that B cell lymphomas and activated B-cells contain CD45 molecules with a MW of 185 kDa that express the CD45RA and CD45RC specificities but neither the CD45RB nor the CD45RO specificities. 185 kDa CD45RA+ molecules were detected in B cell lymphoma B lines, in Epstein-Barr virus (EBV)-transformed lymphoblastoid cell lines, and in tonsillar B cells, but not in normal, unstimulated peripheral blood B cells. These molecules were not detected in neoplastic and normal T cells. CD45RA+ 185 kDa molecules were present in B cells from three non-Hodgkin's patients in leukemic phase were not detected in B lymphocytes of seven of nine CLL patients tested. Trypsin treatment eliminated only 220 kDa CD45RA+ molecules but not 185 kDa CD45RA+ molecules, indicating that the 185 kDa CD45RA+ molecules are not expressed on the cell surface. Pulse-chase experiments, and studies on the effects of tunicamycin, neuraminidase and O-glycosidase, indicated that the 185 kDa molecules are partially glycosylated CD45RABC molecules that constitute precursors of the 220 kDa molecules. The high concentration of 185 kDa CD45RA+ molecules in B lymphoma cells and in activated B cells seems to reflect a high turnover of CD45RA+ molecules characteristic for these cells.
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PMID:Hyposialated 185 kDa CD45RA+ molecules attain a high concentration in B lymphoma cells and in activated human B cells. 1195 18

Cell surface sialylation and beta1-6 branching of L-PHA reactive oligosaccharides play an important role in metastatic capacities of various tumor cell lines. We analyzed the expression and sialylation of L-PHA reactive oligosaccharides in human diffuse large B cell lymphoma (DLBCL). DLBCL was grouped into three types; i). Group A, non-reactive type with no expression of L-PHA reactive oligosaccharides, ii). Group B, sialylated type with expression of sialylated L-PHA reactive oligosaccharides and iii). Group C, non-sialylated type with expression of non-sialylated L-PHA reactive oligosaccharides. To clarify the linkage of sialic acid residues in L-PHA reactive oligosaccharides of Group B cases, L-PHA lectin histochemistry after treatment with two different neuraminidases was performed. In all Group B cases, L-PHA binding reactivity was found after treatment with Vibrio cholerae neuraminidase. But not after treatment with Newcastle disease virus neuraminidase. These data indicate that alpha2,6-linked sialic acid residues were predominantly involved in sialylation of L-PHA reactive oligosaccharides of Group B. To clarify the relationship between expression of N-acetylglucosaminyltransferase V (GnT-V), which catalyzes beta1-6 branching of L-PHA reactive oligosaccharides, and L-PHA reactivities in DLBCL, we investigated the expression of GnT-V using immunohistochemical methods. Most of the Group B and C cases expressed GnT-V while 33% of Group A cases showed no expression of GnT-V. These data suggest that expression of GnT-V is not always correlated with the expression of L-PHA reactive glycoconjugates. Furthermore, survival of patients in Group A which showed no expression of GnT-V was significantly shorter than that of patients in Group C which expressed GnT-V. Therefore, loss of non-sialylated L-PHA reactive oligosaccharides due to lack of expression of GnT-V in lymphoma cells may be associated with aggressiveness of DLBCL.
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PMID:Alpha-2,6-sialylation of L-PHA reactive oligosaccharides and expression of N-acetylglucosaminyltransferase V in human diffuse large B cell lymphoma. 1453 92

Sphingolipid metabolites are important regulators of cell growth and apoptosis. To clarify the biological roles of cell surface sialylation in the effects of sphingomyelinase (SM) treatment on cell viability, the human diffuse large B cell lymphoma cell line, HBL-2 with or without treatment with Vibrio cholerae neuraminidase, was incubated with exogenous bacterial SM which is a key enzyme of ceramide production from sphingolipids in cell membranes. SM treatment enhanced viability of HBL-2 cells compared to non-treatment after 6 h of incubation. On the other hand, viability of HBL-2 cells was decreased by SM treatment with neuraminidase pre-treatment after 6 and 24 h of incubation, and ceramide production on cell surfaces of SM treated cells was enhanced by neuraminidase treatment as shown by flow cytometric analysis. Furthermore, treatment with D-threo-1-phenyl-2-decanoylamino-3-morpholino-1-propanol, an inhibitor which specifically reduces the activity of UDP-glucose:ceramide glucosyltransferase in combination with SM treatment, causes the viability of HBL-2 cells to be decreased more with neuraminidase pre-treatment than without it. Exogenous C6-ceramide induced HBL-2 cell death, and there was no difference in the effects of C6-ceramide after 6 h of incubation between treatment and non-treatment with neuraminidase. Together these data suggest that alteration in susceptibility of HBL-2 cells to SM by neuraminidase treatment may precede the process of ceramide production, and that cell death through the activation of SM, which induces ceramide production, is regulated by cell surface sialylation in DLBCL.
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PMID:Regulatory roles of cell surface sialylation in susceptibility to sphingomyelinase in human diffuse large B cell lymphoma. 1594 62

Two novel lectins were purified from rhizomes of two sweet flag species, namely Acorus calamus (Linn.) and Acorus gramineus (Solandin Ait.) by affinity chromatography on mannose linked epoxy-activated Sepharose 6B. The apparent molecular mass of the lectins, as determined by gel filtration chromatography, was 56 kDa for ACL and 55 kDa for AGL. In SDS-PAGE, pH 8.3, both lectins migrated with a subunit molecular mass of 13.6 kDa and 13.5 kDa, respectively, under reducing and non-reducing conditions thus indicating the absence of disulphide linkages. Acorus lectins readily agglutinated rabbit, rat and guinea pig erythrocytes. Both ACL and AGL also reacted with RBCs from sheep, goat and human ABO blood groups after neuraminidase treatment. ACL and AGL were inhibited by mannose/glucose and their derivatives. The most effective inhibitor was methyl-alpha-D-mannopyranoside. Acorus lectins were stable up to 55 degrees C, did not require metal ions for their activity and were also affected by high concentrations of denaturants like urea, thiourea and guanidine-HCl. These lectins showed potent mitogenic activity towards mouse splenocytes and human lymphocytes. Both ACL and AGL also significantly inhibited the growth of J774, a murine macrophage cancer cell-line and to lesser extent WEHI-279, a B-cell lymphoma.
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PMID:Novel lectins from rhizomes of two Acorus species with mitogenic activity and inhibitory potential towards murine cancer cell lines. 1595 73

Surface sialylation and glycosylation of tumor cells is known to affect various biological phenomena. In the present study, we analyzed the regulatory roles of cell surface sialylation in cell adhesion to galectin-1 in the human diffuse large B cell lymphoma (DLBCL) cell line, HBL-2, and Burkitt's lymphoma cell line, HBL-8. Vibrio cholerae neuraminidase treatment enhanced HBL-2 cell adhesion to galectin-1, suggesting that sialic acid inhibits HBL-2 cell adhesion to galectin-1. The data from employing two different neuraminidases, Vibrio cholerae and Newcastle disease virus neuraminidase, showed that alpha2,6-linked sialic acid plays an important role in the inhibition of HBL-2 cell adhesion to galectin-1. In addition, neuraminidase treatment enhanced the cell adhesion to galectin-1 much more with the highly sialylated HBL-8 3G3 clone than with the hyposialylated HBL-8 3D2 clone. Flow cytometric analysis revealed the expression of partially sialylated L-PHA reactive oligosaccharides on the surfaces of HBL-2 cells. Swainsonine (SW) treatment also enhanced HBL-2 cell adhesion to galectin-1. These data indicate that SW treatment decreased sialylated L-PHA reactive oligosaccharides resulting in cell surface desialylation and leading to enhancement of cell adhesion to galectin-1. In conclusion, alteration of cell surface sialylation or N-glycan expression regulates cell adhesion to galectin-1 in human malignant lymphoma.
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PMID:The regulatory roles of cell surface sialylation and N-glycans in human B cell lymphoma cell adhesion to galectin-1. 1632 92

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