Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0079731 (B-cell lymphoma)
 16,671 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

An EBV-negative B-cell lymphoma cell line designated as HBL-1 was established from the pleural effusion of a patient with malignant lymphoma, diffuse, large cell. Surface marker studies revealed that HBL-1 cell possessed the same phenotypes of a mature B-cell as the original lymphoma cell from pleural effusion. HBL-1 closely resembled morphologically to the original lymphoma cells observed in the lymph node biopsy and pleural effusion. Chromosome analysis revealed that HBL-1 cells showed chromosomal aberrations of a 14q+ marker chromosome as the result of a translocation between chromosomes 14 and 16. Heterotransplantation to subcutaneous tissue of an athymic nude mouse has succeeded, but intraperitoneal heterotransplantation has failed. Tumors were localized in the subcutaneous tissues and no metastasis was found. This newly established cell line may facilitate immunological and oncogenic studies for human B-cell lymphomas.
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PMID:Establishment and characterization of an Epstein-Barr virus negative B-cell lymphoma cell line and successful heterotransplantation. 285 3

A new human B-cell lymphoma-derived cell line, designated HBL-2, was established from peripheral blood of a 17-year-old male during terminal leukemic phase. HBL-2 cells were single cell suspensions when cultured in RPMI 1640 with 10% fetal calf serum promoting a doubling time of about 20 hours. Cell marker studies revealed Ia and surface immunoglobulin positive, cytoplasmic immunoglobulin and Epstein-Barr nuclear antigen negative. Chromosome analysis showed a male aneuploid karyotype with 14q+ and other abnormal markers. Under electron microscopy, the cells exhibited clear nucleoli, fine chromatin, and were in a primary differentiated state. The establishment of HBL-2 cell line provides a powerful tool in studying the oncogenesis of B-cell malignancy.
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PMID:Establishment and characterization of a new human lymphoma-derived cell line--HBL-2. 389 42

Kaposi's sarcoma (KS)-associated herpesvirus or human herpesvirus 8 (KSHV/HHV8) is the likely cause of KS and primary effusion lymphomas or body cavity-based lymphomas (BCBLs). A latency-associated nuclear immunofluorescence antigen (LANA) (D. H. Kedes, E. Operskalski, M. Busch, R. Kohn, J. Flood, and D. Ganem, Nat. Med. 2:918-924, 1996; S. J. Gao, L. Kingsley, M. Li, W. Zheng, C. Parravicini, J. Ziegler, R. Newton, C. R. Rinaldo, A. Saah, J. Phair, R. Detels, Y. Chang, and P. S. Moore, Nat. Med. 2:925-928, 1996) and a 222- to 234-kDa nuclear protein (LNA) (S. J. Gao, L. Kingsley, D. R. Hoover, T. J. Spira, C. R. Rinaldo, A. Saah, J. Phair, R. Detels, P. Parry, Y. Chang, and P. S. Moore, N. Engl. J. Med. 335:233-241, 1996) have previously been described in BCBL cell lines by immunofluorescence and Western blotting techniques, respectively. To identify the viral gene(s) encoding this antigen(s) we screened a cDNA library from HBL-6 cells, a B-cell lymphoma cell line persistently infected with KSHV/HHV8, with KS patient sera. One set of positive clones contained the 3' end of orf73, as well as the complete orf72 and orfK13, and another set contained the 5' end of orf73. Comparison of cDNA sequences with the KSHV/HHV8 genomic sequence revealed a splice event, occurring upstream of orf73. Immunoaffinity purified antibodies to a recombinant carboxy-terminal fragment of the orf73-encoded protein showed the characteristic speckled nuclear immunofluorescence pattern of LANA and reacted with the 222- to 234-kDa LNA on Western blots. Expression of full-length orf73 in bacteria and COS7 cells reproduced the LNA banding pattern. Immunohistochemistry on cases of nodular KS revealed that orf73/LNA is expressed in the nucleus of KS spindle cells. These findings demonstrate that orf73 encodes the 222- to 234-kDa LNA, is a component of LANA, and is expressed in KS tumor cells.
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PMID:The 222- to 234-kilodalton latent nuclear protein (LNA) of Kaposi's sarcoma-associated herpesvirus (human herpesvirus 8) is encoded by orf73 and is a component of the latency-associated nuclear antigen. 922 81

L-PHA reactive oligosaccharides are found on the surface of HBL-2 cells, a lymphoma cell line, established from a human diffuse large B cell lymphoma (DLBCL). Swainsonine (SW) is a potent inhibitor of alpha-mannosidase II which catalyzes the biosynthesis of complex type N-linked oligosaccharides in human cells. CD40L stimulation of HBL-2 cells leads to their prolonged survival. Reduction in the expression of N-linked oligosaccharides, including L-PHA reactive oligosaccharides, on the cell surface by SW treatment resulted in enhancement of HBL-2 cell survival by CD40L stimulation. From an Annexin V assay the enhancement of CD40L-mediated HBL-2 cell survival by SW treatment may have resulted from anti-necrotic effects after 48 h of incubation. Bcl-2 enzyme linked immuno sorbent assay (ELISA) data showed that the expression of bcl-2 protein was enhanced by CD40L stimulation alone and also by CD40L stimulation along with SW treatment. However, there were no significant differences in the amount of bcl-2 protein with these treatments. Therefore, the enhancement of CD40L-mediated cell survival by SW treatment did not depend on the enhancement of bcl-2 protein expression. Furthermore, SW treatment of HBL-2 cells led to degradation of the heavy chain of IgM and rescued HBL-2 cells from anti-IgM-induced growth inhibition. Anti-IgM induced growth inhibition of HBL-2 cells prevented the inhibition of cell death by CD40L. From the present results it is possible that reduction of N-glycosylation of the heavy chain of IgM by SW treatment may reduce anti-IgM-induced growth inhibition, and reduction in anti-IgM-induced growth inhibition due to altered N-glycosylation may enhance CD40-CD40L-mediated cell survival through TRAF2 which interacts with both IgM and CD40 in HBL-2 cells.
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PMID:Regulatory roles of N-glycosylation of immunoglobulin M in CD40-CD40L-mediated cell survival of human diffuse large B cell lymphoma. 1506 43

Beta1-6 branching of L-PHA reactive oligosaccharides, one of the N-glycan structures, plays an important role in the biological behavior of various tumor cell lines. We reported previously that the expression of L-PHA reactive oligosaccharides was closely associated with the prognosis of patients with human diffuse large B cell lymphoma (DLBCL). In the present study, by Western blotting, we analyzed the N-glycosylation patterns in CD45 having L-PHA reactive oligosaccharides. In two cases of DLBCL which do and do not express non-sialylated L-PHA reactive oligosaccharides CD45 was found to be about 180-210 kDa and 180-200 kDa, respectively. Furthermore, after endoglycosidase F3 treatment the CD45 in both cases was found to be 190 or 160 kDa. Therefore, the differences in CD45 molecular weight between the two cases is due to differences in the amount of N-glycosylation. To clarify the biological functions of CD45 N-glycans in DLBCL, we analyzed the antiproliferative effects on human lymphoma cells of bovine galectin-1 (beta-galactoside-binding lectin-1), which reacts with CD45 N-glycans. Bovine galectin-1 stimulation of the DLBCL cell line HBL-2 resulted in inhibition of its growth in vitro. Swainsonine (SW) is a potent inhibitor of alpha-mannosidase II, which catalyzes the synthesis of complex type N-linked oligosaccharides. Reduction in expression of N-linked oligosaccharides, including L-PHA reactive oligosaccharides, on the cell surface by SW treatment prevented the growth inhibition of HBL-2 cells by galectin-1. On Western blots one 190 kDa isoform of the three CD45 isoforms which have N-linked oligosaccharide ligands for galectin-1, was detected with a reduction in molecular weight of about 5 kDa after SW treatment. These data suggested that the amount of CD45 N-glycans is reduced by SW treatment, and that this reduction of N-glycans prevents the interaction between CD45 and galectin-1. Alteration in N-glycosylation of CD45 may regulate lymphoma cell growth in DLBCL through the interaction between the N-glycans of CD45 and galectin-1.
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PMID:Altered N-glycosylation in CD45 and regulatory roles of altered N-glycosylation in galectin-1-induced growth inhibition in human diffuse large B cell lymphoma. 1558 10

To clarify the functions of CD45 N- and O-glycans in diffuse large B cell lymphoma (DLBCL), we analyzed the antiproliferative effects of bovine galectin-1 (beta-galactoside-binding lectin-1), which reacts with CD45 N-glycans and O-glycans, on human lymphoma cells. Bovine galectin-1 induced cell death of the DLBCL cell line HBL-2 in vitro. Swainsonine (SW) is a potent inhibitor of alpha-mannosidase II which catalyzes the synthesis of complex type N-linked oligosaccharides, and benzyl-GalNAc (BZGalNAc) is a potent inhibitor of O-glycosylation. Treatment with SW or BZGalNAc prevented cell death of HBL-2 cells by galectin-1. Western blot analysis revealed SW treatment reduced the molecular weight by about 5 kDa of one isoform at 190 kDa among three isoforms of CD45 which have N-linked oligosaccharide ligands for galectin-1. BZGalNAc treatment reduced the molecular weight of another isoform by about 15 kDa. These data suggest that the amount of CD45 N-glycans or O-glycans was reduced by SW and BZGalNAc treatment, respectively, and that reduction of CD45 N-glycans or O-glycans may prevent the interaction between CD45 and galectin-1. Alteration in CD45 N-glycans or O-glycans may regulate cell death of lymphoma cells through the interaction between CD45 N-glycans or O-glycans and galectin-1 in DLBCL.
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PMID:Regulatory roles of altered N- and O-glycosylation of CD45 in galectin-1-induced cell death in human diffuse large B cell lymphoma. 1575 3

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

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

Sphingolipid metabolites are important regulators of cell growth and death. In the present study, we examined the function of cell surface sialic acid in exogenous sphingosine-1-phosphate (S-1-P) or sphingosine-induced cell death. HBL-2 human diffuse large B cell lymphoma cells were incubated with or without Vibrio Cholerae neuraminidase followed by S-1-P or sphingosine. Flow cytometric analysis using Limax flavus agglutinin, a sialic acid-specific lectin, showed that sialylated glycoconjugates are present on the surface of HBL-2 cells and that they were removed by neuraminidase. In addition, the pretreatment with neuraminidase enhanced S-1-P- and sphingosine-induced cell death, an effect that was not dependent on caspase activation. Furthermore, the cell death induced by S-1-P and sphingosine was morphologically distinct from apoptosis. We further examined S-1-P-induced cell death in two clones of HBL-8 Burkitt lymphoma cells with different amounts of cell surface sialic acid. Clone 3G3, which is hypersialylated, was less sensitive to S-1-P than the 3D2 clone, which is hyposialylated, suggesting that the extent of surface sialylation influences the sensitivity to S-1-P. In conclusion, S-1-P and sphingosine induce cell death, and the sensitivity of human B lymphoma cells to these agents appears to depend on the amount of sialic acid on their cell surfaces.
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PMID:Regulatory roles of cell surface sialylation in sphingolipid-induced cell death in human B cell lymphoma. 1696 5

Galectin-3 is a soluble endogenous lectin in vertebrates and is implicated in a variety of biological functions, including tumor cell adhesion, proliferation, differentiation, apoptosis, cancer progression and metastasis. In the present study, we analyzed the role of galectin-3 in apoptosis in human malignant lymphoma. Galectin-3 induced cell death in the HBL-2 human diffuse large B cell lymphoma cell line. A morphological examination and annexin V assays revealed that galectin-3-induced cell death is consistent with apoptosis and swainsonine, a potent inhibitor of alpha-mannosidase II, which catalyzes the synthesis of complex type N-linked oligosaccharides, inhibited galectin-3-induced apoptosis in HBL-2 cells. These results suggest that galectin-3 induces apoptosis in HBL-2 cells by interacting with cell surface N-linked oligosaccharides. Furthermore, treatment of cells with Vibrio Cholerae neuraminidase enhanced galectin-3-induced apoptosis, suggesting that cell surface sialylation regulates galectin-3-induced apoptosis in human B cell lymphoma. In conclusion, our results indicate that galectin-3-induced apoptosis is regulated by cell surface expression of N-glycans and sialic acid in human diffuse large B cell lymphoma. This mechanism may be involved in the malignant behavior of human lymphoma cells.
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PMID:Cell surface N-glycosylation and sialylation regulate galectin-3-induced apoptosis in human diffuse large B cell lymphoma. 1828 10


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