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

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

Influenza B virus infections are less common than infections caused by influenza A virus in critically ill patients, but similar mortality rates have been observed for both influenza types. Pneumonia caused by influenza B virus is uncommon and has been reported in pediatric patients and previously healthy adults. Critically ill patients with pneumonia caused by influenza virus may develop acute respiratory distress syndrome. We describe the clinical course of a critically ill patient with diffuse large B-cell lymphoma nongerminal center B-cell phenotype who developed acute respiratory distress syndrome caused by influenza B virus infection. This paper emphasizes the need to suspect influenza B virus infection in critically ill immunocompromised patients with progressive deterioration of cardiopulmonary function despite treatment with antibiotics. Early initiation of neuraminidase inhibitor and the implementation of guidelines for management of severe sepsis and septic shock should be considered.
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PMID:Acute respiratory distress syndrome caused by influenza B virus infection in a patient with diffuse large B-cell lymphoma. 2211 May 13

The important role of sialic acid in various biological phenomena is well-established. In order to further clarify the role of sialic acid in cell death induced by various stimuli, the present study compared the cell survival of the HBL-2 human diffuse large B-cell lymphoma cell line upon anticancer drug-induced cell death, with or without neuraminidase pretreatment: Cell survival was assessed using flow cytometry. Upon treatment with doxorubicin or etoposide, the HBL-2 cell viability decreased. In etoposide-induced cell death, the HBL-2 cells demonstrated nuclear fragmentation, which was consistent with morphologically apoptotic cells. In addition, a higher decrease in the cell viability of etoposide-treated HBL-2 cells was observed in cells pretreated with neuraminidase compared with cells that were not pretreated. Furthermore, the caspase-3, caspase-8 and caspase-9 activities in etoposide-induced apoptosis demonstrated a greater increase upon neuraminidase pretreatment compared with no neuraminidase pretreatment. In conclusion, cell surface sialylation appears to protect lymphoma cells from anticancer drug-induced apoptosis.
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PMID:Caspase-dependent drug-induced apoptosis is regulated by cell surface sialylation in human B-cell lymphoma. 2662 54


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