Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:Q06643 (non-Hodgkin's lymphoma)
 11,307 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Human neutrophil gelatinase was purified to apparent homogeneity. The N-terminal amino-acid sequence of the purified enzyme could be aligned to an internal part of the cDNA-derived amino-acid sequence of 92-kDa type IV collagenase from SV 40-transfected human lung fibroblasts and from a TPA differentiated monocytic cell line, U937. Total amino-acid composition of U937 and neutrophil gelatinases was identical. Gelatinase was susceptible to treatment with o- and n-glycanase, indicating that posttranslational addition of oligosaccharide side chains occurs. An enzyme-linked immunosorbent assay for gelatinase was developed using specific polyclonal rabbit antibodies. The assay was specific, sensitive, accurate, and reproducible. Ninety percent range for plasma gelatinase from normal subjects was 17.3 to 102.9 ng/ml. In patients treated with cytostatic agents for non-Hodgkin's lymphoma, there was a parallel drop in plasma gelatinase and peripheral granulocyte count. This indicates that plasma gelatinase is a marker for circulating neutrophils. Plasma gelatinase does not seem to reflect bone marrow cellularity.
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PMID:Human neutrophil gelatinase: a marker for circulating blood neutrophils. Purification and quantitation by enzyme linked immunosorbent assay. 146 61

Little information is available regarding the role of soluble growth factors in neoplastic B cell proliferation. The authors have measured B cell growth factor (BCGF)-induced proliferation in B lymphocytes isolated from 28 patients with malignancies representing different stages of B cell differentiation. The phorbol ester TPA (12-O-tetradecanoyl phorbol-13-acetate), a potent mitogen and inducer of BCGF receptor expression in normal B cells, was added in combination with BCGF to enhance the proliferative response. These results show that many neoplastic B cells are able to respond to BCGF (32%), particularly when combined with TPA (63%). The response was variable in frequency and magnitude within clinicopathologic groups; cells from patients with non-Hodgkin's lymphoma (NHL) were more refractory to stimulation than those from acute lymphocytic leukemia (ALL) and chronic lymphocytic leukemia (CLL). An attenuated response to BCGF plus TPA was observed in neoplastic cells with high rates of spontaneous DNA synthesis from all histologic categories. These observations suggest that some maximally stimulated cells appear incapable of responding to additional exogenous growth stimuli. Within apparently homogeneous clinicopathologic groups, distinct subgroups of B cell neoplasms can be defined by cellular responses to BCGF. The correlation of this biologic feature with the clinical behavior of the neoplasm requires additional study.
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PMID:Response of neoplasms of B cell lineage to the proliferative effects of B cell growth factor and the phorbol ester TPA. 278 41

Mononuclear cells concentrated from the blood of 16 non-Hodgkin's lymphoma (NHL) patients in the leukemic phase, were exposed to 10 ng/ml of TPA in an attempt to induce differentiation. Immunoglobulin (Ig) secretion, surface markers (SmIg, GP-70), tartrate resistant acid phosphatase (TRAP) and surface features were followed for up to six days in vitro. TPA induced 'hairy cell' like features in NHL cells as defined by cell morphology, ultrastructure, cell surface markers and the presence of TRAP. Unlike the results obtained in patients with CLL, cells from different patients at the same stage of disease reacted in a similar way. Differences were evident between NHL mononuclear cells obtained from patients in partial remission and active disease when compared with those derived from patients in complete remission. In the former group, NHL cells were maximally induced by TPA to secrete Ig and higher proportions of TRAP positive cells. In addition hairy cell features as seen by light and scanning electron microscopy were also more pronounced. TPA also induced the maximal expression of SmIg and GP-70 in cells derived from patients in this group. Patients with NHL in leukemic phase in complete remission did not express surface membrane GP-70 before or after TPA treatment while SmIg was expressed to some degree before TPA treatment and further induced following treatment with TPA. GP-70 appears to be a more reliable marker for follow-up of NHL patients than any other marker studied here.
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PMID:Induction of plasmacytoid and hairy cell features by phorbol esters (TPA) in B-lymphoma cells: attempted correlation with disease activity. 326 7

Hairy cell leukemia (HCL) mononuclear cells were incubated with the phorbol ester TPA in an attempt to induce further maturation and were compared with B cell chronic lymphocytic leukemia, prolymphocytic leukemia, and non-Hodgkin's lymphoma cells. Morphology, surface features, membrane markers, tartrate-resistant acid phosphatase, and Ig secretion were examined. HCL cells spread and adhered firmly after TPA, producing elongated filopodia. Cells still retained ribosomal lamellar complexes, and increased numbers of dense bodies were seen. TPA enhanced the adherent and phagocytic properties of HCL cells, producing a modest increase in the expression of membrane Ig, GP-70, and Leu-M5 markers, tartrate-resistant acid phosphatase, and Ig secretion. Other neoplastic B cells behaved differently, forming readily detachable clumps without elongated filopodia. Maturation to plasma cells and hairy cell features were readily evident in all cases. These differences in growth patterns were consistent and may be used to distinguish HCL from other B cell neoplasias.
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PMID:Phorbol esters and hairy cell leukemia: effects on cell morphology and surface membrane features and comparison with other B cell leukemias. 347 38

Mononuclear cells concentrated from 11 patients with chronic lymphocytic leukemia (CLL), 7 with non-Hodgkin's lymphoma in leukemic phase (NHL), 5 with hairy cell leukemia (HCL), 1 with prolymphocytic leukemia (PLL), and 1 with plasma cell leukemia (PCL) were induced to differentiate with various doses of TPA. The degree of induction was followed for up to 6 days by measuring the expression of surface membrane markers (SmIg and GP-70) and Ig secretion, the induction of tartrate-resistant acid phosphatase (TRAP) and by recording ultrastructural changes as seen by electronmicroscopy. The results show a dose and time dependency of the TPA effect and a great heterogeneity in the cellular response, particularly in cells obtained from B-CLL patients. TPA induced two main features, namely the development of "plasmacytoid" or "hairy cell" leukemia features that clearly depended on the dose and duration of treatment with the phorbol ester. The plasmacytoid features were more frequently encountered with lower doses (1 ng/ml) of TPA and were more evident after shorter exposures to TPA (1-2 days). Nevertheless, the hairy cell features were more striking after incubation with higher concentrations of TPA (10-100 ng/ml) after longer periods of incubation (up to 6 days) with lower doses of TPA. The various features of differentiation measured including cell morphology, surface membrane markers, Ig secretion, and TRAP staining, were frequently independent of each other, suggesting an autonomous pathway of differentiation for some of these features. Furthermore, in most of the cases, hairy cell leukemia features were obtained more frequently following TPA exposure than plasmacytic changes.
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PMID:Phorbol ester induction of plasmacytoid and hairy cell leukemia features in B-type lymphocytic leukemias: the relation to B-cell differentiation and maturation. 349 82

In this review we have summarized our experiences of serological analysis of MHC class II antigen expression in human B cell malignant disease. Cells from a large number of cases of B-cell chronic lymphocytic leukaemia (CLL) and non-Hodgkin's lymphoma (NHL) have been examined for expression of class II antigens. Using a number of monoclonal antibodies which in some cases are specific for class II subregion products (DP, DQ and DR), MHC class II antigens were detected by indirect immunofluorescence and fluorescent activated cell sorter analysis in CLL and by immunohistochemical staining in NHL. At the cell surface in many cases of B cell malignant disease, products of the different class II subregion genes are non-coordinately expressed. The most commonly occurring pattern of non-coordinate expression of class II molecules is of expression of DP and DR antigens in the absence of detectable DQ expression. These findings are in contrast to normal B lymphocytes where DP, DQ and DR antigens are expressed together at the cell surface. There is considerable heterogeneity among cases comprising individual histopathological categories of B cell malignancy, and in many instances heterogeneous class II phenotypes are also found on cells from the same tumour. In chronic lymphocytic leukaemia, class II antigen expression is inducible in vitro by treating the cells with the phorbol ester TPA. CLL cells treated with TPA have much increased levels of class II antigen expression at the cell surface and much increased steady state levels of class II specific mRNA transcripts detectable with complementary DNA probes. Aberrant class II antigen expression may be involved in the pathogenesis of B cell malignant disease.
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PMID:Expression of MHC class II antigens in human B-cell leukaemia and non-Hodgkin's lymphoma. 351 12

This report documents phorbol ester (TPA)-induced changes in cell morphology, and in vitro growth patterns in 9 patients with hairy cell leukemia (HCL), 21 with B-type CLL and non-Hodgkin's lymphoma in leukemic phase (NHL), and 10 with acute non lymphoblastic leukemia (ANLL). TPA caused cells from HCL to adhere strongly and produce elongated cytoplasmic extensions. Many of these cells had an appearance resembling fibroblasts, while others showed marked surface ruffling and spreading containing increased dense bodies, and phagolysosomal vacuoles as seen by transmission electron microscopy. This HCL in vitro growth pattern after TPA exposure differed from that seen in B-CLL and NHL cells, which only adhered moderately after 72 hours and readily detached in clumps. CLL and NHL-cells did not show ultrastructural features of macrophages but had either plasmacytic or HCL features. It is suggested that these different growth patterns may aid in distinguishing HCL from other B-cell neoplasias. The expression of surface markers, tartrate resistant acid phosphatase (TRAP) and Ig secretion were studied in some B-CLL, NHL and HCL cells after exposure to different concentrations of TPA for up to 6 days. Results showed that the documented changes were frequently both dose and time dependent and the most striking HCL-features were encountered after 6 days incubation with higher concentrations of TPA. However, individual variation from case to case was noted. Nevertheless, it seems that TPA induces neoplastic B-cells to mature into secreting plasmacytoid lymphocytes, and cells with features of HCL with variable expression of surface markers and TRAP.
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PMID:Phorbol ester (TPA)-induced surface membrane alterations in B-type hairy cell and lymphocytic leukemia cells. 381 25

Primary effusion lymphoma (PEL) is a new lymphoma entity occurring predominantly, but not exclusively in HIV+ patients with acquired immunodeficiency syndrome (AIDS). PEL grows exclusively in body cavities as serous lymphomatous effusion without evidence of mass disease or dissemination. The cells are infected with the newly discovered human herpesvirus-8 (HHV-8), often accompanied by co-infection with Epstein-Barr virus (EBV). Several lymphoma cell lines have been established from patients with AIDS- and non-AIDS-associated PEL. Given their phenotypical relationship to plasma cells, several cytokines may be important for growth and survival of PEL cells. We investigated the spectrum of cytokines produced by nine HHV-8+ PEL cell lines, in comparison with five Burkitt lymphoma, seven other B non-Hodgkin's lymphoma (B-NHL) and seven multiple myeloma-derived cell lines. In addition, we tested the response of the PEL cells to selected cytokines and the effects of neutralizing anti-cytokine and anti-cytokine receptor antibodies. Using specific ELISAs, PEL cell lines were found to produce large amounts of interleukin-6 (IL-6; 10-5000 pg/ml), IL-6 soluble receptor (IL-6sR; 30-600 pg/ml), IL-10 (600-80,000 pg/ml) and oncostatin M (OSM; 50-80 pg/ml) which in most cases were significantly higher than the levels produced by the Burkitt, B-NHL or myeloma cell lines; on the contrary, PEL cell lines did not elaborate significant levels of macrophage inhibitory protein (MIP-1alpha) and leukemia inhibitory factor (LIF). However, the levels of MIP-1alpha were increased 10- to 100-fold by treatment with phorbol ester TPA. PEL cell lines did not respond proliferatively to IL-6, IL-10, IL-11, LIF, MIP-1alpha, or OSM. Incubation with IL-6sR and IL-6 inhibited cell growth. Anti-IL6 neutralizing antibodies had no effect on PEL cell line proliferation; conversely, whereas anti-IL6R alone inhibited only weakly, anti-gp130 and anti-gp130 plus anti-IL6R showed strong inhibitory effects (>20% inhibition in 5/9 lines and >60% inhibition in 3/9 lines). In summary, PEL cell lines produce high amounts of cytokines (IL-6, IL-10, OSM); proliferation could be inhibited by blocking the receptors of the IL-6 signaling pathway.
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PMID:Constitutive cytokine production by primary effusion (body cavity-based) lymphoma-derived cell lines. 1021 73