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)

Injection of a nonlymphomagenic ecotropic virus 24-666 isolated from a B cell lymphoma of AKR origin into young AKR mice (1-60 days old) inhibited spontaneous T cell lymphoma development. The reduction in T cell lymphoma incidence (16/106-15%) was accompanied with the appearance of B cell lymphomas (16/106-34%) in older mice (500 days mean latency). Infection of newborn to 60-day-old AKR mice with 24-666 prevented changes in thymus subpopulations and expression of MuLV-related cell surface antigens, normally observed in the thymus of 5- to 6-month-old AKR mice prior to lymphoma development. Thymuses of 24-666-infected 9- to 12-month-old mice lacked recombinant dual tropic virus (DTV) expression and retained the thymus pattern of 2-month-old AKR mice. At 12 months after 24-666 administration a striking decrease in Thy1.1 level and in the CD4+ CD8+ population and an increase in CD4- CD8- cells and in mu+ B cells, predominantly Ly1+, were observed. The presence of B cells in these thymuses was also reflected in the high response of thymocytes to LPS blastogenesis accompanied by a decreased response to PHA. Although T cell lymphoma development was markedly reduced by 24-666 administration, the establishment of potential lymphoma cells (PLC) was not affected. Transfer of lymphoid cells from 12-month-old grossly normal 24-666-infected mice to the appropriate recipients resulted in a high incidence (64-80%) of B cell lymphoma development. Thus, 24-666 seems to act through interference with the establishment of DTV in the thymus, thereby preventing PLC promotion to overt T cell lymphomas. Lack of the favorable microenvironment for PLC development in the T cell pathway enables PLC development in the B cell pathway in older mice.
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PMID:Prevention of spontaneous AKR T cell lymphomagenesis by 24-666, a virus isolated from an AKR B cell lymphoma. 167 38

Three predominantly CD8+ CTL lines, TIL 501, TIL 620, and TIL 660, were generated from three HLA-A2+ melanoma patients by culturing tumor-infiltrating lymphocytes in 1000 U/ml IL-2. These tumor-infiltrating lymphocytes lysed 12 of 18 HLA-A2+ autologous and allogeneic melanomas, but none of 20 HLA-A2-negative melanomas. They also did not lyse the MHC class I negative lymphoma-leukemia cell lines, Daudi, K562, or HLA-A2+ non-melanoma cell lines including PHA or Con A-induced lymphoblast, fibroblast, EBV-transformed B cell, Burkitt's B cell lymphoma, and colon cancer cell lines. Autologous and allogeneic melanoma lysis was inhibited by anti-CD3, by anti-MHC class I, and by anti-HLA-A2 mAb, indicating recognition of shared tumor Ag among melanoma cell lines in a TCR-dependent, HLA-A2-restricted manner. Six HLA-A2-negative melanoma cell lines obtained from five HLA-A2-negative patients were co-transfected with the HLA-A2.1 gene and pSV2neo. All 17 cloned transfectants expressing cell surface HLA-A2 molecules, but none of 12 transfectants lacking HLA-A2 expression, were lysed by these three HLA-A2-restricted, melanoma-specific CTL. Lysis of the HLA-A2+ transfectants was inhibited by anti-CD3, by anti-MHC class I, and by anti-HLA-A2 mAb, indicating recognition of shared tumor Ag on transfectants in a TCR-dependent, HLA-A2-restricted manner. These results identify the HLA-A2.1 molecule as an Ag-presenting molecule for melanoma Ag. They also suggest that common melanoma Ag are expressed among melanoma patients regardless of HLA type. These findings have implications for the development of melanoma vaccines that would induce antitumor T cell responses.
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PMID:Shared human melanoma antigens. Recognition by tumor-infiltrating lymphocytes in HLA-A2.1-transfected melanomas. 172 79

We investigated the expression of fos oncogene proteins in lymphoproliferative disorders, using a monoclonal antibody (FO-120) that was prepared against a synthetic oligopeptide of fos protein (amino acid sequence from 127 to 152). Although peripheral blood leukocytes were rarely positive for FO-120, they were transiently stained after lectin (PHA) stimulation. After culture with IL-2 for 1 or 2 weeks, less than 40% of the lymphocytes weakly reacted with FO-120, whereas strongly positive cells were detected in more than 70% of cells in half the T-cell lines established from preleukemic state of adult T-cell leukemia (pre-ATL) and all of ATL derived T-cell lines. All in vivo specimens of non-Hodgkin's malignant lymphomas, except for one case of T-cell lymphoma were also strongly positive. In addition, the extent of the antibody reactivity correlated with the histopathological grade of malignancy in B-cell lymphoma. The reactivity to most AILD-IBL lesions overlapped with that to T-lymphomas, and could be distinguished from that to reactive lesions. FO-120 appears to be a useful tool for detecting early neoplastic changes in lymphoproliferative disorders.
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PMID:Detection of fos oncogene products by monoclonal antibody FO-120 in lymphoproliferative disorders. 251 20

We report on 11 patients from 8 independent families (3 pairs of sibs) with a complex clinical pattern including microcephaly, peculiar "bird-like" face, growth retardation, and, in some cases, mild-to-moderate mental deficiency. Most of the patients have recurring respiratory tract infections. One girl has developed B-cell lymphoma. A detailed anthropometric study of 15 physical parameters, including 3 cephalic traits, was performed. It was possible to study the chromosomes of PHA-stimulated lymphocytes in all of the patients. We found structural aberrations with multiple rearrangements, preferentially involving chromosomes 7 and 14 in a proportion of metaphases in all individuals. Profound humoral and cellular immune defects were observed. Serum AFP levels were within normal range. Radioresistant DNA synthesis was strongly increased in all 8 patients who were hitherto studied in this respect. Our patients fulfill the criteria of the Nijmegen breakage syndrome, which belongs to the growing category of ataxia telangiectasia-related genetic disorders. In light of the increased predisposition to malignancy in this syndrome, an accurate diagnosis is important for the patient.
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PMID:Eleven Polish patients with microcephaly, immunodeficiency, and chromosomal instability: the Nijmegen breakage syndrome. 754 70

CD3 engagement has been used as a surrogate for antigen-specific stimulation to trigger T cell effector functions. Exogenous IL-2 has been used to prolong and amplify CD3-induced T cell activation. Previous studies have been shown that CD3 reactivity is increased in cancer patients with preactivated (> 10% HLA-DR+) T cells in the peripheral blood. In this study, we report 9 courses of a single infusion of anti-CD3 mAb (OKT3) followed by continuous infusion of intermediate dose IL-2 in 4 cancer patients [2 multiple myeloma (MM), 1 B-cell lymphoma (NHL), 1 metastatic melanoma (ME)] with advanced disease and > 10% HLA-DR+ T cells in the peripheral blood. An increase of lymphocytes, equally distributed between CD4+ and CD8+ subsets, was observed during treatment. Activation was phenotypically documented by the emergence of CD25+ cells in the peripheral blood. Unexpectedly, functional studies [including proliferation to mitogens (PHA, OKT3) and cytotoxicity assays (NK and LAK activities)] did not parallel phenotypic data and a slight decrease of all functions was observed after OKT3 and IL-2 treatment. OKT3 and IL-2 infusions were well tolerated and no limiting toxicity was observed. The treatment did not revert tumor progression in the 2 patients with progressive disease (NHL, ME) and had only minimal effects in the 2 MM patients with stable disease. These data indicate that the sequential administration of OKT3 and IL-2 had no anti-tumor activity in this small series of patients with advanced cancer who were selected for treatment because of an increased number of HLA-DR+ T cells in the peripheral blood. A discrepancy was observed between the emergence of CD25+ T cells and the clinical outcome.
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PMID:Clinical and immunological studies in advanced cancer patients sequentially treated with anti CD3 monoclonal antibody (OKT3) and interleukin-2. 872 15

The results of cytogenetic studies are reported in 76 patients with B-chronic lymphoproliferative disorders (B-CLPD): 60 patients with chronic lymphocytic leukemia (CLL), six with follicular lymphoma in leukemic phase (FLLP), five with splenic B-cell lymphoma with villous lymphocytes (SLVL), two with chronic prolymphocytic leukemia (CPL), two with hairy cell leukemia (HCL), and one with plasma cell leukemia (PCL). PHA (phytohemagglutinin), PWM (pokeweed mitogen), LPS (lipopolysaccharide from Escherichia Coli), TPA (phorbol 12-myristate acetate), IL6 (interleukin 6), and DxS (dextran sulfate) were used as mitogens. Mitoses were obtained in 75 cases. Clonal aberrations could be demonstrated in 34 cases (44%). In CLL, classical type, chromosomes 6, 11, and 13 were more frequently involved, whereas trisomy 12 was frequently found in CLL mixed-cell type, in FLLP, and CPL. In SLVL the deletion del(7)(q32) is noteworthy and miscellaneous chromosome abnormalities in the remaining patients were observed. Regarding the efficiency of mitogens, PHA turned to be the most effective in obtaining metaphases and in detecting clonal chromosomal aberrations.
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PMID:Cytogenetic studies in seventy-six cases of B-chronic lymphoproliferative disorders. 907 2

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

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

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


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