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

We analyzed the overall structures of N-linked oligosaccharides on glycoproteins of various murine lymphocytic and lymphoma cells employing a newly developed method which was performed on high-performance liquid chromatography after derivatization of oligosaccharides with 2-aminopyridine. A total of 15 types of bi, tri- and tetra-antennary N-acetyllactosamine-type oligosaccharides with or without fucose and oligomannose-type oligosaccharides were identified on these cells in variable amounts depending on the type and maturation stage of the cells. It was found that all murine lymphocytic cells carry N-acetyllactosamine-type oligosaccharides with the additional alpha-linked galactose residue on the non-reducing ends. Thymocytes had exceptionally large amounts of oligosaccharides with one or even two alpha-galactose residues per molecule. In contrast, peripheral resting T cells possessed those oligosaccharides only in a small amount, although the cells produced more the oligosaccharides after stimulation with Con A. Two thymoma lines such as BW 5147 and EL-4 and one B cell lymphoma line WEHI231 contained relatively large amount of oligosaccharides with alpha-galactose residues. Significant change of the molar ratio of component carbohydrates by cell activation was observed also in oligommanose-type oligosaccharides which were few in resting T cells but were markedly increased in Con A activated cells. Molar ratio of triantennary oligosaccharides in total N-acetyllactosamine type oligosaccharides was high in thymocytes and low in resting T cells, but was increased in T cells after Con A activation. It was also very high in WEHI 231 B cell lymphoma. Although BW 5147 and EL-4 thymoma did not contain tri-antennary oligosaccharides in high proportion, they carried larger tetra-antennary oligosaccharides with an N-acetyllactosamine repeating unit in definitive amounts. It is suggested from these results that overall structures of oligosaccharides on cell surface proteins of lymphocytes are finely controlled with link to cell differentiation, activation and transformation.
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PMID:Cell type and maturation stage-dependent polymorphism of N-linked oligosaccharides on murine lymphocytes and lymphoma cells. 192 4

Different types of tumors developed in transgenic mice following the introduction of the entire coding region of ras, myc or SV40 large T gene (T) linked to the same regulatory unit, consisting of a human immunoglobulin gene enhancer (Ig) and SV40 early gene promoter (Tp) with a 21-bp repeat. All the 12 transgenic mice harboring the intact T gene developed a variety of tumors including choroid plexus tumor, B cell lymphoma, histiocytic lymphoma, thymoma and others. This suggests that the Ig/Tp regulatory unit has transcriptional activity in these heterologous tissues. With this regulatory unit, myc gene induced solely pre-B cell lymphomas (five out of nine mice). Contrary to our expectation, however, the mutated ras gene induced lung adenomatous tumors in six out of eight transgenic mice over the 10-month observation period; the tumors are histologically comparable to adenocarcinomas in man. The tumors developed as early as 4 weeks after birth and the introduced ras gene was as efficiently expressed in both normal and neoplastic bronchioloalveolar epithelial cells as in normal lymphoid cells. An unidentified secondary event thus appears to be necessary for these ras-expressing cells to become neoplastic, as observed for myc (Leder et al., 1986). In a variety of tumors induced by Ig/Tp-T, on the other hand, T gene was expressed only in the tumor cells, but not in normal cells. Thus, derepression of T gene in normal cells appears to be closely related to their malignant change as observed in development of pancreatic acinar cell tumors by the T gene (Ornitz et al., 1985). These results suggest that ras and myc oncogenes penetrate differentially specific types of cells, while the SV40 T gene is tumorigenic in a variety of cell types.
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PMID:Driven by the same Ig enhancer and SV40 T promoter ras induced lung adenomatous tumors, myc induced pre-B cell lymphomas and SV40 large T gene a variety of tumors in transgenic mice. 283 50

In 3 patients suffering from follicular center-cell-derived B-cell lymphoma with primary cutaneous manifestation, antiadult T-cell leukemia-associated antigen antibodies were detected by the ELISA. In one of the patients, the husband and the dog had died from thymoma and from malignant lymphoma, respectively.
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PMID:Antihuman T-cell leukemia/lymphoma virus antibodies in three patients with primary cutaneous B-cell lymphoma. 283 89

T cell hybridomas with specificity for VSV (vesicular stomatitis virus)-infected cells were generated in an attempt to better define the la-restricted helper T cell response to VSV. The hybridomas were created by fusing BALB/c (H-2d) anti-VSV immune spleen cells to the murine thymoma BW 5147. These hybridomas produce IL-2 when stimulated with VSV-infected spleen cells. They were found to recognize viral antigens in association with I-Ad and, in addition, could also be stimulated by VSV-infected A20 cells (an Ia-positive B cell lymphoma of H-2d origin). The purified viral membrane glycoprotein, G protein, and Gs (secreted G protein that lacks the hydrophobic and intracytoplasmic domains) both stimulated IL-2 production when added to cultures of A20 and the hybridomas. These hybridomas therefore recognize a viral antigenic determinant on G protein. Since chemically-fixed antigen-presenting cells fail to stimulate the hybridomas after exogenous addition of purified G protein we can conclude that these T cell hybridomas recognize a processed form of the G protein. Stimulator cells created by expression in A20 of a transfected cDNA encoding G protein were also recognized. Recognition in this case was I-Ad-restricted, as anti-I-Ad monoclonal antibodies blocked stimulation, and an Ia-negative cell (P815) expressing a transfected G protein gene failed to stimulate the hybridomas. Even after paraformaldehyde fixation, G gene-transfected, Ia-positive cells could stimulate the hybridomas, suggesting that processing of this endogenously-synthesized antigen has occurred.
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PMID:T cell hybridomas define the class II MHC-restricted response to vesicular stomatitis virus infection. 285 79

Rapamycin, a potent immunosuppressive drug that prevents rejection of organ transplants in many animals, caused profound growth inhibition in an immature B cell lymphoma, BKS-2, at very low concentrations (2 ng/ml). Similar growth inhibition was also observed in a series of B cell lymphomas (i.e., L1.2, NFS.1.1, and WEHI-279) as well as in thymoma cells. The cell death induced by rapamycin in BKS-2 lymphoma was found to be via programmed cell death, or apoptosis. In contrast to rapamycin, neither FK506 nor CsA affected the normal growth of these cells. FK506, but not CsA antagonized the effect of rapamycin and rescued the BKS-2 cells from undergoing apoptosis. Further, suboptimal concentrations of anti-IgM antibodies and rapamycin acted synergistically in causing the growth inhibition of BKS-2 cells and this inhibitory effect was also completely reversed by FK506. Thus, rapamycin appeared to inhibit lymphoma growth by binding to FK506 binding protein. These results indicate that rapamycin should be evaluated as an effective immunosuppressive therapeutic agent to prevent the incidence of lymphoma after transplantations.
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PMID:Rapamycin, a potent immunosuppressive drug, causes programmed cell death in B lymphoma cells. 754 36

beta-Endorphin affects mononuclear cell proliferation, cytokine production and calcium uptake in a naloxone-resistant manner. The presence of naloxone-insensitive binding sites for beta-endorphin have been demonstrated on murine EL4-thymoma cells, transformed human mononuclear cells and normal murine splenocytes. Since murine splenic B cells have been shown to express naloxone-resistant receptors for beta-endorphin in response to the mitogen, concanavalin A (Con A), the A20 B-cell lymphoma line was used to further study regulation of this site by Con A and dexamethasone. Analyses showed two sites: a high-affinity site, Kd1 = (8.7 +/- 2.3) x 10(-11) M and binding capacity (Bmax1) of (2.6 +/- 2.0) x 10(3) receptors/cell; and a low-affinity site, Kd2 = (2.2 +/- 0.8) x 10(-8) M with Bmax2 of (1.5 +/- 0.8) x 10(5) receptors/cell. Competition studies showed that N-acetyl-beta-endorphin was approx. 5-fold and beta-endorphin6-31 10-fold less potent than beta-endorphin1-31. Neither beta-endorphin1-27 nor naloxone, morphine or other opioid receptor agonists displaced [125I]beta-endorphin. Con A (20 micrograms/ml) significantly increased the Bmax (3.5-fold; expressed per cell) and resulted in a loss of the higher-affinity site. However, the increased Bmax occurred in proportion to the Con-A-induced increase in protein/cell. Dexamethasone (Dex) also increased Bmax, primarily by increasing (2-3-fold) the number of lower affinity sites. In contrast to Con A, two binding sites persisted after treatment with Dex, which exerted a minimal effect on protein/cell. Therefore, binding/cell and binding/protein/cell were both significantly enhanced by Dex. The combined effects of Dex and Con A on binding failed to show additivity or synergy. When binding was analyzed per protein/cell, the effect of Con A appeared to dominate; the Dex-enhanced binding/protein/cell was no longer evident in the presence of Dex plus Con A. Thus, Dex and Con A may enhance binding by independent mechanisms.
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PMID:Expression of naloxone-resistant beta-endorphin binding sites on A20 cells: effects of concanavalin A and dexamethasone. 785 49

A20 is a B cell lymphoma that constitutively expresses the costimulatory molecule B7-2 yet grows readily as a tumor in syngeneic BALB/c mice. We have compared the tumorigenicity of A20 variants expressing either B7-1 (A20/B7-1) or B7-2 (A20/B7-2) with an A20 variant expressing B7-1 and B7-2 with 4-1BBL (A20/4-1BBL), a costimulatory member of the TNF family. Mice injected with tumors expressing the vector backbone (A20/CMV) or B7-1 developed tumors within 25 days of s.c. injection. In contrast, mice injected with A20/4-1BBL were tumor free for the 150-day follow-up period, while 25% of mice injected with A20/B7-2 developed tumors. Tumorigenicity experiments using nude mice indicated the requirement for T cells for variant rejection. Almost all mice that resisted the initial tumor challenge were resistant to further challenge with the parental tumor. Splenocytes from these mice showed high CTL lytic activity against the parental tumor, A20, as well as the syngeneic BALB/c lymphoma K46J, but showed background levels of lytic activity against the congenic SCID thymoma line ST-D2 or the allogeneic EL4 thymoma. In vitro blocking experiments with anti-B7-1 plus anti-B7-2 and/or soluble 4-1BB receptor showed B7-1, B7-2, and 4-1BBL all contributed to the CTL activity. Thus, the data show that neither B7-1 or B7-2 alone can confer full immunogenicity to the A20 lymphoma but that the addition of 4-1BBL results in a tumor that is highly immunogenic and can confer long-lasting protection against challenge with parental tumor in vivo.
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PMID:4-1BBL cooperates with B7-1 and B7-2 in converting a B cell lymphoma cell line into a long-lasting antitumor vaccine. 1020 49

This report describes a low-grade B-cell lymphoma of mucosa associated lymphoid tissue (MALT) involving the thymus of a 63-year-old woman with features suggestive of a connective tissue disease. Sections of the thymic lesion and of a lung biopsy performed at the same operation were examined histologically and by immunohistochemistry using the monoclonal antibodies CD45, CD20, CD79a, CD3, CD45RO, and AE1/AE3. Polymerase chain reaction (PCR) for immunoglobulin heavy chain gene rearrangement was also performed. The dense infiltrate of small lymphoid cells intimately admixed with ramifying epithelial elements, some of which had undergone cystic change, closely resembled a thymoma. The lymphoid infiltrate comprised centrocyte-like cells, small lymphocytes, plasma cells, and blasts. Most of the lymphoid cells were immunoreactive with the B-cell markers CD20 and CD79a, and PCR showed clonal immunoglobulin heavy chain gene rearrangement. The lung biopsy showed dense infiltration by small lymphoid cells, morphologically suggestive of lymphoid interstitial pneumonia. However, PCR showed a weak band in the amplification for immunoglobulin heavy chain gene rearrangement, identical to that within the thymus and suggesting either recirculation of cells to accumulated MALT or subhistological lymphoma. MALT lymphoma may rarely involve the thymus, and pathologists should be aware of this to avoid misdiagnosis as a thymoma. Immunohistochemical and/or molecular studies are of value in this regard. MALT lymphomas of the thymus, common with those arising in other organs, may develop in the setting of a connective tissue disease.
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PMID:Low-grade B-cell lymphoma of mucosa-associated lymphoid tissue (MALT) of thymus. 1068 45

alpha beta+ TCR T cells recognize peptide fragments displayed by MHC-class I or -class II molecules. Recently, additional mechanisms of antigen recognition by T cells have been identified, including CD1-mediated presentation of nonpeptide antigens. Only a limited number of CD1 antigens is retained in the mouse, i.e., the group II CD1 antigens, which are split into CD1D1 and CD1d2. Several T cell subsets have been shown to interact with murine CD1 antigens, including NK cells or "natural T cells" with the invariant V alpha 14 J alpha 281 TCR chain. Even if TAP defects may prevent classical endogenous antigen presentation in tumor cell lines, antigen presentation via CD1 is still functional. Therefore, CD1-mediated recognition of transformed cells by NK cells or "natural T cells" may represent an alternative way for immune surveillance. CD1 cell surface expression in murine tumor cell lines of different histology, including the B cell lymphoma A20, macrophage cell lines J774 and P388D1, mastocytoma P815, thymoma EL-4, melanoma B16, colon adenocarcinoma MC-38 and renal carcinoma Renca is regulated by Th1- (IFN-gamma), Th2- (IL-4, IL-10 and vIL-10) or GM-CSF (Th1/Th2) cytokines, depending on the tumor histology. In order to distinguish between CD1D1 and CD1d2 molecules, we examined differential expression of these CD1 isoforms by ratio RT-PCR: A20, EL-4, P815 and MC-38 cells exclusively express CD1D1 transcripts but not CD1D2 mRNA independent of cytokine treatment. Decreased CD1d expression leads to reduced immune recognition of CD1d+ tumor cells by freshly isolated NK1.1(+) effector cells as defined by cytolysis and IFN-gamma release. Thus, modulation of CD1 expression on tumor cells by cytokines may be advantageous to drive cellular anti-tumor antigen directed immune responses directed against TAP-independent, non-classical MHC restricting molecules.
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PMID:Regulation of CD1d expression by murine tumor cells: escape from immunosurveillance or alternate target molecules? 1192 May 90

Flow cytometry (FC) has become the routine technique in the evaluation of hematopoietic neoplasms. Since the anterior mediastinum is a frequent site of involvement by both primary and secondary lymphoma/leukemia, flow cytometry plays an important role in the evaluation of mediastinal masses. The present study reviews 100 flow cytometry cases from patients presenting with mediastinal lesions. In 5 cases (5%) flow cytometry was not diagnostic due to either insufficient cell yield or low viability. In the remaining cases (95/100) cell suspensions were adequate for flow cytometry evaluation. Results showed that in 31/32 (96.8%), 2/3 (66.7%), 7/9 (77.8%), 7/8 (87.5%) and 11/11 (100%) cases of B-cell lymphoma, T-cell lymphoma, carcinoma, T-ALL/LBL and thymoma/thymic hyperplasia, respectively, the diagnosis could be reached by flow cytometry alone. Excluding HL, the general sensitivity of FC in diagnosing mediastinal tumors was approximately 92%. Among the 100 cases, flow cytometry gave non-informative results in 3 cases of diffuse large B-cell lymphoma, 1 case of peripheral T-cell lymphoma, and 3 cases of carcinoma. No false positive results were encountered. The phenotypic pattern, especially surface CD3 expression versus forward scatter, reliably discriminated between immature thymocytes from thymoma/thymic hyperplasia from T-ALL/LBL. Flow methodology has the advantage of rapid turn-around time as well as high sensitivity, enabling patients with large anterior mediastinal masses and/or superior vena cava syndrome to begin treatment as promptly as possible. In experienced hands, flow cytometry plays a valuable and complementary role to histology and immunohistochemistry in diagnosing mediastinal tumors.
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PMID:Flow cytometry in the diagnosis of mediastinal tumors with emphasis on differentiating thymocytes from precursor T-lymphoblastic lymphoma/leukemia. 1516 Sep 15


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