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)

A case of small lymphocytic B-cell lymphoma with seropositivity for human T-cell leukemia virus type I (HTLV-I), whose clinical features were closely related to those of mucosa-associated lymphoid tissue (MALT) lymphoma, is presented. The neoplastic cells of the lymph node were immunologically positive for CD5, in addition to several B-cell markers, but negative for CD10, and cytogenetically carried a t(11;14)(q13;q32). These findings were fully consistent with so-called mantle cell lymphoma (MCL). In addition to the lymph nodes and bone marrow, multiple extranodal sites including lacrimal and salivary glands, lung and stomach (where MALT is present) were occupied by lymphoma cells. These extranodal lesions were immunologically identical to the lymph nodes (CD5(+), CD10(-)), but histologically showed lymphoepithelial lesions (LEL) characteristic of MALT lymphoma. These findings suggest a possible relationship between MCL and MALT lymphoma, and the neoplastic cells are thought to originate from the CD5-positive B cells, which are present near the areas across the mantle and marginal zones. Furthermore, HTLV-I-infection, which appears to create an immunodeficient state or modulate the B-cell response, is thought to play a role in B-cell lymphomagenesis.
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PMID:Mantle cell lymphoma with the features of mucosa-associated lymphoid tissue (MALT) lymphoma in an HTLV-I-seropositive patient. 753 56

Cross-linking of membrane Ig receptors by anti-mu antibodies (Ab) or treatment with ionomycin induced complete growth arrest and subsequent apoptotic cell death in an immature B cell lymphoma, BKS-2. The growth-inhibitory signals delivered by anti-mu and ionomycin were overcome by anti-CD3-activated Th2 clones D10.G4 and F1 and by Th1 cell clone S53. In this report the Th-mediated growth reversal in BKS-2 cells was shown to require contact-dependent interactions when the inhibition was caused by immobilized anti-mu or ionomycin. Th2 cells in transwells (lymphokines) failed to protect BKS-2 cells from the growth-inhibitory effect of immobilized anti-mu or ionomycin. Monoclonal antibodies to CD5 or CD40 ligands on activated Th cells partially inhibited the Th2 contact-dependent growth reversal of BKS-2 cells whereas simultaneous addition of both antibodies effectively prevented the delivery of contact-mediated growth signal. In contrast, anti-class I or class II Ab did not affect Th cell mediated growth reversal of BKS-2 cells. These data demonstrated that noncognate physical interaction with Th cells was essential for the recovery of BKS-2 cells when the latter were growth-arrested by strong inhibitory stimuli such as immobilized anti-mu and ionomycin. Further CD5 as well as CD40 ligands on Th cells are important for signal transduction in this type of T-B interaction.
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PMID:Involvement of CD5 in Th1 and Th2 contact-mediated rescue of anti-mu and ionomycin induced growth inhibition in a B cell lymphoma. 753 38

The phenotypically immature B cell lymphoma WEHI-231 undergoes apoptotic cell death when cultured with anti-immunoglobulin (Ig) antibodies, via a bcl-2-independent mechanism. We have therefore studied the role of the bcl-2-related protein bcl-x in controlling cell death in WEHI-231. We find that overexpression of the long form of bcl-x (bcl-XL) renders these cells refractory to anti-Ig-induced cell death. Stimulation of WEHI-231 via CD40 has similar protective effects. We show here that ligation of CD40 rapidly induces the appearance of the bcl-XL protein in WEHI-231, while stimulation via sIgM, sIgD, CD5 or CD45 receptors, or with phorbol esters plus ionomycin does not. WEHI-231 cells also rapidly undergo massive apoptosis following culture with thapsigargin, a specific inhibitor of the Ca(2+)-ATPase of the endoplasmic reticulum: this is also reversed by anti-CD40, or by overexpression of bcl-XL. We, therefore, conclude that bcl-XL plays a key role in the regulation of antigen receptor-mediated apoptosis via CD40 in WEHI-231. In addition, the fact that this protein is not induced in WEHI-231 in response to phorbol dibutyrate plus ionomycin points to a fundamental signaling defect in these cells, which could conceivably be a reflection of their immature, apoptosis-susceptible phenotype.
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PMID:The role of bcl-XL in CD40-mediated rescue from anti-mu-induced apoptosis in WEHI-231 B lymphoma cells. 753 57

Cyclin D1/PRAD1 (bcl-1) is a recently discovered proto-oncogene that is overexpressed in mantle cell lymphomas and several other human tumors. In a previous study, the authors demonstrated expression of cyclin D1 in 15 of 15 cases of mantle cell lymphoma and 1 of 8 cases of B-chronic lymphocytic leukemia (B-CLL) using a polyclonal antibody and microwave enhanced immunohistochemical staining method on paraffin-embedded tissue sections. In this study, 107 additional B- and T-cell neoplasms were studied, including 47 cases of high grade lymphoma (33 diffuse large B-cell type, 9 Burkitt and Burkitt-like, 4 precursor T-lymphoblastic lymphoma, and 1 adult T-cell lymphoma/leukemia), 38 additional cases of low grade B-cell lymphoma (18 CLL, 15 hairy cell leukemia and 5 mantle cell lymphoma), and 22 plasmacytomas for expression of cyclin D1 using the same immunohistochemical staining technique. All cases of mantle cell lymphoma showed diffuse nuclear staining. No additional cases of CLL showed cyclin D1 expression. In contrast, 1 of 15 hairy cell leukemias and 1 of 22 plasmacytomas showed cyclin D1 staining. None of the high grade lymphomas demonstrated expression of cyclin D1 protein by immunostaining, including three cases of large B-cell lymphoma that coexpressed CD5. The authors conclude that cyclin D1 is expressed in all cases of mantle cell lymphoma, and only in very rare cases of B-CLL, hairy cell leukemia and plasmacytoma/myeloma. Cyclin D1 does not appear to play an important role in high grade lymphomas. In addition, most CD5 positive high grade B-cell lymphomas do not express cyclin D1, and are not likely to be derived from mantle cell lymphoma or other lymphomas with t(11;14).
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PMID:Cyclin D1 expression in non-Hodgkin's lymphomas. Detection by immunohistochemistry. 754 Mar 62

A case of cutaneous B-cell lymphoma successfully treated by MACOP-B therapy is described. The patient was a 43-year-old man with reddish tumors measuring 3 to 7 cm in diameter on the right cheek and the post-auricles. Histopathologically, massive infiltrations of medium-sized atypical lymphoid cells were found in the reticular dermis and subcutis. A clear zone beneath the epidermis was also detected. The atypical lymphoid cells were positive for CD19, CD20, CD22 and HLA-DR but negative for CD3, CD4, CD5, CD10, CD43, CD45RO and CDw75. The patient was treated successfully with the MACOP-B protocol from March of 1990 to May of 1990. Since April of 1990, he has been free of disease.
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PMID:A case of cutaneous B-cell lymphoma treated successfully with MACOP-B. 768 13

A case of lymphoma presenting with features shared by hairy cell leukemia (HCL) and its variant, intermediate lymphocytic lymphoma (ILL) and monocytoid B-cell lymphoma (MBCL) is described. Clinical presentation and the morphological findings observed in peripheral blood and in bone marrow biopsy suggested an HCL; however, the tartrate-resistant acid phosphatase negativity of peripheral blood lymphocytes, the histologic pattern observed in the spleen, and the immunophenotyping of peripheral blood, spleen and bone marrow neoplastic lymphocytes (expression of CD5 and lack of CD25), were strongly against this hypothesis. The clinical course was aggressive. This report emphasizes the concept of the equivocal presentation of some 'low-grade' B-cell lymphomas. It is further pointed out that, even with complete and exhaustive morphological and immunological analyses, atypical cases may be encountered.
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PMID:A CD5+ leukemic lymphoma with monocytoid features: an unusual B-cell lymphoma mimicking hairy-cell leukemia. 768 80

We describe a patient with stage IV non-Hodgkin's lymphoma (NHL) and a t(11;18)(q21;q21) translocation. He presented with a gastric small B-cell lymphocytic lymphoma, expressing IgAL immunoglobulins without expression of CD10, CD5, and CD23 antigens. The lymphoma was the final development of a 6-year history of a monoclonal IgAL increase complicated by severe renal failure due to membranoproliferative glomerulonephritis. The clinical, histological, immunologic, and cytogenetic features of this patient are very similar to those observed in the five other patients with t(11;18) reported to date. This translocation therefore seems to delineate a new subtype of diffuse small B-cell lymphoma with involvement of mucosal sites. Involvement of the BCL2 oncogene on 18q21 could not be detected using molecular techniques with 5' as well as 3' BCL2 probes, indicating that other, so far unknown, genes relevant to lymphoid differentiation could be located in 18q21 and 11q21.
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PMID:t(11;18)(q21;q21) may delineate a spectrum of diffuse small B-cell lymphoma with extranodal involvement. 768 56

Patients with B-cell chronic lymphocytic leukemia (CLL) infrequently may develop high-grade B-cell lymphoma, or Richter's syndrome lymphoma (RS lymphoma). Such lymphomas differ from the original leukemia in both histology and clinical behavior. Studies seeking to define the clonal relationship between the cells of the two malignancies in any one patient have yielded conflicting reports. We examined the clonal relationship between the early and late neoplastic cells of a patient who underwent Richter's transformation. In contrast to the original leukemia cells, the secondary high-grade lymphoma was CD5-. However, both the leukemia cells and the evolved RS lymphoma expressed surface IgM lambda reactive with Lc1, a murine monoclonal antibody specific for a supratypic cross-reactive idiotype encoded by a subset of human Ig variable region genes of the VH4 subgroup. Nucleic acid sequence analyses of the heavy and light chain variable region genes expressed by both leukemia and lymphoma cells show that the CD5- B-cell lymphoma constitutes a clonal expansion of mutant cells derived from the original CD5+ B-cell leukemia. Moreover, certain sets of somatic mutations distinguish the Ig variable region genes used by RS lymphoma from those expressed by the CLL B cells. This is the first study to establish the clonal relationship between CLL and RS lymphoma through primary structural analyses of the expressed Ig genes.
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PMID:Common clonal origin of chronic lymphocytic leukemia and high-grade lymphoma of Richter's syndrome. 769 38

In human T cells CD45 is reported to associate with both cell surface and intracellular molecules including CD2, CD4/CD8, CD5, p56lck and p59fyn. In this study the association of molecules with CD45 in murine T lymphocytes was explored using biotinylation, chemical cross-linking, immunoprecipitation and 32P-labelling. Sodium dodecyl sulphate-polyacrylamide gel electrophoresis (SDS-PAGE) analysis of CD45 monoclonal antibody (mAb) (S-450-15.2) immunoprecipitates from Triton X-100 lysates of murine thymocytes that were surface biotinylated and treated with the chemical cross-linker 3,3'-dithio-bis(sulpho-succinimidylpropionate) (DTSSP) showed that CD45 can be chemically linked to molecules of 25,000-32,000, 42,000 and 60,000-70,000 MW. The CD45 mAb also co-precipitated a prominent 32,000 MW molecule from digitonin lysates of surface biotinylated murine thymocytes, splenocytes and D10 cells, but a weaker association was also detected on splenic B cells and on the murine B-cell lymphoma line A20. The results suggest that in these cells CD45 is associated with a 32,000 MW molecule which is exposed extracellularly. Experiments in which thymocytes were biotinylated after permeabilization with lysolecithin showed that additional molecules of 33,000, 55,000, 60,000 and 90,000 MW, presumably localized intracellularly, also co-precipitated with CD45. Labelling of murine thymocytes or D10 cells with H3(32)PO4 in vivo, and of CD45 immunoprecipitates by in vitro kinase reaction, revealed that the 32,000-33,000 MW molecules are phosphoproteins. The relationship of these molecules with the 30,000-34,000 MW molecules previously reported to associate with CD45 in human T cells is not clear as a number of differences were observed. Firstly, the molecular weight of the CD45-associated 32,000-33,000 MW molecule(s) on murine T cells and B cells is slightly lower than that observed in the human T-cell line Jurkat (34,000 MW). Secondly, phosphoamino acid analysis after in vitro kinase labelling of CD45 immunoprecipitates showed that the murine 32,000-33,000 MW molecules are phosphorylated exclusively on serines. Thirdly, although in vitro phosphorylation of the 32,000-33,000 MW molecules was inhibited by preincubation with either GTP-gamma-S or GDP-beta-S, the 32,000-33,000 MW CD45-associated molecules did not bind 32P-GTP, GDP-agarose, or react with antisera to a consensus sequence of G proteins. The crucial role of CD45 for proper function of the T-cell receptor (TCR), suggests that the CD45-associated 32,000-33,000 MW molecules and kinases also may play a role in the signalling events leading to T-cell activation.
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PMID:Evidence for an association of CD45 with 32,000-33,000 MW phosphoproteins on murine T and B lymphocytes. 783 67

Employing Northern blot analysis and the polymerase chain reaction, we investigated PRAD1 gene overexpression in the tumour tissues of 58 patients with B-cell lymphoma. These findings were then examined in relation to the patients' clinical and immunohistological characteristics. The over-expression of this gene was detected in 6/8 patients with mantle cell lymphoma (MCL) and in only 1/50 other lymphomas, indicating its close association with MCL. The patients with MCL had common clinical findings of advanced disease with generalized lymphadenopathy on admission, and they had a CD5+CD10-IgD+ phenotype. The patients with chronic lymphocytic leukaemia (CLL) also showed findings indicating a distinctive disease entity: a CD5+CD10-IgD+ phenotype and lack of PRAD1 over-expression. In contrast, most patients with diffuse low-grade lymphoma other than MCL and CLL had localized extranodal disease, expressed a CD5-CD10-IgD- phenotype, and lacked PRAD1 over-expression. These findings suggest that extranodal low-grade lymphomas differ from nodal MCL and are not part of the spectrum of CLL.
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PMID:PRAD1 gene over-expression in mantle-cell lymphoma but not in other low-grade B-cell lymphomas, including extranodal lymphoma. 791 73


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