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

In more than 80% of tumor cells in the pericardiac effusion of a case of malignant B-cell lymphoma, Epstein-Barr virus-determined nuclear antigen (EBNA) was detected by the anticomplement immunofluorescence test. Moreover, herpestype virus particles, although few in number, were demonstrated in the nucleus of lymphoma cells by an electron microscope. Tumor cells in the pericardiac effusion were seeded at 98% purity after centrifugation on Ficoll-Conray and, soon after plating, they proliferated continuously without any lag phase of growth or cell death. Therefore, the established cell line was regarded as of tumor cell origin and named Fujimaki-II cell after patient's name. On the other hand, Fujimaki-I cells were established from the biopsied tumor in the same way. These two cell lines, B-lymphocyte in nature, had both EB virus-related antigens and herpes-types virus particles. Heterotransplantation of cultured cells and tumor tissue obtained at autopsy into athymic nude mice was not successful. Transformation of cord blood lymphocytes by the virus released from Fujimaki-II cell also failed. This might be the first case of non-Burkitt type lymphoma in which the EB virus genome was directly detected in the tumor cells.
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PMID:Detection of Epstein-Barr virus in biopsied malignant lymphoma cell and its continuous culture. 21 75

Activation of the alternative complement pathway by human B cell lymphoma lines is correlated with the presence of Epstein Barr virus (EBV) in the cell genome. EBV-negative B cell lymphoma lines produce little activation of the alternative pathway as measured either by C3 deposition on the cell surface or C3 conversion and consumption of alternative pathway activity in the supernatant serum. By contrast, EBV-positive sublines derived by in vitro EBV conversion of EBV-negative parental lines produce considerable activation of the alternative pathway. This membrane-associated complement-activating mechanism reflects an EBV-induced membrane change in these cells and may provide a mechanism whereby EBV-transformed cells are controlled in vivo.
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PMID:Activation of the alternative complement pathway by human B cell lymphoma lines is associated with Epstein-Barr virus transformation of the cells. 21 Oct 40

Although chromosome aberrations in T lymphocytes and bone marrow cells have been reported in atomic bomb survivors, the presence of chromosome abnormalities has not been demonstrated in B lymphocytes because of the technical difficulties involved in B-lymphocyte separation. A method for detecting chromosome aberrations in B lymphocytes was established by "stimulation" of B lymphocytes with Epstein-Barr virus (EBV) instead of "separation" of B lymphocytes by rosette formation. The EBV-stimulated lymphocytes were isolated as single colonies in soft agar and transferred to liquid culture for further cell growth. The EBV-stimulated B lymphocytes of two heavily exposed survivors showed 50% and 12.5% chromosome abnormalities 30 yr after exposure to the effects of the atomic bomb. The former patient seemed to have a karyotypically abnormal clone of B lymphocytes in vivo. The method used in this study and the evidence of chromosome aberrations in B lymphocytes for long periods after radiation exposure will be useful and important in elucidating the malignant processes of acute lymphocytic leukemia, B-cell lymphoma, and multiple myeloma among high-risk groups having a history of accidental or therapeutic exposure to radiation or radiomimetic drugs.
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PMID:Chromosome aberrations in B lymphocytes of atomic bomb survivors. 22 Oct 56

In recent years, techniques, probes, and reagents became available to reliably visualize individual Epstein-Barr virus (EBV)-infected cells, to assess EBV gene expression, and to analyze the clonal composition of EBV genomes in human tissues. Application of these techniques to more than 1000 lymphoid tissue specimens revealed (1) characteristic cellular and compartmental distribution patterns of EBV-infected cells in normal lymph nodes, reflecting the interference of EBV with physiologic B cell differentiation pathways, (2) an association of EBV with various mono- and oligoclonal lymphoproliferations ranging from benign conditions to overtly malignant lymphomas, and (3) characteristic patterns of EBV gene expression among EBV-associated lymphoproliferations. In the context of the established immortalizing and transforming properties of EBV, the findings support the concept of an etiologic role of EBV for cases of certain lymphomas such as Burkitt's lymphoma, anaplastic large cell lymphoma, Hodgkin's disease, and lymphomas arising in immunocompromised individuals. In contrast, lymphomas harboring EBV in only proportions of the tumor cells (such as cases of peripheral T cell lymphoma and some B cell lymphoma types) argue against an etiologic role in the primary process of malignant transformation for the virus in these instances. Since in many of these cases a proportion of the EBV infected tumor cells express the EBV oncoprotein LMP (latent membrane protein) the virus may influence, however, the proliferative properties as well as the morphological and molecular phenotype of the neoplastic cells.
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PMID:[Epstein-Barr virus associated lymphocyte proliferation]. 128 80

We investigated the association of Epstein-Barr virus (EBV) with African cases of Burkitt's lymphoma (BL) and high grade B cell non-Burkitt's lymphoma (non-BL) occurring in areas where BL is endemic. The presence of EBV genomes was analysed in 24 cases using in situ hybridization with a 35S-labelled EBV probe applied to paraffin sections. EBV DNA was detected in each of 10 cases of BL in which technically satisfactory results were obtained, the virus being homogeneously distributed in all identifiable tumour cells. Two other cases of BL could not be evaluated because of technical problems. In contrast, EBV DNA was not detected in any case of high-grade non-BL (10 centroblastic and two immunoblastic lymphomas). These results confirm previous reports of the strong association of EBV with endemic BL, but suggest that the virus is not important in the pathogenesis of other types of African high-grade B cell lymphoma from regions where BL is endemic.
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PMID:Analysis of African Burkitt's and high-grade B cell non-Burkitt's lymphoma for Epstein-Barr virus genomes using in situ hybridization. 131 Nov 94

Human Immunodeficiency Virus type 1 (HIV-1) infects CD4+ T lymphocytes and various other cell types, including B cells. Since HIV-1 seropositive individuals have high numbers of B cells carrying Epstein-Barr Virus (EBV), and are at high risk for development of EBV-associated lymphoproliferative diseases, we studied the mode of HIV-1 infection in four EBV-positive lymphoblastoid B-cell lines (LCLs) as well as some molecular and biological features of the B cells infected by both viruses. We found that LCL cells were successfully infected in vitro by HIV-1, despite the lack of CD4 antigen expression on the cell membrane. LCL cells displayed a persistent, productive, and non-cytopathic infection. Moreover, HIV-1 infection induced reactivation of EBV latent genomes in one cell line. Following HIV-1 infection, LCL cells showed a decrease in B-cell activation markers CD23 and CD39, and an increase in CD10 immature B-cell antigen. Not all cells in each LCL expressed HIV-1 antigens, but all CD10+ cells also co-expressed the HIV-1 envelope protein gp 120. Furthermore, HIV-1 infected LCL cells grew as disperse suspensions, and formed more agar colonies than control, non-HIV-1-infected LCLs. These findings raise the possibility that HIV-1 might play a role in EBV reactivation, and in B-cell lymphoma pathogenesis in AIDS patients.
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PMID:Morphological and phenotypical changes in EBV positive lymphoblastoid cells infected by HIV-1. 131 75

Inoculation of the cottontop tamarin with Epstein-Barr virus (EBV) invariably gives rise to mono- or oligoclonal large cell lymphoma occurring at multiple sites, and which resembles to a certain extent B cell lymphoma that occurs in the immunodeficient patient. The viral transcriptional pattern in tamarin tumour biopsies and in the corresponding tumour cell lines was investigated by means of the synthesis of radioactive single-stranded cDNA. It was found that the EBV transcripts came mainly from the fragments BamH1-H, BamH1-S, BamH1-A and EcoR1-Dhet. Transcripts from a few other early or late genes, namely BARF1, BSLF1/BMLF1, BBLF-4, BLLF1 and BXLF2, were also detected in one of the three biopsies tested. It would be important to characterize the transcripts that originate from the region where viral latent expression has not previously been observed. Our results also revealed that there is a sharp increase in EBV transcription in the tumour cell lines derived from the tamarin lymphomas. Simultaneously, the copy number of the viral genome was found to be amplified. Such a significant change in viral activity might be indicative of a close virus-host cell interaction in vivo.
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PMID:Transcriptional expression of the viral genome in the Epstein-Barr virus-induced tamarin lymphoma and the corresponding lymphoblastoid tumour lines. 133 74

Recombinant human growth hormone (rhGH) previously has been demonstrated to promote human or mouse T-cell engraftment in immunodeficient mice. We then wanted to examine long-term effects of rhGH on human cell engraftment in these mice. Mice with severe combined immune deficiency (SCID) were given human peripheral blood lymphocytes or human bone marrow cells and daily injections of rhGH (20 micrograms ip every other day). Upon later assessment for engraftment by flow cytometric analysis, it was determined that rhGH strongly promoted human T-cell engraftment in the thymus and spleens of these mice. However, there was considerable variability in both the incidence and extent of engraftment which appears to be due to donor-to-donor variation. Additionally, rhGH promoted B lymphomagenesis in these mice since long-term treatment of these xenogeneic chimeras with rhGH resulted in the increased incidence of human Epstein-Barr virus (EBV)-infected B-cell lymphoma. Thus, while rhGH can be used to optimize human T-cell engraftment in SCID mice, it also increases the likelihood of B-cell lymphoma generation when the donor is EBV infected. The results suggest that the activation of human T cells by rhGH results in an increased ability of these cells to traffic to the peripheral lymphoid organs of the SCID mice and results in a lymphoid microenvironment conducive to the outgrowth of EBV-transformed B lymphocytes.
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PMID:Recombinant human growth hormone promotes human lymphocyte engraftment in immunodeficient mice and results in an increased incidence of human Epstein Barr virus-induced B-cell lymphoma. 133 93

Cyclosporine (CsA) is a potent immunosuppressive agent primarily affecting T-lymphocyte function. Patients receive CsA following organ transplantation to prevent rejection. These patients are at high risk for developing Epstein-Barr virus (EBV)-induced lymphoproliferative disease (LPD) or B-cell lymphoma (BCL). Severe Combined Immunodeficient (SCID) mice reconstituted with human peripheral blood leukocytes (PBL) develop fatal B-cell lymphomas of human origin following latent or active infection with EBV. This model was utilized to determine the role of CsA in the development of human BCL. SCID mice were reconstituted with PBL, latently or actively infected with EBV, and treated with CsA. Following active EBV infection, mice developed human BCL with or without CsA treatment. In contrast, treatment with CsA prevented the development of BCL in mice latently infected with EBV. This suggests a T-cell interaction with latently infected B-cells which is perturbed by CsA. Further understanding of this interaction and the occurrence of human BCL may allow the development of strategies to prevent, detect, or treat malignancies associated with immunosuppression.
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PMID:Effects of cyclosporine on human B-cell lymphoma development in vivo. 134 Dec 39

We studied 23 cases of angioimmunoblastic lymphadenopathy (AILD) and AILD-like lymphoma for evidence of Epstein-Barr virus (EBV) using the polymerase chain reaction (PCR) and in situ hybridization studies. EBV nucleic acid sequences were found by either PCR or in situ hybridization in 96% of the cases. There was a wide range in the number of EBV-positive cells among the different cases as detected by in situ hybridization. The EBV-positive cells most often possessed nuclei of intermediate to large size. Double-labeling immunohistochemistry/in situ hybridization studies demonstrated that most of the EBV-positive cells expressed the B-lineage antigen CD20 (as detected by L26), with a minority of the EBV-positive cells stained for the T-lineage associated antigen, CD43 (as detected by Leu 22). The abnormally high amounts of EBV found in AILD and AILD-like lymphoma may be a reflection of decreased immunocompetence in these patients. The presence of EBV-positive B cells may explain the presence of B-cell clones found by others as well as the paradoxical occurrence of B-cell lymphoma in a primary T-cell lymphoproliferative disorder.
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PMID:Detection and localization of Epstein-Barr viral genomes in angioimmunoblastic lymphadenopathy and angioimmunoblastic lymphadenopathy-like lymphoma. 137 88


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