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)

Lines of Epstein-Barr virus (EBV)-transformed lymphoblastoid B-cells (B-LCLs) differ in the expression of surface CD4 glycoproteins. The aim of the present study was to correlate the expression of CD4 molecules on B-LCL cells with the synthesis of CD4 mRNA. RT-PCR assays were performed with oligonucleotide primers designed to detect mRNA corresponding to intracellular, transmembrane, or extracellular portions of the CD4 molecule. RT-PCR assays with all sets of primers were positive in T-cell populations, but were negative in various B-cell lymphoma lines. The majority of the LCLs established by EBV transfection of non-selected B-cells yielded positive results with at least some of the primer sets used for detection of CD4 mRNA. A significant positive correlation was found between the proportion of CD4+ cells in various B-LCLs and the concentration of CD4 mRNA. LCLs established from B-cells which synthesized various antibodies did not express CD4 molecules and either failed to synthesize CD4 mRNA or produced very low concentrations. These findings indicate that the expression of CD4 on B-LCLs is directly correlated with the concentration of CD4 mRNA synthesized and with the differentiation stage in which B-cells were immortalized by EBV infection.
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PMID:Correlation between the expression of CD4 and the level of CD4 mRNA in human B-cell lines. 1214 39

We observed in the same patient the development of a tonsil mucosa-associated lymphoid tissue-type lymphoma in 1994, a mediastinal Hodgkin's disease in 1998, and a colonic CD30+ anaplastic diffuse large B-cell lymphoma in 2000. A same-sized FR3-JH fragment was demonstrated by polymerase chain reaction, both at the level of total DNA and of single micromanipulated cells, showing monocytoid, Reed-Sternberg, or anaplastic morphology. Moreover, an identical IgH nucleotide sequence was detected in mucosa-associated lymphoid tissue-type lymphoma and colonic CD30+ anaplastic diffuse large B-cell lymphoma, whereas mediastinal Hodgkin's disease IgH rearrangement involved different VH and JH genes. CD30+ Reed-Sternberg and diffuse large B-cell lymphoma cells contained Epstein-Barr virus EBER sequences that were not observed at the level of mucosa-associated lymphoid tissue-type lymphoma. Therefore, Epstein-Barr virus infection may have played a role in diffuse large B-cell lymphoma transformation of mucosa-associated lymphoid tissue-type lymphoma and in the lymphomagenesis of Hodgkin's disease. In addition to their different clonal origin, Reed-Sternberg cells of Hodgkin's disease expressed a CD15+, CD20+ (rare cells), CD30+, Oct-2-, EBNA2-, LMP1+ phenotype, whereas anaplastic and Reed-Sternberg-like cells of diffuse large B-cell lymphoma were CD15-, CD20+, CD30+, Oct-2+, EBNA2+, and LMP1+. Interestingly, we also detected scattered CD30+ Epstein-Barr virus- large cells with prominent nucleoli in the initial tonsil mucosa-associated lymphoid tissue-type lymphoma, suggesting that these cells could be prone to Epstein-Barr virus infection and/or large cell transformation.
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PMID:Sequential development of Hodgkin's disease and CD30+ diffuse large B-cell lymphoma in a patient with MALT-type lymphoma: evidence of different clonal origin of single microdissected Reed-Sternberg cells. 1245 31

We report a rare case of composite angioimmunoblastic T-cell lymphoma (AILT) and diffuse large B-cell lymphoma occurring in a 48-year-old woman with generalized lymphadenopathy and hepatosplenomegaly. The patient initially sought care at a local hospital with a single enlarged left cervical lymph node. Histologic examination of the node was interpreted as an atypical immunoblastic proliferation. She developed generalized lymphadenopathy 10 months later and was referred to our institution for further evaluation. The recent biopsy of the cervical node showed typical features of AILT Flow cytometric immunophenotyping identified an aberrant CD4+ T-cell population that lacked surface CD3. Polymerase chain reaction analysis of the T-cell receptor gamma gene revealed a clonal rearrangement. In addition to the AILT, the lymph node showed partial involvement by a diffuse large B-cell lymphoma. The B lymphoma cells and admixed immnunoblasts and Reed-Sternberg-like B cells in the AILT were positive for Epstein-Barr virus (EBV) by in situ hybridization. Ourfindings raise the possibility that the EBV-associated large B-cell lymphoma is a secondary event in AILT via EBV infection or reactivation followed by clonal expansion of an immortalized EBV-infected B cell clone.
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PMID:Composite angioimmunoblastic T-cell lymphoma and diffuse large B-cell lymphoma: a case report and review of the literature. 1247 77

Methotrexate has proven to be effective in treating rheumatoid arthritis (RA), and is believed to be nononcogenic in the low weekly dose typically employed in the patients with RA. We report, however, a patient with RA in whom a rapidly enlarging diffuse large B-cell lymphoma developed in the left upper lung after weekly treatment with methotrexate for 5 years. The patient had a positive serum IgG for Epstein-Barr virus but a negative in situ hybridization of the resected specimen. Methotrexate therapy was discontinued, and the patient elected for clinical observation instead of chemotherapy or radiation therapy. There has been no clinically detectable recurrence of the lymphoproliferative disorder for 2 years. We believe that methotrexate has an oncogenic potential even in low weekly dosing in a subset of patients with RA and latent Epstein-Barr virus infection. The strongest causal link is demonstrated by the persistent tumor remission after stopping treatment with methotrexate.
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PMID:Methotrexate-induced pulmonary lymphoma. 1279 4

We report here a case of mantle cell lymphoma (MCL) in a patient who, following Epstein-Barr virus (EBV) infection, developed diffuse large B-cell lymphoma (DLBCL). A 47-year-old woman was diagnosed as having MCL with clinical stage IIIA in July 1990. After treatment with a third-generation chemotherapy without response, she was kept under observation for 8 years. In January 1999, fever and night sweats appeared with laboratory evidence for EBV infection, and acute swelling of lymph nodes and hepatosplenomegaly developed in May 1999. Histopathological examination confirmed the diagnosis of DLBCL. Sequence analysis of the complementarity-determining region (CDR)-III of the immunoglobulin heavy chain gene demonstrated clonal identity between the initial MCL and the subsequent DLBCL. Immunohistochemistry revealed that cyclin D1, CD5, and CD20 were expressed in the MCL but lost in the DLBCL cells, and EBER-ISH confirmed that EBV infection was absent in the former but present in the latter. Southern hybridization with the EBV terminal repeat probe showed a clear monoclonal pattern in the DLBCL specimen. All these results suggest that EBV infection may have been the molecular event that caused transformation of MCL cell(s) to DLBCL in this case. This is, to the best of our knowledge, the first well-documented case of EBV-associated transformation of MCL.
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PMID:Case of Epstein-Barr virus-associated transformation of mantle cell lymphoma. 1282 58

In the new World Health Organization (WHO) classification of malignant lymphoma, anaplastic large cell lymphoma of B-cell phenotype is classified either as the anaplastic large cell variant of diffuse large B-cell lymphoma or as Hodgkin's lymphoma. A 71-year-old Japanese man developed fever and generalized lymphadenopathy. Biopsy of the right axillary node revealed morphology of malignant lymphoma in which large cells with abundant cytoplasm and pleomorphic nuclei were scattered among small lymphocytes. Immunostaining with various monoclonal antibodies revealed the large cells to be CD79+, CD20/L26+, CD45RO/UCHL-(1-), CD3-, CD10-, CD30+, NPM/ALK-, EMA-, CD15-, and bcl-(2-). Amplification of the J region of the immunoglobulin heavy chain by polymerase chain reaction revealed a single rearranged band. Therefore the diagnosis of anaplastic large cell variant of diffuse large B-cell lymphoma, stage IIIB, was made from the standpoint of the new WHO classification of malignant lymphoma. Biopsy led to findings of Epstein-Barr virus (EBV)-associated lymphoma with positive in situ hybridization results for EBV small RNAs, positive results of immunostaining with EBV latent membrane 1 antibody, and negative results of immunostaining with Epstein-Barr nuclear antigen 2. Results of immunostaining of the mass with p53 antibody also were positive for lymphoma cells. The findings in this case may suggest a close relationship between p53 expression and latent EBV infection.
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PMID:Epstein-Barr virus-associated anaplastic large cell variant of diffuse large B-cell-type non-Hodgkin's lymphoma with concurrent p53 protein expression. 1284 89

To identify molecular features of neoplasms associated with EB virus, human peripheral blood lymphocytes (huPBL) were isolated from healthy volunteer donors and were transplanted intraperitoneally into SCID mice, and then huPBL/SCID mice were infected with EB virus. Serum levels of human IgG were measured by unidirectional immunodiffusion assay. Human Alu sequence and EBER-1 in tumor tissues were detected with PCR and in situ hybridization. Immunohistochemical staining was used to examine leukocyte differentiation antigens (LCA, L26, UCHL1, PS1), viral gene products (LMP1, EBNA2, BZLF1) and cellular oncoproteins (p53, C-myc, Bcl-2 and Bax). The experiments showed that tumors developed in 24 of 34 surviving huPBL/SCID mice by EBV infection. Histopathological and immunohistochemical observations demonstrated that all of the induced tumors in SCID mice were malignant lymphomas derived from human B-lymphocytes. In situ hybridization showed that tumor cells had EBV-encoded small RNA-1 (i.e. EBER-1). Alu sequence could be amplified by PCR from human genome of tumor tissues. Immunohistochemistry detected positive staining of BZLF1-encoded protein in a small population of tumor cells of almost all cases, and positive staining of LMP1 and EBNA2 only in small number of tumor cells. Human IgG could be found in the serum of 12 SCID mice on the 15th day after huPBL engraftment, and then increased with time and with the development of induced tumors in 6 mice. Positive rates of p53, C-myc, Bcl-2 and Bax expression were 83.33%, 100%, 95.83%, 91.67%, respectively, in 24 cases of the EBV-induced lymphomas. The results indicate that molecular lesions associated with the induced B-cell lymphoma involved EBV infection, expression of oncogenic viral genes, and abnormal expression of cellular oncogenes in human xenografts. Human IgG level in the serum of huPBL/SCID mice can be considered as a useful index for tumor development.
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PMID:[Molecular pathological characteristics of human B-cell lymphomas induced by Epstein-Barr virus]. 1451 11

Human herpes virus type 8 (HHV8) has been strongly associated with Kaposi sarcoma, primary effusion lymphoma (PEL), and Castleman's disease. To our knowledge, infection by this virus has not been strongly associated with other hematopathologic malignancies. We examined five oral cavity lymphomas from men with AIDS for HHV8 and HIV-1 by reverse transcriptase in situ polymerase chain reaction, as well as for Epstein-Barr virus (EBV) (EBER-1, -2) using in situ hybridization and HHV8 protein with immunohistochemistry. Four of these tumors were plasmablastic lymphomas; the final case was diffuse large B-cell lymphoma. Most of the neoplastic cells in these five lymphomas contained HHV8 RNA and protein. Further, the four plasmablastic lymphoma cases had tumor cells that contained EBV. HIV-1 RNA was not detected in the tumor cells but was noted in surrounding benign T cells. In comparison, HHV8 RNA was not detected in any of the five oral cavity lymphomas from people who did not have acquired immunosuppression nor in five lymphomas from AIDS patients that were located at a site other than the oral cavity. It is concluded that oral cavity lymphomas from people with AIDS are strongly associated with infection by HHV8 and EBV. Given the poor prognosis of oral cavity lymphomas in immunocompromised patients, therapy directed against the HHV8 and EBV infection may be of therapeutic value.
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PMID:Oral plasmablastic lymphomas in AIDS patients are associated with human herpesvirus 8. 1548 61

Epstein-Barr virus (EBV)-infected B cell lymphomas are resistant to apoptosis during cancer development and treatment with therapies. The molecular controls that determine why EBV infection causes apoptosis resistance need further definition. EBV-positive and EBV-negative BJA-B B cell lymphoma cell lines were used to compare the expression of selected apoptosis-regulating Bcl-2 and caspase proteins in EBV-related apoptosis resistance, after 8 hr or 18-24 hr etoposide treatment (80 microM). Apoptosis was quantified using morphology and verified with Hoechst 33258 nuclear stain and electron microscopy. Fluorescence activated cell sorting (FACS) was used to analyse effects on cell cycle of the EBV infection as well as etoposide treatment. Anti-apoptotic Bcl-2 and Bcl-XL, pro-apoptotic Bax, caspase-3 and caspase-9 expression and activation were analysed using Western immunoblots and densitometry. EBV-positive cultures had significantly lower levels of apoptosis in untreated and etoposide-treated cultures in comparison with EBV-negative cultures (p < 0.05). FACS analysis indicated a strong G2/M block in both cell sublines after etoposide treatment. Endogenous Bcl-2 was minimal in the EBV-negative cells in comparison with strong expression in EBV-positive cells. These levels did not alter with etoposide treatment. Bcl-XL was expressed endogenously in both cell lines and had reduced expression in EBV-negative cells after etoposide treatment. Bax showed no etoposide-induced alterations in expression. Pro-caspase-9 and -3 were seen in both EBV-positive and -negative cells. Etoposide induced cleavage of caspase-9 in both cell lines, with the EBV-positive cells having proportionally less cleavage product, in agreement with their lower levels of apoptosis. Caspase-3 cleavage occurred in the EBV-negative etoposide-treated cells but not in the EBV-positive cells. The results indicate that apoptosis resistance in EBV-infected B cell lymphomas is promoted by an inactive caspase-3 pathway and elevated expression of Bcl-2 that is not altered by etoposide drug treatment.
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PMID:Epstein-Barr virus-mediated protection against etoposide-induced apoptosis in BJA-B B cell lymphoma cells: role of Bcl-2 and caspase proteins. 1474 96

We report a case of composite lymphoma consisting of peripheral T-cell lymphoma and an anaplastic variant of diffuse large B-cell lymphoma (DLBCL) and associated with Epstein-Barr virus (EBV) infection and strong p53 expression. A 65-year-old Japanese woman developed fever and generalized lymphadenopathy. A biopsy of the cervical node revealed the morphology of malignant lymphoma with 2 kinds of lymphoma coexisting in 1 lymph node. One lymphoma type consisted of immunoblastic large cells with the T-cell marker phenotype CD3+, CD45RO/UCHL-1+, CD20/L26-, CD79-, CD10-, CD30-, and CD15-; the other type consisted of large cells with abundant cytoplasm and pleomorphic nuclei with the marker phenotype CD79+, CD20/L26+, CD45RO/UCHL-1-, CD3-, CD10-, CD30+, NPM/ALK-, and CD15-. Therefore, the diagnosis was composite lymphoma of peripheral T-cell lymphoma and an anaplastic variant of DLBCL, stage IVB, because the patient had bone marrow involvement with peripheral T-cell lymphoma. The biopsy led to findings of latent type II EBV-associated lymphoma in both the peripheral T-cell lymphoma and the anaplastic variant of DLBCL as the result of positive signals for EBV small RNAs by in situ hybridization, positive immunostaining results for EBV latent membrane protein 1 antibody, and negative immunostaining results for EBV nuclear antigen 2. Immunostaining of the mass with p53 antibody also yielded positive results for both types of lymphoma cells. This case suggests that the immunocompromised state of this patient with EBV-related peripheral T-cell lymphoma allowed the emergence of an EBV-related anaplastic variant of DLBCL and suggests a close relationship between p53 expression and latent EBV infection.
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PMID:Epstein-Barr virus-associated composite lymphoma composed of peripheral T-cell lymphoma and an anaplastic variant of a diffuse large B-cell type of non-Hodgkin's lymphoma and strongly expressing p53 protein. 1516 95


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