Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019829 (Hodgkin's disease)
 30,247 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Recent nucleic acid hybridization studies have implied that Reed-Sternberg/Hodgkin (RS/H) cells are infected with Epstein-Barr virus (EBV) before malignant transformation, and hence, that Hodgkin's disease could develop as a consequence of malignant transformation of an EBV-infected cell. This study is a detailed immunohistochemical and in situ hybridization characterization of the various lymphoid cells in nine cases of infectious mononucleosis (IM), the acute manifestation of EBV infection. The RS/H-like cells of IM were similar in most respects to their morphologically identical counterparts in Hodgkin's disease; they expressed the EBV-encoded protein LMP1, EBV EBER1 transcripts, and CD30 and rarely, if ever, expressed CD45/LCA or T cell markers. Dissimilarities were limited to CD15 negativity and the absence of a collarette of T cells around the RS/H-like cells of IM compared with their Hodgkin's counterparts. Expression of the immortalizing bcl-2 oncoprotein was variable in the RS/H-like cells of IM, as has been demonstrated in the RS/H cells of Hodgkin's disease by other investigators. An apoptosis assay suggested that many apoptotic cells in IM were EBV-infected T cells, in keeping with the previous in vitro observation that IM-derived T cells succumb to apoptosis. Additionally, the apoptosis assay suggested that RS/H-like cells of IM can succumb to programmed cell death, reminiscent of the mummified RS/H cells seen in Hodgkin's disease. The accumulation of evidence suggests that RS/H-like cells of IM are more similar to true RS/H cells than previously recognized.
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PMID:New characterization of infectious mononucleosis and a phenotypic comparison with Hodgkin's disease. 753 53

Non-Hodgkin's (1ii)lymphoma is an AIDS-defining event in a significant percent of U.S. patients infected with the human immunodeficiency virus (HIV). Advances in anti-retroviral treatment and management of opportunistic infection have been accompanied by an increase in the incidence of these lymphomas. In the immunocompromised state of patients late in the course of HIV infection, these lymphomas represent a complication of HIV infection that is associated with an extremely poor prognosis. Currently, there is little understanding of the pathogenesis of HIV-associated lymphomas, which are nearly exclusively of B-cell origin. Experimental data do not support HIV infection in these lymphomas. While some lymphomas show evidence of EBV infection, the majority do not. Polyclonal B-cell hyperactivity during the early phases of HIV infection argues that chronic B-cell stimulation may be the major process predisposing B-cells in the HIV-infected individual to malignant transformation. The mechanism of this stimulation of normal B cells and its relationship to AIDS-associated lymphomas remain poorly understood. In this review, we will summarize current information on HIV-associated B lymphoma and then discuss our views on the association and regulation of HIV-related hyperactivity on the pathogenesis of this lymphoma.
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PMID:HIV-mediated B-lymphocyte activation and lymphomagenesis. 755 9

Severe immunodeficiency is associated with reactivation of latent Epstein-Barr virus (EBV) that is manifested by virus replication. It is unknown whether EBV replication also occurs in the Hodgkin's disease (HD) tissue of patients infected with the human immunodeficiency virus (HIV). Therefore, we studied paraffin-embedded lymph nodes from 13 cases of HIV-associated HD to determine the latent or replicative state of EBV infection. All patients were seropositive HIV-infected men; additional clinical information was available for 12 patients. The risk factor(s) for HIV infection were homosexuality (n = 7), intravenous drug abuse (n = 2), homosexuality and intravenous drug abuse (n = 1), sexual promiscuity (n = 1), or hemophilia (n = 1). Advanced clinical stage and B symptoms were common at the time of initial diagnosis of HD. The histological subtype of Hodgkin's disease was universally mixed cellularity, except for a single case classified as nodular sclerosis. Seven cases exhibited foci of relative lymphoid depletion. Five cases contained foci of necrosis. Reed-Sternberg (RS) cells and RS cell variants were positive for CD30/BerH2 and negative for CD45/LCA, CD45RO/UCHL1, and CD20/L26 in all cases. Tumor cells were positive for CD15/LeuM1 in seven cases. In all 13 cases, RS cells and RS cell variants were infected by latent EBV as shown by in situ hybridization to EBV-encoded ribonucleic acid (EBER1). In 12 of 13 cases neoplastic cells coexpressed EBV latent membrane protein 1 (LMP1). EBV replication was examined by two different methods: immunohistochemistry to identify EBV-encoded BZLF1 protein and in situ hybridization to detect EBV BHLF1 transcripts. No positivity in RS or RS cell variants was detected with either assay of EBV replication (95% confidence interval [CI] = 0% to 23%). The findings confirm that EBV is detected more frequently in HIV-associated HD when compared with immunocompetent patients with HD. The findings also suggest that EBV is tightly latent within RS and RS cell variants of HIV-associated HD. It appears that factors other than host immune status are important in maintaining EBV latency in HIV-associated HD.
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PMID:Human immunodeficiency virus-associated Hodgkin's disease contains latent, not replicative, Epstein-Barr virus. 881 1

The Epstein-Barr virus (EBV) is closely related to Hodgkin's disease (HD), while the BCRF-I (viral [v] IL-10) gene of the EBV is highly homologous to the human interleukin-10 (h IL-10) gene. To investigate the relationship of IL-10 and HD, we performed both immunostaining and in situ hybridization (ISH) in 30 cases of HD. The presence of EBV in Hodgkin (H) and Reed-Sternberg (RS) cells was seen in 16 of the 30 cases, by ISH of the EBV EBER-I region and/or immunostaining of latent membrane protein (LMP-I). Of the 16 EBV-positive cases, 12 also showed IL-10 antigen (Ag) in H and RS cells by immunostaining, 5 of the 16 demonstrated hIL-10 RNA by ISH and 14 of the 16 showed vIL-10 RNA. But only 2 of the 14 EBV-negative cases showed IL-10 Ag, and one of them showed hIL-10 RNA, while none demonstrated vIL-10 RNA. The T cells in the HD-involved tissues were found to be mainly CD4-positive T cells, and had no association with EBV infection. However, the lymphocytes surrounding H and RS cells were more frequently CD4 cells and rarely CD8 cells in the EBV-positive cases, in contrast with the EBV-negative cases. The above results indicate that an EBV infection influenced both cytokine synthesis and the response of T cells in HD.
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PMID:Human and viral interleukin-10 in Hodgkin's disease, and its influence on CD4+ and CD8+ T lymphocytes. 760 67

A polymerase chain reaction (PCR) assay for the detection of Epstein-Barr virus (EBV) sequences in various clinical samples, especially peripheral blood leukocytes (PBL) and serum, was carried out and the results obtained were compared with specific EBV serology. One hundred seventy patients were enrolled in the study: 89 healthy blood donors, 22 asymptomatic patients, 36 individuals with primary EBV infection (including 19 patients with infectious mononucleosis [IM]), 22 HIV-infected subjects (including 4 with hairy oral leukoplakia, 3 with central nervous disorders, and 15 with non-Hodgkin's lymphoma). All the serum samples from the healthy blood donors were negative. In patients with IM and in AIDS-non Hodgkin's lymphoma (ARNHL), PCR was strongly positive in leukocytes (> 2,000 genome equivalents/10(4) cells), which was correlated with detectable amounts of EBV DNA in serum. The overall positivity rate of PCR in serum was 58.8%, 68%, and 73% of cases for non-IM primary EBV infections, IM, and ARNHL, respectively. In two cases of EBV primary infection, the viral DNA was detected in serum, respectively 1 month and 2 months before IgM positivity and IgG rise. In one case of ARNHL followed up for several months, PCR (viral load of 2,000 genome equivalents/10(4) cells) became positive concurrently with appearance of lymphoma. In immunocompromised individuals, PCR EBV, if carried out in larger prospective studies, could be considered as a tumor marker, useful for predicting EBV-driven lymphoma and follow-up therapy.
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PMID:Measurement by the polymerase chain reaction of the Epstein-Barr virus load in infectious mononucleosis and AIDS-related non-Hodgkin's lymphomas. 762 9

The prevalence of Epstein-Barr virus (EBV) markers in nodal lesions from Algerian (Al) patients (n = 47) was compared to French (Fr) patients (n = 21) with Hodgkin's disease. Initial characteristics were: males Fr 57%, Al 53%; median age Fr 29, Al 26; histologic subtypes: lymphocytic predominance (LP) Fr 1, Al 2; nodular sclerosis (NS) Fr 16, Al 19; mixed cellularity (MC) Fr 4, Al 12; lymphocytic depletion (LD) Al 2. The latent membrane protein (LMP) was expressed in Reed-Sternberg cells (RSC) in 16 Al (4 NS, 12 MC) and 4 Fr (2 NS, 2 MC) cases. All LMP-positive cases were also positive by DNA or RNA in situ hybridization (ISH). ISH was positive in RSC of 29% of Fr and 66% of Al patients (p < 0.02); the positivity was more frequent in MC (80%) than in other histologic types (39%). EBV genome was detected by PCR on DNA extracted from frozen samples in 84% of Fr and 95% of Al patients (100% of MC and 86% of other histologic types). The discrepancy between PCR and ISH results can be due to a lesser sensitivity of the latter technique, or, alternatively, to the presence of EBV in lymphoid cells surrounding RSC. ISH positivity was more frequent in young Al adults than in Fr ones. This more pronounced HD-EBV link in patients from a developing country compared with an industrialized one can result from the age at primary EBV infection, which occurs earlier in Algeria than in France.
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PMID:[Association of Epstein-Barr virus and Hodgkin's disease: comparison between Algerian and French patients]. 762 43

The growth transforming potential of Epstein-Barr virus (EBV) for Burkitt's lymphoma and nasopharyngeal carcinoma is now extended to other neoplasia, such as Hodgkin's disease, peripheral T-cell tumor and gastric cancer. We have generated an EBV recombinant with a selectable marker at the viral thymidine kinase locus. Recombinant EBV was successfully infected into a human T-cell line, MT-2. Following incubation in the selective medium, drug resistant MT-2 cell clones were isolated and proved to be infected with recombinant EBV. EBV-infected MT-2 cell clones expressed EBNA 1 and LMP 1 and very little of EBNA 2, showing the BamHI F promoter-driven latency II form of infection, which is seen in non-B-cell tumors. This is the first report of in vitro generation of latency II type EBV infection. The present system of persistent EBV infection in T cells should be a good model for investigating the pathogenic role of EBV in non-B-cell tumors.
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PMID:Persistent Epstein-Barr virus infection in a human T-cell line: unique program of latent virus expression. 764 89

We report in 4 patients the rare association of Hodgkin's disease and high grade B malignant lymphoma. In 2 cases, both tumours were disclosed at the same time but in different tissues from the same region. In the 2 other patients, the second tumour was found 11 months and 12 months after the first respectively. In all cases Hodgkin's disease was of the nodular sclerosing type, the tumour cells expressing CD 30 and CD 15. The high grade lymphomas were of the polymorphic centroblastic (large non cleaved) type and expressed the B markers. One (case 4) was secondary to a follicular lymphoma. In 2 cases (2 and 4) the search for a latent EBV infection was negative in both tumours. In case 1, only the Reed-Sternberg cells were positive with both techniques. Such an association is different from so-called composite lymphomas, and can be called "discordant lymphoma". Different related conditions are discussed. This association is distinct from lymphomas or Hodgkin's disease complicating the treatment of Hodgkin's disease or malignant lymphomas.
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PMID:Discordant malignant lymphoma synchronous or successive high-grade B lymphoma associated with Hodgkin's disease. A clinico pathologic and immunophenotypic study of 4 cases. 765 37

Epstein-Barr virus (EBV) encodes genes that permit its persistence in human B lymphocytes and genes that ensure its replication in epithelial cells. Immune restraints on the virus are usually so effective that most EBV infections are limited to a minute fraction of B lymphocytes and of epithelial cells. As a result, most EBV infections are never symptomatic. Occasionally, the virus causes disease, often with the cooperation of the immune system or other less characterized cofactors. Infectious mononucleosis, a generally self-limited lymphoproliferative illness common in adolescents and young adults, is due to primary EBV infection and to the brisk cellular immune response it elicits. Lymphoproliferative disorders of EBV-infected B cells arise almost exclusively when cellular immunity is grossly compromised. EBV-positive Burkitt's lymphoma contain a translocated and deregulated c-myc oncogene and EBV-positive non-Hodgkin's lymphomas are characterized by the presence of Reed-Sternberg's and Hodgkin's cells, features that have not been directly linked to EBV. Many recent observations, however, including evidence that virus infection precedes malignant transformation and is often associated with a characteristic pattern of viral gene expression, provide continued interest in the relationship between the virus and these haematological malignancies.
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PMID:Epstein-Barr virus as an agent of haematological disease. 766 46

Recent studies have indicated that nodular lymphocyte predominance Hodgkin's disease (nLP-HD) is a B-cell lymphoma. Although molecular events in the neoplastic transformation of B-cells are not well understood, Epstein-Barr virus infection and bcl-2 protein overexpression have been postulated to have etiologic roles in some lymphomas. Epstein-Barr virus has been demonstrated in the Reed-Sternberg cells of Hodgkin's disease cases (other than nLP-HD) as well as in some B-cell lymphomas; bcl-2 overexpression is found in the majority of follicular lymphomas. The biologic role for bcl-2 in HD is controversial. Some reports have indicated the presence of bcl-2 gene rearrangements, associated with the t(14;18) (q32;q21), detected by the polymerase chain reaction in HD; recent studies have failed to confirm this finding. Reports in the literature describe only a few such analyses in the nLP-HD subtype. To address these conflicting issues, we examined 12 cases of nLP-HD to determine whether bcl-2 protein expression (by immunohistochemistry) and Epstein-Barr virus (by in situ hybridization) could be detected in the Reed-Sternberg variants. None of the cases showed expression of bcl-2 protein or Epstein-Barr virus RNA in the neoplastic cells. Epstein-Barr virus does not appear to play an important role in the pathogenesis of nLP-HD. Similarly, we cannot substantiate a role for bcl-2 in the development of this type of Hodgkin's disease.
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PMID:Epstein-Barr virus and bcl-2 protein overexpression are not detected in the neoplastic cells of nodular lymphocyte predominance Hodgkin's disease. 767 75


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