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)

Epstein-Barr virus (EBV) has been associated with a wide variety of neoplastic conditions including nasopharyngeal carcinoma, gastric carcinoma, lymphoproliferative disorders in immunocompromised hosts, Hodgkin's disease, and non-Hodgkin's lymphomas of either B or T-cell phenotype. Although the presence of EBV in neoplastic lymph nodes has been well studied, very few studies have examined the distribution of EBV in normal or reactive lymph nodes. We studied normal or reactive lymph nodes from patients in Peru, a geographical region with a relatively high prevalence of EBV infection as compared with the United States or Europe. EBV DNA-RNA in situ hybridization was performed using a 30-base biotinylated oligonucleotide complementary to the EBER1 gene of EBV. Ten cases showed the presence of EBV RNA in scattered cells (less than 50 per section) and were utilized in the study. Most of the cells labeling for EBV RNA were small lymphocytes although some large lymphocytes also labeled. These cases were then subjected to double-labeling immunohistochemical/in situ hybridization studies using monoclonal antibodies L26(CD20), Leu22(CD43), Leu7(CD57), and the polyclonal antibody CD3. In their respective sections, of those cells that showed positive labeling for EBV RNA, 44% double labeled for L26, 24% double labeled for CD3, and 23% double labeled for Leu22. No cells double labeled for Leu7. This study shows that EBV RNA is expressed in both B and T-cells in nonneoplastic lymph nodes. These findings are compatible with other studies that have shown the presence of EBV in both B and T-cell non-Hodgkin's lymphomas.
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PMID:Epstein-Barr virus distribution in nonneoplastic lymph nodes. 830 16

Recent work has shown that p53 gene mutations are frequently found in Epstein-Barr virus (EBV)-positive and EBV-negative cases of Burkitt's lymphoma but not in EBV-associated undifferentiated nasopharyngeal carcinomas (NPCs). Similar viral gene expression patterns are observed in undifferentiated NPCs and in EBV-positive cases of Hodgkin's disease (HD), suggesting that the contribution of the virus to the pathogenesis of these malignancies may also be similar. We have analysed 116 cases of HD for EBV association and for immunohistologically detectable overexpression of p53. p53 overexpression was detected in the tumour cell population of 37 (32 per cent) of the cases. Fifteen cases showed p53-specific labelling of more than 40 per cent of tumour cells; in six of these, virtually all tumour cells were stained. In eight cases, between 5 and 40 per cent of tumour cells were labelled, and in another 14 cases, less than 5 per cent of tumour cells expressed detectable amounts of p53. EBV-positive HD cases were found in all groups with different levels of p53 overexpression as well as amongst p53-negative cases. While a more detailed analysis of the p53 gene in HD is required, these data show that overexpression of p53 in HD is heterogeneous and that there is no simple correlation between EBV infection and p53 overexpression.
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PMID:Overexpression of p53 in Hodgkin's disease: lack of correlation with Epstein-Barr virus infection. 838 96

Epstein-Barr virus (EBV) is linked to a spectrum of human diseases including epithelial and lymphoid malignancies in which it exists predominantly in a latent state. EBV is capable of establishing replicative infection at oropharyngeal and genital sites. Replicative EBV infection also occurs in oral hairy leukoplakia, in EBV associated lymphoproliferative disorders, and to a minor degree in nasopharyngeal carcinomas. Recent evidence also suggests that EBV replication, also, may be associated with AIDS related lymphomas and Hodgkin's disease. However it is widely believed that virus in circulating B-lymphocytes and in B-cell malignancies is stringently latent. We now show that by Southern blot analysis we can detect replicative forms of virion DNA in 14.5% (8 of 55) of EBV-positive Burkitt's lymphoma biopsies. This may be the explanation for the elevation of the titres of lytic cycle EBV antigens that is associated with presentation and relapse of EBV associated Burkitt's lymphoma.
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PMID:Replicative viral DNA in Epstein-Barr virus associated Burkitt's lymphoma biopsies. 838 79

In recent years an increasing number of reports have described Epstein-Barr virus (EBV)-induced lymphoproliferative disease, or portrayed EBV as a cofactor in lymphoproliferative diseases (e.g. Hodgkin's disease, Burkitt's lymphoma and nasopharyngeal carcinoma), in the presence of congenital or acquired immune defects. Improved molecular biological and immunological techniques now permit detailed investigation of EBV itself and of the immune system's reaction to EBV infection. Our analysis of X-chromosome-transmitted lymphoproliferative syndrome (XLP), an immune defect that occurs after EBV infection, depicts the whole spectrum of symptoms of EBV-associated diseases, explains various theories regarding pathogenesis, and discusses diagnostic and therapeutic measures.
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PMID:[X-chromosomal recessively inherited lymphoproliferative syndrome. An analysis of EBV-induced immune deficiency]. 838 21

Latent Epstein-Barr virus (EBV) infection is associated with a variety of malignancies. Rapid in situ hybridization techniques have been described for various lytic viral infections because of limited gene expression. However, EBERS (Epstein Barr early RNAs) are expressed in abundance in tumour cells which are latently infected with EBV. We have targeted these transcripts in a rapid (3 h) in situ hybridization assay fo the detection of latent EBV in clinical specimens, including formalin-fixed paraffin-embedded material. EBER RNA was detected in control cell lines which have two copies of the EBV genome and in paraffin-embedded biopsy specimens from patients with nasopharyngeal carcinoma, EBV-associated Hodgkin's disease, Burkitt's lymphoma and post-transplant lymphoma. The technique did not detect EBER RNA in oral hairy leukoplakia, a pathologic process previously characterized as associated with lytic EBV infection. The sensitivity, specificity and rapidity of this technique make it ideal for the diagnostic detection of EBV in latently infected clinical specimens.
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PMID:Rapid in situ hybridization for the diagnosis of latent Epstein-Barr virus infection. 839 39

Lymphoma represents a major source of morbidity and mortality among AIDS patients. AIDS-associated non-Hodgkin lymphomas (AIDS-NHL) are almost invariably B-cell derived, are classified as high or intermediate grade lymphomas, and display three main histologic types: namely, small non-cleaved cell lymphoma (SNCCL), large cell immunoblastic plasmacytoid lymphoma (LC-IBPL), and large cell lymphoma (LCL). Here we report the in vitro establishment of three new AIDS-NHL cell lines (termed HBL-1, HBL-2, and HBL-3) derived from three AIDS-SNCCL patients differing in primary tumor sites and risk factors for HIV infection. The derivation of the cell lines from the original tumor clones was established by immunophenotypic and molecular genetic analysis. These cell lines display clonal immunoglobulin gene rearrangement, express surface immunoglobulin and B-cell restricted markers, and exhibit a phenotype consistent with SNCCL. Monoclonal Epstein-Barr virus infection was found in only one of the cell lines (HBL-1). Cytogenetic analysis demonstrated the presence of a chromosomal translocation involving the c-myc proto-oncogene and an immunoglobulin locus in all three cell lines. The pattern of genetic lesions detected in HBL-1, HBL-2, and HBL-3 reflects that found in primary AIDS-SNCCL and includes activation of the c-myc oncogene as well as inactivation of the p53 tumor suppressor gene. These cell lines should prove useful in studies of the biological, immunological, and viral factors involved in AIDS-associated lymphomagenesis.
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PMID:In vitro establishment of AIDS-related lymphoma cell lines: phenotypic characterization, oncogene and tumor suppressor gene lesions, and heterogeneity in Epstein-Barr virus infection. 841 24

Although immunophenotypic abnormalities have been reported in B-cell non-Hodgkin's lymphomas (NHLs) occurring in the general population, there are no extensive studies on such abnormalities in AIDS-related B-cell NHLs. Reactivity of CD45RO/UCHL1 and expression of other T-cell associated antigens (CD43, OPD4, CD3, CD5, EMA) were examined by immunohistochemistry in 66 diffuse aggressive AIDS-related B-cell NHLs and in 296 AIDS-unrelated B-cell NHLs of similar morphology analyzed in the same institution. EBER in situ hybridization studies were also carried out in 57 of the 66 AIDS-related B-cell NHLs investigated. CD45RO/UCHL1 was expressed in 27% of AIDS-related B-cell NHLs, but only in 8% of diffuse aggressive AIDS-unrelated B-cell NHLs. The difference was highly significant (P < .001) overall and, within the Working Formulation subtypes, especially marked among small noncleaved cell (SNCC) lymphomas. Conversely, the reactivity of other T-cell associated antigens seemed to be very similar in AIDS-related and AIDS-unrelated NHLs. However, for CD43, a significantly lower number of positive cases was found in AIDS-related NHLs among SNCC lymphomas. Among AIDS-related B-cell NHLs, the highest frequency of CD45RO/UCHL1 expression was found in the immunoblastic subset with plasmacytoid differentiation. In the latter CD45RO/UCHL1 preferentially associated with EMA expression and EBV infection of the tumor clone, but not with CD45RA. The present finding of an excess of CD45RO/UCHL1 expression in AIDS-related B-cell lymphomas may reflect the preferential expansion of CD45RO expressing B-cell clones with putative autoreactive potential, as suggested by the expansion of CD45RO expressing B-cells in autoimmune disorders.
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PMID:High frequency of CD45RO expression in AIDS-related B-cell non-Hodgkin's lymphomas. 852 13

Hodgkin's disease (HD) has seldom been reported after transplantation. Epstein-Barr virus (EBV) is present in about 50% of Reed-Sternberg cells in HD developing in immunocompetent individuals, but is more frequently found in HD of acquired immune deficiency syndrome patients. We report 7 cases of HD that occurred in transplant recipients. Clinical and pathological data and studies of EBV reveal specific features of HD after transplantation. Six patients received kidney transplants and 1 patient received combined kidney and pancreas transplantation. Immunosuppressive therapy consisted of cyclosporine, steroids, azathioprine, and antilymphocyte globulins. One patient received, in addition, anti-CD3 mAb therapy and an EBV+ B cell lymphoma developed. Retrospective EBV serological data from patients were collected. Tumors were classified according to pathology. EBV studies were conducted by immunohistochemical methods with monoclonal antibodies to EBV-latent membrane protein (LMP) or EBV-nuclear antigen 2 (EBNA2), and by in situ hybridization for latent nuclear EBV-early RNAs (EBERs). The mean lapse of time between transplantation and HD was 49 months. Six patients presented with enlarged lymph nodes and 1 patient presented with liver involvement. HD was classified as IA in 2 patients, IIA in 3 patients, IIIB in 1 patient, and IVB in 1 patient. Four patients had primary EBV infection after graft, before HD, and the others reactivated latent EBV infection. Histological subtypes were mixed cellularity in 6 cases and lymphocytic depletion in 1 case. Latent EBV infection was detected with EBERs in all tumors. Reed-Sternberg cells expressed LMP, and were negative for EBNA2 expression. Six patients were treated: 2 patients at stage I received radiotherapy, and relapsed within 1 year with a more advanced stage of HD; chemotherapy was indicated as primary therapy in 5 patients, and as salvage therapy in 2 patients; it was associated with radiotherapy in 4 patients. Immunosuppressive therapy was reduced in all patients. Four patients were alive and in complete remission 18, 25, 31, and 67 months after chemotherapy, with a functioning graft in 3 patients. Two patients died of infection. Mixed cellularity is the most frequent histological subtype observed in HD occurring in transplant patients. EBV is present in all Reed-Sternberg cells. Posttransplant HD shows similarities with human immunodeficiency virus-associated HD. These facts argue for a role of EBV infection and immunosuppression in the progression of HD after transplantation.
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PMID:Hodgkin's disease after transplantation. 856 May 77

Seventeen of 40 cases of Hodgkin's disease (HD) and eight of 46 non-Hodgkin's lymphomas (NHL) were associated with Epstein-Barr virus (EBV) infection, judged by the EBER-1 in situ hybridization (ISH) method. Approximately 40% incidence in HD was comparable to previous reports. Young children and elderly HD patients were more prone to be found EBV positive. Fourteen of 17 HD and two of 8 NHL cases with positive EBER-1 ISH were also positive on LMP-1 immunostaining. EBV might have a role in lymphomagenesis in these cases. The fact that 7 of 8 EBV-related NHL were peripheral T cell lymphoma indicates the necessity of a larger-scale survey on this subject. As the present study revealed four cases with positive LMP-1 immunostaining but negative EBER-1 ISH (1 HD, 3 NHL), LMP-1 alone should not be regarded as a tool to prove EBV infection.
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PMID:Epstein-Barr virus genomes in Hodgkin's disease and non-Hodgkin's lymphomas. 856 34

Two-hundred and four cases of peripheral T cell lymphoma (PTCL) occurring in Europeans without any sign of HIV-infection were investigated for their association with an Epstein-Barr virus (EBV) infection. Polymerase chain reaction (PCR) was applied for EBV-DNA detection, in situ hybridisation (ISH) for the cellular localization of EBV-encoded small nuclear RNA (EBER) and immediate early gene expression (BHLF) and immunohistology (IH) for the detection of EBV-encoded latent membrane protein 1 (LMP1) and EBV nuclear antigen 2 (EBNA2) expression. PCR and EBER-ISH produced congruent results in almost all cases with amplifiable DNA, leading to the finding of an overall frequency of EBV presence in 87/204 (42.6%) of the PTCL cases. Through EBER-ISH, the virus was identified to be exclusively present in small and blastic bystander lymphocytes in 29 cases, whilst an additional infection of neoplastic T cells was observed in the remaining 58 EBV-positive cases. The entity presenting with the most frequent EBV infection of tumour cells was that of angioimmunoblastic type PTCL, whilst the primary cutaneous PTCLs only seldom harbored the virus. Forty-eight of the EBV-positive TCLs showed an infection of a small proportion (1-20%) of the tumour cell population, whilst another ten cases, belonging to the pleomorphic TCL (PMTCL) group, displayed an infection of several to almost all neoplastic T cells (20-100%). Additional lytic EBV-infected cells could be detected in four cases by BHLF-ISH. LMP1 expression was present in a small proportion of the neoplastic T cells in 24 of the 58 cases with tumour cell infection, whilst an EBNA2 expression was detectable only in one case. Some non-malignant EBV-infected B-immunoblasts and Hodgkin/Reed Sternberg-like cells also expressed LMP1 in several cases. Our data imply a role of EBV in the pathogenesis of only a few PMTCL cases with predominant tumour cell infection, whilst the pathogenic significance of an EBV infection in the other PTCLs remains unclear due to the usually partial infection of the neoplastic cell component.
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PMID:Frequent presence of latent Epstein-Barr virus infection in peripheral T cell lymphomas. A review. 857 54


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