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)

The presence of Epstein-Barr virus (EBV) DNA in biopsy tissues from patients with Hodgkin's disease (HD) was investigated by the polymerase chain reaction (PCR) using primers specific to a sequence within the EBV Bam H1W region. EBV genome was detected in 33 of 57 (58 per cent) cases of HD. Viral DNA was, however, also demonstrated in nine of 24 non-Hodgkin's lymphomas, in three of nine non-neoplastic lymph nodes and in seven of 12 normal peripheral blood samples used as controls. In all cases, the band obtained following PCR was verified using Southern blotting and hybridization with highly specific Bam H1W probes. The results suggest that the technique is sufficiently sensitive to detect EBV in persistent latent infection in B-lymphocytes. Distinction between virus present as a possible aetiological agent of malignancy or as a latent infection is not possible when PCR is used under these conditions. The possible role of EBV as an aetiological agent of HD remains unresolved.
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PMID:Epstein-Barr viral DNA in Hodgkin's disease: amplification and detection using the polymerase chain reaction. 132 Jun 71

Epstein-Barr viral DNA (EBV DNA) has been detected in 20 to 58% of Hodgkin's disease tumors analyzed by Southern blotting or polymerase chain reaction (PCR). Because patients with Hodgkin's disease are generally immunodepressed, it is possible that the EBV is not directly involved in the pathogenesis of Hodgkin's disease but is merely detectable by molecular techniques because of reactivation of a latent infection. The purpose of this study was to determine if EBV DNA could be detected in an even higher percentage of cases of Hodgkin's disease, including acquired immunodeficiency syndrome (AIDS)-related Hodgkin's disease, by using newly designed, PCR amplification primers, and to compare the incidence of EBV DNA with the incidence of another common, latent virus (cytomegalovirus) in Hodgkin's disease tissue. The PCR was performed on DNA extracted from cells from 15 benign hyperplastic lymph nodes and from 15 cryopreserved cases of Hodgkin's disease, including 2 cases of AIDS-related Hodgkin's disease. For negative controls, PCR was also performed without template DNA and on genomic DNA from E. coli, calf thymus, a murine myeloma, and from a human cell line. After 32 cycles of amplification, a 225 base-pair amplification product comigrating with an EBV-positive control was detected in none of the negative controls but was present in 14 out of 15 cases (93%) of Hodgkin's disease, including both cases of AIDS-related Hodgkin's disease, and in 2 out of 15 cases of benign lymphoid hyperplasia. By contrast, cytomegalovirus DNA was undetectable by PCR in any of our specimens. We conclude that in our study set, the PCR procedure detected EBV-DNA but not cytomegalovirus DNA in a high percentage of cases of Hodgkin's disease, including two cases of AIDS-related Hodgkin's disease. These findings strengthen the hypothesis that EBV may be involved in the pathogenesis of Hodgkin's disease and AIDS-related Hodgkin's disease.
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PMID:Frequent detection of Epstein-Barr viral deoxyribonucleic acid and absence of cytomegalovirus deoxyribonucleic acid in Hodgkin's disease and acquired immunodeficiency syndrome-related Hodgkin's disease. 166 51

The Epstein-Barr virus (EBV)-encoded latent gene products, latent membrane protein (LMP) and EBV nuclear antigen 2 (EBNA 2), seem to have important roles in EBV-induced cell transformation in vitro, and have been implicated as important effector molecules in EBV-associated lymphomagenesis. Because up to 35% of Hodgkin's disease (HD) samples have been reported to contain EBV genomes, the expression of LMP and EBNA 2 in these tumours was investigated. 84 cases of HD were studied with monoclonal antibodies and immunohistochemical labelling of acetone-fixed cryostat sections. LMP, but not EBNA 2, was demonstrated in Reed-Sternberg (RS) cells of 40 cases (48%); the two proteins were easily detected in transformed lymphocytes of positive control acute infectious mononucleosis tonsils. LMP expression in RS cells varied according to the histological subtype of HD (1/10 cases [10%] of lymphocyte predominance subtype, 16/50 cases [32%] of nodular sclerosis, 23/24 [96%] cases of mixed cellularity type). That the LMP antibodies showed no substantial cross-reactivity with negative control tissues shows that they are useful probes for the diagnosis of latent EBV infection in tissue sections. The findings suggest that EBV is associated with more cases of HD than was previously recognised, that in positive cases RS cells express a latent infection protein phenotype (LMP+, EBNA 2-) which differs from that of other EBV-associated lymphomas, and that LMP expression is related to histologically aggressive subtypes of HD.
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PMID:Expression of Epstein-Barr virus latent gene products in tumour cells of Hodgkin's disease. 167 37

Paraffin wax sections of lymph node biopsies from a total of thirteen patients with the morphologic and clinical features of Castleman's disease were analyzed for the presence of the Epstein-Barr virus (EBV) by in situ hybridization for the noncoding EBV early RNAs (EBERs) and by immunohistochemistry for the EBV-encoded latent membrane protein-1 (LMP-1). Of twelve cases of localized Castleman's disease EBER-positive cells were identified in five, and in these cases were only rarely found and were always confined to the interfollicular regions. LMP-1 was not detected in any of these cases, either alone or after dual staining for EBERs and LMP-1. (A similar pattern of EBER expression is seen in nonneoplastic lymphoid tissue from EBV-positive individuals.) No EBER-positive or LMP-1 positive cells were identified in a single case of multicentric Castleman's disease. In two additional patients initially diagnosed with Castleman's disease of localized plasma cell type, repeat biopsy showed Hodgkin's disease. In both cases Reed-Sternberg cells and their variants were identified in the original biopsy on which the diagnosis of Castleman's disease was made. In one of these cases these cells showed expression of EBERs and LMP-1, indicating latent infection with EBV. The results suggest that EBV is not generally associated with Castleman's disease. Further analysis of a series of cases of multicentric Castleman's disease is indicated.
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PMID:Localization of Epstein-Barr virus in Castleman's disease by in situ hybridization and immunohistochemistry. 762 95

Epstein-Barr virus (EBV) is associated with a wide spectrum of benign and malignant diseases. Recent additions to the list include oral hairy leukoplakia; a subset of Hodgkin's lymphomas, particularly those with mixed cellularity histology or those occurring in underdeveloped countries; a subset of diffuse large cell/immunoblastic lymphoma in the immunocompromised, particularly primary central nervous system lymphoma; a subset of peripheral T cell lymphomas; and a subset of gastric carcinomas, particularly undifferentiated carcinomas. There are several distinctive aspects of the biology of the virus that are important in investigations of virus in clinical specimens. The presence of repeated elements in the genome facilitates detection of viral nucleic acids by a variety of hybridization techniques as well as the characterization of the clonality of virus-infected tissues. Latent viral infection is associated with several different patterns of viral gene expression in infected cells. Latent gene products are important because of their growth-regulating and -transforming properties as well as the potent cytotoxic T cell response they elicit. The abundant expression of the EBER RNA transcripts makes possible the sensitive detection of latent infection in EBV-associated tumors. Lytic infection can be inhibited by antiviral nucleoside analogues. Two lytic gene products are of special interest because of their homology to the cellular proteins BCL-2 and interleukin-10. Two viral biotypes or strains with different properties in terms of lymphocyte immortalization and transformation have recently been characterized. Current evidence suggests a differential biotype association with particular malignancies. Characterization of the association of EBV with various disease processes promises to be important for diagnosis and treatment as well as for a better understanding of the epidemiology and pathogenesis of these diabetes.
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PMID:Detection and characterization of Epstein-Barr virus in clinical specimens. 805 85

Some acquired immunodeficiency syndrome (AIDS)-related lymphomas (ARLs) are infected with Epstein-Barr virus (EBV), although the frequency and importance of this association is disputed. Using paraffin section RNA in situ hybridization (ISH) with digoxigenin-labeled riboprobes, we screened 16 central nervous system (CNS) non-Hodgkin's lymphomas (NHLs), 101 systemic NHLs, and 11 Hodgkin's disease cases arising in human immunodeficiency virus-seropositive individuals for EBV-encoded small RNA (EBER 1) expression, an EBV gene product transcribed in abundance during latent infection. Tumor cells contained EBV in 85 of 128 ARLs (66%), but infection rates differed with lymphoma type. EBER 1 was expressed in tumor cells in 11 of 11 Hodgkin's disease cases (100%), 15 of 16 CNS NHLs (94%), and 46 of 60 systemic immunoblast-rich/large-cell lymphomas (77%), but in only 12 of 35 Burkitt-type (small noncleaved cell) (34%) and 1 of 6 monomorphic centroblastic (diffuse large noncleaved cell) (17%) lymphomas. In most EBV-positive ARLs, all recognizable viable tumor cells expressed EBER 1. We conclude that (1) EBV infects tumor cells in all AIDS-related Hodgkin's disease cases, in virtually all primary CNS ARLs, and in most systemic immunoblast-rich/large-cell ARLs; (2) only a minority of Burkitt-type and monomorphic centroblastic lymphomas are associated with EBV; and (3) EBER-ISH is ideal for the histopathologic detection of latent EBV in routine tissue specimens.
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PMID:In situ demonstration of Epstein-Barr virus small RNAs (EBER 1) in acquired immunodeficiency syndrome-related lymphomas: correlation with tumor morphology and primary site. 839 1

Viral infections have been implicated in the pathogenesis of several malignancies. A high incidence of the Epstein-Barr virus (EBV) genome and increased EBV-specific antibody titers were frequently observed in Hodgkin's disease. Some epidemiologic and clinical similarities have been demonstrated between Hodgkin's disease and human testicular germ-cell carcinoma. However, we investigated testicular biopsies from 16 patients with testicular cancer and 16 noncancer controls for the presence of EBV, cytomegalovirus (CMV), and herpes simplex virus (HSV) genomes with in situ hybridization and evaluated serum antibodies against EBV, CMV, and mumps among 52 patients with testicular carcinoma and 54 age-matched controls without cancer. There were no statistically significant differences in increased virus titer between patients with testicular cancer and controls, and we detected no EBV or CMV DNA in tumor cells, although the HSV genome was found in 50% of the testicular-tumor patients and 37.5% of controls. The findings suggest that viral infections have no direct role in the etiology of testicular carcinoma. The detection of HSV DNA in both tumor patients and controls might be a sign of latent infection, rather than a risk factor for testicular cancer.
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PMID:Virus-related serology and in situ hybridization for the detection of virus DNA among patients with testicular cancer. 839 88

Tumor cells of Epstein-Barr virus (EBV)-associated Hodgkin's disease (HD) express the viral protein, latent infection membrane protein-1 (LMP1), but evade cytotoxic responses normally directed at this antigen. We tested whether local production of the immunoregulatory interleukins (IL)-4 and -10 may have a role in this process. IL-4 RNA was not detectable in any of the HD cases. By contrast, isotopic in situ hybridization and correlation with the presence of EBV gene products showed significantly higher proportions of cases with IL-10 expressing tumor cells in LMP1-positive (17 of 26, 66%) as compared with LMP1-negative HD cases (six of 37, 16%). Absence of EBV BCRF1 RNA indicated that the transcripts originated from the cellular IL-10 gene. Similarly, an association between IL-10 expression and EBV-infection of tumor cells was found in AIDS-related malignant non-Hodgkin lymphomas (ARL). Very small proportions of EBV-infected cells, mainly blasts, expressed IL-10 in infectious mononucleosis tonsils. Thus, although not entirely exclusive to EBV-positive cases, IL-10 expression is frequently associated with EBV-infection in HD and ARL and appears to be upregulated by EBV, most likely through LMP1. In view of the established inhibitory effects of IL-10 on cell mediated immunity, it is suggested that IL-10 expression may contribute to evasion of LMP1-positive cells from cytotoxicity directed at viral antigens.
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PMID:Frequent expression of interleukin-10 by Epstein-Barr virus-harboring tumor cells of Hodgkin's disease. 863 12

Primary infection with human herpesviruses 6 and 7 (HHV-6 and HHV-7) during early childhood causes permanent latent infection, usually without any ill effects; only a small percentage of primary infections will lead to exanthem subitum. Like other herpesviruses. HHV-6 and HHV-7 can be reactivated at any time if host defence mechanisms become defective (e.g. in transplant recipients, AIDS, tumour patients). HHV-6 can be reactivated under such conditions and cause a variety of clinical problems, such as exanthems along with interstitial pneumonia or hepatitis for example. In addition, the reactivated virus may influence the course of autoimmune and proliferative diseases such as systemic lupus erythematosus and Hodgkin's disease. While, HHV-7 may be associated with similar disorder, more systematic studies are needed to clarify the clinical implications and the pathogeetic mechanisms of both viruses.
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PMID:[Human herpesviruses 6 and 7. Basic principles and possible significance for dermatology]. 870 78

A patient is described with angioimmunoblastic T-cell lymphoma (AIL) (angioimmunoblastic lymphadenopathy with dysproteinemia [AILD]-type T-cell lymphoma), which was later followed by Hodgkin's disease. At the time of the initial diagnosis, histological examination of a cervical lymph node showed a typical picture of AIL with abundant clear cells which were CD45RO+, CD43+, and CD20-, and there was no evidence of a monoclonal B-cell proliferation by immunohistochemical analysis. In situ hybridization for Epstein-Barr virus (EBV) was negative. Interposed by a bout of recurrence, the patient developed, 16 years later, a left subparotid mass which showed histologic features of Hodgkin's disease, mixed cellularity type. Diagnostic Reed-Sternberg cells and their variants were CD30+, CD15- and CD20+. Neither rearrangement of TCR beta and gamma chain genes nor of immunoglobulin heavy chain and kappa light chain genes was detected in DNA extract from fresh material. In situ hybridization showed the presence of EBV within the Reed-Sternberg cells. The data show that EBV was not etiologically related to AIL in this case. Further, the deficit in cellular immunity that accompanied AIL conceivably permit primary EBV infection or reactivation of latent infection, which eventuated in development of Hodgkin's disease, but the exact pathogenesis remains uncertain.
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PMID:Angioimmunoblastic T-cell lymphoma (angioimmunoblastic lymphadenopathy with dysproteinemia [AILD]-type T-cell lymphoma) followed by Hodgkin's disease associated with Epstein-Barr virus. 880 2


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