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Query: UMLS:C0019829 (Hodgkin's disease)
 30,247 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Paraffin-embedded tissue specimens from 46 cases of Hodgkin's disease (HD) were studied by in situ hybridization with biotinylated probes for the presence of EBV genomes. EBV specific DNA sequences were detected in the nuclei of Reed-Sternberg (RS) and Hodgkin cells (H), in 14 of these 46 cases. There was no correlation between positive hybridization and morphological subtype or site of tumor. By demonstrating an exclusive localization of the viral DNA in the tumor cells of HD, our study adds to the growing body of evidence to suggest an involvement of EBV in the pathogenesis of at least some cases of HD.
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PMID:Demonstration of Epstein-Barr virus genome in neoplastic cells of Hodgkin's disease by in situ hybridization, in paraffin-embedded tissue using biotinylated probes. A study of 46 cases. 132 Jul 58

We studied 44 cases of Hodgkin's disease for the presence of Epstein-Barr virus (EBV) DNA, its localization and the expression of the EBV receptor on the tumour cells. EBV DNA was found in 52% (16/31) of the Hodgkin's lymphomas using the polymerase chain reaction. With a very sensitive non-radioactive DNA in situ hybridization technique in combination with immunohistochemistry for CD 30 or CD 15 antigens, EBV DNA was localized to Reed-Sternberg cells and its mononuclear variants. The relationship between the presence of EBV DNA and the expression of the EBV-receptor CR2 (CD 21) on Reed-Sternberg cells was studied using the same techniques and two different monoclonal anti-CD 21 antibodies. CR2 could be detected on a substantial number of the Reed-Sternberg cells in EBV DNA positive Hodgkin's lymphomas (9/12; 75%), whereas in EBV negative cases positivity with anti-CD 21 was rare (1/13; 8%). The results indicate that CR2 expression on Reed-Sternberg cells and the presence of EBV DNA sequences are frequently associated in Hodgkin's lymphomas.
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PMID:Epstein-Barr virus DNA in Reed-Sternberg cells of Hodgkin's disease is frequently associated with CR2 (EBV receptor) expression. 132 87

The prevalence of Epstein-Barr virus (EBV) and human immunodeficiency virus (HIV) in acquired immunodeficiency syndrome (AIDS)-related primary central nervous system (CNS) lymphoma was examined. Deoxyribonucleic acid (DNA) extracted from 12 formalin-fixed, paraffin-embedded tumors was used as substrate for the polymerase chain reaction (PCR). Targets for amplification were the EBNA-1 region of EBV, the gag region of HIV, and a single copy cellular sequence as a control. The cases studied were autopsy and surgical specimens collected between the years 1985 and 1989. By the working formulation for non-Hodgkin's lymphomas, five had large cell, four had mixed large and small cleaved cell, two had small cleaved cell, and one had an unclassified histology. Epstein-Barr virus was detected in 6 of 12 tumors studied. Human immunodeficiency virus was not detected in any of the tumors. The presence of EBV was not correlated with any particular histologic tumor type. It is concluded that EBV, not HIV, can be detected in a large percentage (50%) of AIDS-related primary central nervous system (CNS) lymphomas. This viral association may be significant in light of the demonstrated ability of EBV to induce lymphoid tumors in experimental mammalian systems.
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PMID:Epstein-Barr and human immunodeficiency viruses in acquired immunodeficiency syndrome-related primary central nervous system lymphoma. 132 21

Ki-1 (CD30)-positive, large-cell anaplastic lymphoma (LCAL) is a distinctive subset of non-Hodgkin's lymphoma; morphologically, the neoplastic cells of LCAL may closely resemble Reed-Sternberg cell variants of Hodgkin's disease. The neoplastic cells in Hodgkin's disease are often CD30-positive, as are some of the transformed lymphocytes in infectious mononucleosis. Recent evidence suggests an etiologic role for the Epstein-Barr virus (EBV) in Hodgkin's disease. Because of the phenotypic similarities between Hodgkin's disease and LCAL, we used the polymerase chain reaction (PCR) to analyze eight specimens of LCAL for EBV genome. Diagnoses were established by paraffin section morphology and immunohistochemistry. For comparison, we also analyzed nine non-Hodgkin's lymphomas other than the LCAL type, three Hodgkin's disease specimens, and nine non-neoplastic lymph nodes. PCR was performed using DNA extracted from frozen tissue; DNA was amplified using two sets of oligonucleotide primers corresponding to the BamH1 W-fragment of the EBV genome. Amplified EBV genome was obtained from all specimens except for one mantle zone lymphoma, one diffuse mixed-cell lymphoma, and six non-neoplastic lymph nodes. EBV terminus region probing and in situ hybridization techniques, each less sensitive than PCR, were performed in selected cases in an attempt to corroborate our PCR results. Only 2 of 13 specimens contained EBV detectable by these other techniques, and neither specimen was a LCAL. In view of the high incidence of latent EBV infections in humans, the biologic significance of our PCR results is uncertain. Despite the detection of EBV genome by PCR in a high percentage of lymphomas, we were unable to substantiate an etiologic role for EBV in LCAL. The PCR technique may be too sensitive to provide meaningful data on the possible role of EBV in lymphomagenesis.
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PMID:Detection of Epstein-Barr virus genome in Ki-1 (CD30)-positive, large-cell anaplastic lymphomas using the polymerase chain reaction. 132 22

Eleven cases of Hodgkin's disease (HD) were examined for the presence of the Epstein-Barr virus (EBV) genome, using the polymerase chain reaction (PCR) to detect EBV DNA in whole paraffin-embedded tissue specimens and in single cells picked out from the specimens with a micromanipulator. The EBV genome was detected in 5 of the 11 cases by conventional PCR. Single cell PCR demonstrated the EBV genome in Reed-Sternberg cells from all the EBV-positive cases, but not from any of the EBV-negative cases. Background lymphocytes and lysozyme-positive histiocytes from EBV-positive cases did not contain the EBV genome. These results indicate an etiological association of EBV with some cases of HD.
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PMID:Direct detection of Epstein-Barr virus DNA from a single Reed-Sternberg cell of Hodgkin's disease by polymerase chain reaction. 132 34

There is a clear association between the Epstein-Barr virus (EBV) and Hodgkin's disease (HD). EBV is not, however, detectable within the affected tissues of all cases. The proportion of positive cases varies from 15-79% depending on the assay used to detect EBV. The techniques utilised vary not only in sensitivity but in their ability to detect viral DNA, RNA, or protein and in their ability to demonstrate the cellular localisation of the virus. Thus, the biological significance of a positive result will vary depending on the method of analysis. In the present study, four different methods of detecting EBV were compared. RNA in situ hybridization was found to be the most practical method of detecting EBV in tumour cells. Using this assay EBV was detected in the Reed-Sternberg cells of 33% and 45% of the two series of HD cases examined in this study. We believe that these cases should be considered EBV-associated.
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PMID:Criteria for the definition of Epstein-Barr virus association in Hodgkin's disease. 132 80

In previous studies, Epstein-Barr virus was considered a possible etiologic factor in Hodgkin's disease. Two hundred twenty-nine cases of Hodgkin's disease were investigated for the presence of Epstein-Barr virus DNA using the polymerase chain reaction technique on formalin-fixed, paraffin-embedded lymph node tissue to clarify the clinical importance of the incidence of this genome. In 42 cases (18.3%), genomic DNA was not amplifiable. The remaining 187 cases included the following subtypes: lymphocyte-predominant type (n = 13), nodular sclerosis type (n = 98), mixed cellularity type (n = 68), and lymphocyte-depleted type (n = 8). Sixty-six cases (35.2%) were positive for Epstein-Barr virus DNA. In the statistical analysis of available follow-up data from 130 patients, no influence of a positive Epstein-Barr virus DNA finding on length of survival time was revealed. This was true within the cohort of all patients and within the histologically defined subtypes of Hodgkin's disease. In this investigation, detection of Epstein-Barr virus DNA by polymerase chain reaction showed no prognostic relevance for patients with Hodgkin's disease.
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PMID:Influence of Epstein-Barr virus genomes on patient survival in Hodgkin's disease. 132 90

To evaluate whether the expression of T-cell receptor (TCR) V beta families in eight cases of malignant T-cell lymphomas took place in a preferential manner, we analyzed four cases of mycosis fungoides (MF), the most common form of primary cutaneous T-cell non-Hodgkin's lymphomas (NHL), and four cases of primary nodal T-cell NHL. The usage of V beta families in T-cell populations was investigated on mRNA that was transcribed to cDNA using a C beta primer and reverse transcriptase. Subsequently, the specific usage of the families was analyzed by polymerase chain reaction (PCR) using combinations of the selected C beta-oligonucleotide primer and one of the family-specific V beta primers. Peripheral blood lymphocytes from four healthy volunteers and 1 "reactive" lymph node served as a control and expressed all 20 V beta families tested for. In T-cell lines, with restricted V beta expression, and in three patients with advanced MF, only one or two V beta families were expressed at the mRNA level. In an early MF lesion this monoclonal expression was absent: several V beta families were expressed with a weak intensity. This may indicate either a polyclonal origin of MF, or that too few monoclonal neoplastic cells were present in the tissue specimen. In the four nodal T-cell NHL, only one family could be clearly distinguished, whereas some of the other V beta families showed only a weak expression. These latter families represent the reactive T-cell component in the nodal T-cell NHL. Both in nodal T-cell NHL and in MF there was no preferential expression of a particular V beta family. There was a good correlation between PCR data and the expression of V beta-family protein products observed by immunohistochemistry on tissue sections of the T-cell lymphomas. All T-cell lines, three cases of MF, and three cases of nodal T-cell NHL showed a rearrangement of the TCR beta chain on DNA level.
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PMID:T-cell receptor V beta-family usage in primary cutaneous and primary nodal T-cell non-Hodgkin's lymphomas. 796 67

Epstein-Barr virus is associated with many diseases. Today, the pathologist may study either by immunohistochemistry or in situ hybridization on tissue sections: EBV genome, EBV messenger RNA, EBV latent and replicative proteins. Several technics can be performed on fixed paraffin-embedded tissue to demonstrate the presence of EBV DNA, EBER-1 RNA, LMP-1 protein. Frozen tissues are required for the study of EBNA-2, ZEBRA and replicating proteins expression. The results, obtained during the study of benign and malignant proliferations always or often associated with EBV, such as infectious mononucleosis, Burkitt's lymphomas, AIDS associated lymphomas, lymphoproliferations in immunocompromised patients, Hodgkin's disease, and some epithelial proliferations, are summarized.
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PMID:[Contribution of immunohistochemistry and in situ hybridization techniques in diseases caused by or associated with Epstein-Barr virus]. 133 77

The following manuscript reviews data presented at the Cologne meeting relating to oncogene expression in Hodgkin's disease. Presented data ranged from investigations of oncogene expression in cell lines, where transcripts of unique size were identified and lineage related expressions of transcription factors described to detailed cytogenetic investigations of fresh Hodgkin's biopsy tissue. Particular attention was centred on discrepancies in the described expression of t(14; 18) and the molecular demonstration of translocated bcl-2 breakpoints in Hodgkin's disease. A large volume of data was presented relating to the relative expression of bcl-2 breakpoints by either genomic hybridization or hybridization following DNA amplification, the expression of the bcl-2 protein or the defined cytogenetic presence of the translocation. Certain other cytogenetic abnormalities of interest in Hodgkin's disease were discussed.
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PMID:Oncogenes in Hodgkin's disease. 133 73


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