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

Southern blot and polymerase chain reaction (PCR) were used to analyse rearrangements of antigen receptor genes in 27 cases (fresh tissues) and 51 cases (paraffin-embedded specimens) of non-Hodgkin's lymphomas (NHL). Thirty in 31 cases of NHL detected by Southern blotting showed IgH and/or IgK and/or TCR beta gene rearrangements. Of NHL with T-cell phenotype, 12 of 14 cases presented rearrangement of TCR beta gene. All the cases of analysed B-cell lymphomas displayed rearrangements of IgH and/or IgK genes. Two cases of NHL were considered bi-genotypic. Both showed IgH and TCR beta gene rearrangements. Three cases unclassified with immunophenotyping showed IgH and/or IgK gene rearrangements. In contract to the above findings all cases of reactive lymphoid hyperplasias demonstrated a germline configuration of antigen receptor genes, PCR analysis showed that monoclonal bands were observed in 77% of B-NHLs with IgH primers and 91% of T-cell lymphomas with TCR gamma primers. Besides, 4 cases of "borderline" lymphoid hyperplasias showed clonal bands of IgH and/or TCR gene rearrangements. The results suggested that gene rearrangements of antigen receptors is one of the most sensitive and valuable clonal markers in the diagnosis of lymphomas, and an important supplement to morphological diagnosis and immunophenotyping.
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PMID:[Application of gene rearrangement analysis in the diagnosis of non-Hodgkin's lymphomas]. 811 44

Cutaneous B-cell lymphomas constitute approximately 20% of primary cutaneous lymphomas. Most histologic subtypes of nodal B-cell lymphomas also occur primarily in the skin. The recently described T-cell-rich B-cell lymphomas (TCRBCLs) manifest mainly in the lymph nodes. This article presents a case of TCRBCL arising primarily in the skin, the origin of which could be traced back 13 years. The patient is a 59-year-old man. Plaque-like and nodular skin infiltrates had first appeared in the left preauricular region. Repeated examinations never found any extracutaneous involvement. A skin biopsy and a retrospectively studied 10-year-old skin specimen showed identical histologic features. Immunohistochemistry identified the TCRBCL previously considered as cutaneous Hodgkin's disease or a diffuse centroblastic centrocytic non-Hodgkin's lymphoma. A clonal B-cell population was detected by polymerase chain reaction, showing a rearrangement of IgH gene. The case of this patient shows that primary cutaneous TCRBCLs, similarly to other B-cell lymphomas in the skin, may have a good prognosis, in contrast to their nodal counterparts.
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PMID:Primary cutaneous T-cell-rich B-cell lymphoma. A case report with a 13-year follow-up. 859 80

The development of rapid PCR protocols for amplification of rearranged IgH gene sequences has greatly facilitated the identification of clonal IGH rearrangements in non-Hodgkin's lymphomas (NHL) and leukemias. However, the 15-35% incidence of false negative results with this approach has been a constant and unresolved problem. To assess the reliability of a previously published framework region 3 (FR3A) IgH-CDR3-PCR for detection of monoclonal IgH gene rearrangements we compared the PCR and Southern results in a series of 44 NHL and leukemias of B cell lineage showing a JH-rearrangement in Southern analysis with genomic DNA and hybridization with a IgH joining region (JH) probe. IgH-CDR3 regions were amplified using DNA extracted from clinical specimens by PCR using fluorescent dye-labeled consensus primers homologous to conserved regions within the variable (VH) and the joining (JH) gene segments. The PCR products were size separated on a high resolution polyacrylamide gel and analyzed for clonality by exact size determination and fluorescence quantification in an automated DNA sequencer. With commonly used DNA polymerases monoclonal IgH-CDR3 junctions were identified in 36/44 samples (82%). However, in the remaining eight cases (18%) with pathohistologically clearly demonstrated B cell malignancies which were also monoclonal on JH-Southern analysis, monoclonality could be demonstrated by FR3A-IgH-CDR3-PCR only with the proofreading UITma DNA polymerase. In four of these monoclonal VH--N--DH--N--JH junctions sequence analysis was performed which showed a point mutation in one and a single nucleotide deletion at the 3' terminus of the primer target site in the other case. In the remaining two cases no primer mismatches could be identified. Thus we conclude that the marked improvement of the PCR-detection rate of monoclonal IgH-CDR3 junctions was achieved at least in part due to the ability of UITma DNA polymerase to remove mismatched bases at the 3' terminus of the primers with respect to the target during the first amplification cycles. Our results suggest, that UITma is the DNA polymerase of choice for amplification of IgH-CDR3 junctions with consensus FR3A-VH- and JH-primers.
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PMID:Use of UITma DNA polymerase improves the PCR detection of rearranged immunoglobulin heavy chain CDR3 junctions. 860 29

Bcl-x is a member of the bcl-2 family of proteins which are characterized by their ability to modulate apoptosis. Alternative splicing results in two distinct bcl-x mRNAs encoding a long isoform, bcl-xL, which acts as a bcl-2 agonist; and a short isoform, bcl-xS, which inhibits bcl-2 effects. The aim of the study was to determine whether bcl-x is expressed in lymphoma tissues and to characterize the respective production of bcl-xs and bcl-xL. We investigated the expression of bcl-x mRNA in a series of 50 non-Hodgkin's lymphomas (NHL) and Hodgkin's disease (HD) cases using a RT-PCR method in order to amplify both transcripts simultaneously, and to estimate their relative abundance. The rearrangements of the bcl-2 gene were analysed by RT-PCR expression of the hybrid bcl-2-lgH mRNA. In addition, 20 PCR-positive NHL cases and three HD cases were analysed by immunohistochemistry using bcl-x polyclonal antisera. RT-PCR showed bcl-x expression in 43/45 NHLs and 5/5 HD cases. The bcl-xL transcript was predominant in all positive cases and was associated with variable amounts of bcl-xS. There was no significant correlation between the profile of bcl-xL/bcl-xS expression and the histological and immunological subtyping. Bcl-x immunodetection was positive in the neoplastic cell component in all analysed cases, but the degree of staining was highly variable between cases. Expression of the hybrid bcl-2-IgH gene was detected by RT-PCR in five cases of follicular NHL and in one case of HD, but this group of tumours did not display a particular profile of bcl-xL/bcl-xS expression. We conclude that bcl-x is commonly expressed by malignant cells in various types of malignant lymphomas, with a predominance of the bcl-xL transcript. Since the corresponding bcl-xL isoform can block the cell death machinery and potentialize bcl-2 effects, it may be involved in some pathways of lymphomagenesis.
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PMID:Predominant expression of the long isoform of Bcl-x (Bcl-xL) in human lymphomas. 861 83

Mantle cell lymphoma (formerly known as intermediate lymphocytic lymphoma, diffuse centrocytic lymphoma, or diffuse small cleaved lymphoma) is one of the small cell non-Hodgkin lymphoma entities that is clinically more aggressive than small lymphocytic lymphoma, and needs to be separated from it. Mantle cell lymphoma is strongly associated with the t(11;14) chromosomal translocation that rearranges the bcl-1 oncogene (PRAD-1 gene) and immunoglobulin heavy chain gene. In this study, we developed a nested polymerase chain reaction system to evaluate the t(11;14) translocation. The study material consisted of 10 mantle cell lymphomas fulfilling the criteria suggested by other authors (P. M. Banks et al. Surg Pathol 16:637, 1992). A novel nested polymerase chain reaction system was used to evaluate the bcl-1 breaks in the major translocation cluster using two successive polymerase chain reaction amplifications. This reaction yielded a background-free single product of the size of 200 to 300 base pairs in four of 10 mantle cell lymphomas. The identity of the product from the nested polymerase chain reaction was confirmed by Southern blotting followed by hybridization with a specific probe. The amplification products were also evaluated by Sst-I, Alu-I, Dde-I, and Ita-I restriction enzymes and showed different patterns of digestion reflecting individual differences between the MTC/ IgH junctions. A selection of other low-grade lymphomas, including lymphocytic, follicular, and mucosa-associated lymphoid tissue lymphoma, and hairy cell leukemia and 29 hyperplastic lymph nodes were negative. This nested polymerase chain reaction system for the t(11;14) translocation involving major translocation cluster offers a convenient specific identification for mantle cell lymphoma. However, this test has a limited diagnostic power because only about half of the mantle cell lymphomas show the bcl-1 breaks in the major translocation cluster. The test performs well in formaldehyde-fixed and paraffin-embedded material, allowing the study of large numbers of retrospective cases of mantle cell lymphomas.
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PMID:Molecular diagnosis of mantle cell lymphoma in paraffin-embedded tissue. 872 72

The cellular origin and the type of proliferation of the Hodgkin and Reed-Sternberg (HRS) cells, the malignant cells of Hodgkin's disease (HD), is an issue of constant debate. Immunohistochemical and molecularbiological studies of different research groups revealed contradictory results among the different groups ranging from a complete absence to a frequent presence of B-cell or T-cell characteristic features in the HRS cells. The determination of their clonality by cytogenetic means produced no conclusive results. To unequivocally clarify these questions we and others isolated single HRS cells and amplified their immunoglobulin (Ig) rearrangements. Most groups found Ig rearrangements within the HRS cells pointing to a B-cell nature of these HD cases. Individual IgH rearrangements were found in a proportion of the HD cases whereas most cases harbor monoclonal HRS cells with or without additional polyclonal rearranged HRS cells. Further studies are needed to clarify whether the differences among the different groups are caused by the selection of the HD cases used for investigation.
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PMID:Ig rearrangements in isolated Reed-Sternberg cells: conclusions from four different studies. 883 6

Molecular analysis of leukemias has been demonstrated to be useful for understanding the pathogenesis of leukemias or for detection of minimal residual disease. We present studies on the application of molecular diagnosis in malignant lymphomas. Although follicular lymphomas, a part of non-Hodgkin's lymphomas (NHL), often involve a t (14;18) chromosomal translocation, it is difficult to detect the translocation in some cases by conventional chromosomal analysis. We showed the usefulness of amplification of mbr/JH and mcr/JH junction by PCR to detect the translocation. The PCR products of mbr/JH junction were positive in 7 out of 8 cases of follicular lymphomas some of which were negative in tests on the translocation in the malignant cells. However, most NHL do not have cytogenetically specific translocations, indicating the necessity for another way to diagnose the malignant lymphomas. We used IgH gene probes as tumor specific markers in B-cell lineage malignant lymphomas. We determined DNA sequences for complementarity-determining region 3 (CDR3) of IgH in the malignant clone of each case. Then, we prepared a unique 5' primer for PCR or an oligonucleotide probe for detecting the clone-specific VH gene in each case, amplified the DNA by PCR and finally tried to detect minimal disease in bone marrow or peripheral blood, which brought into sequential detection of minimal residual disease in NHL. Thus, molecular diagnosis in hematopoietic malignancy will be more important in diagnosis, staging, and clinical management of patients with NHL.
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PMID:[Molecular diagnosis in hematopoietic malignancy]. 885 Nov 93

Analysis of IgH and TcR-gamma genes using consensus primers identifying junctional regions of rearranged genes by polymerase chain reaction (PCR) was performed on tissues involved by Hodgkin's disease (HD) in 90 cases and was correlated with the immunophenotype of Hodgkin and Reed-Sternberg (HRS) cells and the presence of Epstein-Barr virus (EBV) within these cells. Clonal IgH gene rearrangements were found in 1/5 cases of lymphocyte predominance (LP) subtype and none was positive for EBV. In 85 cases of classic HD, no IgH or TcR-gamma gene rearrangements were found in 51 (60 per cent) cases. A similar percentage, but not the same cases, were of null (non-B, non-T) phenotype. Of 30 cases where a B phenotype was assigned to HRS cells, nine had IgH gene rearrangements, three had TcR-gamma gene rearrangements, and two had both genes rearranged. None of the five cases assigned to T phenotype of HRS cells showed rearrangement of TcR-gamma genes, but two cases showed rearranged IgH genes. Among 41 cases of null phenotype, ten had IgH gene rearrangements, five had TcR-gamma gene rearrangements, and three cases had both genes rearranged. Whereas EBV was detectable in HRS cells in 17/43 classic HD cases of assigned B phenotype, EBV was also detectable in 2/5 cases of assigned T phenotype and in 21 cases with the null phenotype. Furthermore, there was no correlation of EBV with the presence or lack or IgH or TCR-gamma gene rearrangements. Of the remainder, half (30 per cent) expressed antigens associated with lymphocytes without an appropriate genotype. The results confirm lymphocyte-lineage committed cells at the origin of HRS cells in 40 per cent of cases. Any hypothesis of a non-lymphocytic origin of HRS cells will require the inducibility of CD30 on candidate precursors and the methodology for probing genetic events in such cells to be addressed.
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PMID:IgH and TcR-gamma gene rearrangements identified in Hodgkin's disease by PCR demonstrate lack of correlation between genotype, phenotype, and Epstein-Barr virus status. 919 35

The aims of this study are to evaluate the frequency of clonal immunoglobulin heavy chain gene rearrangements in paraffin-embedded samples of Hodgkin's disease (HD) with use of the polymerase chain reaction method and to correlate the molecular findings with the histologic and immunocytochemical features. DNA extracts from paraffin-embedded sections from 212 HD samples were used for amplification of the IgH gene by use of framework 2 and framework 3 region primers. Immunohistochemical studies were performed on paraffin sections by use of monoclonal antibodies for CD20 and latent membrane protein-1 and polyclonal antibody for CD3. With use of both primer combinations, monoclonality was detected in 18.7% of lymphocyte-predominant HD cases and in 32.2% of classical HD cases. These results suggest that immunoglobulin heavy chain gene clonal rearrangements are relatively frequent in classical HD. In addition, the statistical analyses of the genotypic and immunocytochemical data revealed that the detection of B-cell populations is significantly associated with the expression of CD20 on HRS cells. There was, however, no correlation between the histologic subtype, the percentage of HRS cells, the presence of latent membrane protein-1 expression, and the molecular analysis results.
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PMID:Molecular analysis of the IgH gene in 212 cases of Hodgkin's disease: correlation of IgH clonality with the histologic and the immunocytochemical features. 923 78

Lymph nodes from the incipient or early neoplastic phase of adult T-cell leukemia/lymphoma (ATLL) histologically resemble Hodgkin's disease. Integrated proviral human T-lymphotrophic virus type I (HTLV-I) has been demonstrated in such lesions. We studied 18 patients with this disease, and about half of the cases developed typical ATLL within 2 or 3 years. In all cases, either mono- or oligoclonal cell populations with proviral HTLV-I DNA were detected by Southern blot analysis and/or inverse polymerase chain reaction (IPCR). In addition, either a mono- or oligoclonal rearrangement of T-cell receptor genes was demonstrated. Giant cells with Reed-Sternberg-like histological features revealed CD15 and CD30 positivity. The background infiltrating lymphocytes represented either no or only minimal nuclear abnormalities with a CD4+ T-cell phenotype. In less than half of all cases, Epstein-Barr virus (EBV) infected the giant cells. A mixed EBV-A and -B type was found in 3, and a multiple genotype of EBV lymphocyte-determined membrane antigen (LYDMA) was found in 6 cases. These results could have been due to the immunodeficient status of the patients. A single-cell PCR of the giant cell, B cell, CD4+ or CD8+ T cells could be performed after cell sorting in 4 cases. HTLV-I infection was frequently found in the CD4+ T cells, but in neither the giant cells nor the B cells. The CD4+ T cells exhibited clonality. The giant cells showed various PCR products of IgH, and also expressed recombination activating genes (RAG). In summary, the giant cells were reactive cells, which resembled the immature B-lineage cells, while HTLV-I infected the CD4+ T cells, which demonstrated clonality. Based on these above findings, we consider CD4+ cells to play an important role in ATLL tumorigenesis.
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PMID:Clonal HTLV-I-infected CD4+ T-lymphocytes and non-clonal non-HTLV-I-infected giant cells in incipient ATLL with Hodgkin-like histologic features. 925 96


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