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

Based on observations of 66 cases, in which tissues were specially processed to optimize the simultaneous preservation of cell membrane antigens and morphology, we provide evidence in favor of a relationship between follicular dendritic reticulum cells (FDRC) and Reed-Sternberg (RS) cells of Hodgkin's disease (HD) other than the lymphocyte predominance subtype. RS cells were intimately related to the FDRC network (75% of cases), and the expression of CD21 antigen was frequent (41% of cases). Exclusive expression of CD21 antigen was found in 11 cases of HD, while the expression of other B-cell-associated markers (CD19, CD20, CD22) was both variable and inconsistent. The expression of T-cell antigens (CD3, CD4, CD8) was rare. Null phenotype of RS cells was observed in 27 of 66 cases (41%). Epstein-Barr virus (EBV) nucleic acids were found in 34 of 66 (51.5%) cases. Double labeling techniques showed the presence of EBV-positive RS cells within the FDRC network. A non-B-cell origin of RS cells was supported by the differential expression of EBV latent antigens in HD (latent membrane protein+, EB nuclear antigen 2-), which is unusual in EBV-driven lymphoblastoid cell lines and EBV-positive B-cell lymphomas. FDRC and RS cells are known to share morphological traits (binucleated cells), and both cell types possess Fc receptor for IgG. The hypothesis is further backed by the findings of CD15 antigen expression by occasional RS-like dysplastic FDRC in Castleman's disease (five cases), which is characterized by hyperplasia of FDRC. Whether FDRC might be the only cells involved in the conversion to RS cells by the loss or gain of antigens remains to be determined.
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PMID:Relation of follicular dendritic reticulum cells to Reed-Sternberg cells of Hodgkin's disease with emphasis on the expression of CD21 antigen. 768 51

Several reports of chronic lymphocytic leukemia (CLL)/small lymphocytic lymphoma (SLL) and of coexisting or subsequent Hodgkin's disease (HD) have raised the question how these two disorders are related. The authors have identified eight new cases of B-cell low-grade lymphoproliferative disorders (LGLPD) and HD. Six of these cases were similar to those previously reported on by others in that the HD were mixed cellularity, nodular sclerosing, and lymphocyte depleted subtypes. The morphology in these cases was typical of HD, as was the immunohistochemical profile. However, the two remaining cases were notable in that the HD was of the nodular lymphocyte predominant type (NLPHD). To our knowledge, this association has not been well documented previously. In the two cases in this study, CLL and NLPHD were found simultaneously when each patient presented with lymphadenopathy and a lymphocytosis that was comprised of small monoclonal B lymphocytes coexpressing CD5. Lymph node biopsies in each case revealed typical NLPHD, with large, indistinct nodules containing scattered lymphocytic-histiocytic (L&H) cells. Focal, but distinct areas of CLL/SLL were also present. Immunostaining of the lymph node biopsy specimens showed the L&H cells to be CD20- and CD45 positive, and to lack CD15 or evidence of light chain restriction. In one of these patients, a NLPHD-associated large cell lymphoma developed 8 months later. The large cells were CD20- and CD45 positive, with lambda light chain restriction. In contrast, the original CLL cells in this patient expressed kappa light chains. This report indicates that LGLPD can be associated with all subtypes of HD, including the NLP type. The discordant light chain restriction between the CLL and the NLPHD-associated large cell lymphoma in one of these cases indicates that the CLL and HD were probably not derived from the same clone.
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PMID:Hodgkin's disease associated with chronic lymphocytic leukemia. Eight additional cases, including two of the nodular lymphocyte predominant type. 772 47

A new cell line, SBH-1, with the morphologic, immunophenotypic, and karyotypic features consistent with those of Reed-Sternberg (RS) and Hodgkin (H) cells, has been established from the pleural effusion of a patient. The cytologic appearance of SBH-1 cells is characteristic of multinucleate RS and mononuclear H cells, all containing inclusion-like nucleoli. The SBH-1 cells express CD30, CD15, CD25, CD71, CD45, CD20, CD22, and bcl-2 protein and are negative for epithelial membrane antigen. Cytogenetic analysis showed multiple clonal abnormalities with breakpoints at 14q32, 6q21, and 11q23. The Ig heavy chain genes and both Ig light chain genes were rearranged in SBH-1 cells, whereas the bcl-2 gene was in germline configuration. Messages for the cytokines interleukin-1 beta (IL-1 beta), tumor necrosis factor-alpha, and transforming growth factor-beta and the cytokine receptors IL-2R, IL-4R, IL-6R, and IL-7R were detected by reverse transcription-polymerase chain reaction analysis. Xenotransplantation of SBH-1 cells into severe combined immunodeficient (SCID) mice led to local and disseminated tumor growth. The cytologic, histologic, and immunohistochemical features of SBH-1 cells in SCID mouse tumors were typical of RS and H cells. The SBH-1 cell line will be useful in the study of RS and H cell biology, inasmuch as it represents a cell line obtained from a previously untreated patient.
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PMID:SBH-1, a novel Reed-Sternberg-like cell line capable of inducing tumors in SCID mice: immunophenotypic, cytogenetic, and cytokine expression profiles. 774 44

Two post mortem examinations from the Institute of Pathology, Albert-Ludwigs-University of Freiburg, will be presented. In both cases diagnosis of a T-cell-rich B-cell-lymphoma was first established after necropsy and evaluation of the immunohistochemical results. In the first case a peripheral T-cell-lymphoma was diagnosed after a peripheral T-cell-marker test. A liver biopsy showed suspicion of a Hodgkin-lymphoma. In the second case a biopsy of an extended retroperitoneal tumor showed a centroblastic non-Hodgkin-lymphoma 3 weeks before death. By autopsy we found in both cases a wide infiltration with small monomorphic lymphocytes. Less than 20% of the infiltrate consisted of polymorphous blasts with a wide morphologic range and prominent nucleoli. Immunohistochemistry showed the blasts to be CD20-positive, while the small monomorphic lymphocytes expressed the CD3 marker. In the first case kappa-light-chain-restriction was shown in the blasts by immunohistochemistry. Differential diagnosis difficulties, diagnostic criteria, prognosis and classification of these cases in the common non-Hodgkin-lymphoma classification will be discussed in view of the current literature.
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PMID:[T-cell rich B-cell lymphoma: diagnosis, differential diagnosis, and classification of two representative cases]. 774 28

The authors analyzed the frequency of immunophenotypic abnormalities in 1,474 cases of routinely fixed, paraffin-embedded B-lineage non-Hodgkin's lymphomas. B-lineage was determined by immunoreactivity for CD20 (L26, 92%); CD45RA (4KB5, an additional 3%) or immunoglobulin (Ig) light chain restriction (remaining 5%). CD45RA was found to be especially helpful on Bouin's-fixed or decalcified tissue and Ig staining was most helpful in plasmacytoid lesions. Coexpression of the T-cell marker CD43 (Leu-22) was the most common immunophenotypic abnormality, seen in 60% of mantle cell lymphomas (MCL), 39% of CLL/small lymphocytic lymphomas, 16% of diffuse large cell lymphomas (DLCL), but only 5% of follicular lymphomas (FL). Antibodies to CD45RO (A6 and UCHL1) and CD3 (polyclonal) were useful in distinguishing infiltrating T cells from B cells coexpressing CD43. Ig light chain restriction was the next commonest immunophenotypic abnormality, which was identified in 67% of plasmacytoid diffuse small cell lymphomas, 43% of MCLs, 35% of monocytoid B-cell lymphomas and 28% of FLs. Overexpression of bcl-2 oncogenic protein was observed in 71% of FLs (n = 96), but not in a control group of reactive follicular hyperplasias (n = 34). Combining two criteria increased the sensitivity of immunodiagnosis in certain circumstances.
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PMID:Detection of immunophenotypic abnormalities in paraffin-embedded B-lineage non-Hodgkin's lymphomas. 780

The case of a 36-year-old woman is presented. She had a voluminous tumour inside the 1/3 average part of the right thigh at 12 cm from the inguinal region. Apart from some local pains, she had a normal haematological formula, normal spleen, liver and lymph nodes. As the tumour of 5.5 x 5 x 4.5 cm was well incapsulated between the sartorius muscle and the great adductor tendon it was easily extirpated and presented a whitish-light yellow section. The histological cellular aspect was pleiomorphic with round, ovalar cells; some were big and clear cells of centroblast-type with several mitoses and giant multinucleated cells and collagenic bundles in between. The nodular Hodgkin sclerosis is not confirmed immunohistochemically because of the negative reaction for antigen Kil (CD30) so that the diagnosis was lymphoma with lymphoma with big B cells by CD20 reaction. We also found positive T cells at CD43 that might be reactive lymphocytes. The tumour ranks a rare malignant lymphoma and for the first time, an extraganglionar lymphoma in thigh was found. We have not met such a location in the literature.
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PMID:Voluminous solitary non-Hodgkin extraganglionary lymphoma of thigh. 784 84

Follicular dendritic cells (FDC) are restricted to the B-cell regions of secondary lymphoid tissue and to non-Hodgkin's lymphomas derived from the follicular center or the mantle zone. With their cytoplasmic ramifications they form a dense network which contains the B-lymphocytes. In situ, FDC are only detectable at the ultrastructural level or when stained with anti FDC-reagents. On the surface of their dendritic extensions they express transferrin receptors (CD71), the B-cell epitope CD20, class II antigens, the myelomonocytic molecule CD14, the glycoprotein gp50 (CD40), and several receptors for components of the complement system (CD11b, CD21, CD35). Subsequent to an antigen challenge, FDC trap and retain immune-complexes for a long period of time. In vitro FDC and neoplastic lymphocytes spontaneously form small cellular aggregates. This adhesion is mediated by the LFA-1-alpha/beta = ICAM-1, the VLA-4 = VCAM-1, and the ICAM-1 = C3bi- receptor ligand pathways on B-cells and on FDC, respectively. The loss of LFA-1- alpha/beta and ICAM-1 molecules may enable neoplastic lymphocytes to detach from FDC. The monoclonal B-cells now invade new compartments. In vitro, FDC have the capacity to activate resting B-cells and to save them from dying by apoptosis. Signals involved in this activation include cell-surface immunoglobulin and CD40. Immunocytochemistry and autoradiography with single cell suspensions of neoplastic B cells suggest that FDC also provide signals leading to the continued stimulation of lymphoma lymphocytes. During the early stage of HIV infection lymph nodes show an immense follicular hyperplasia, with a massive increase of the dendritic network of FDC. In the later stage of the disease, the continuous involution of the germinal centers is associated with a progressive destruction of FDC.
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PMID:Follicular dendritic cells in non-Hodgkin's lymphomas. 785 1

A 70-year-old woman with a 2-year history of B-cell chronic lymphocytic leukemia (CLL) developed headache, fever, chills, and weakness. Bone marrow examination revealed both CLL and large cell immunoblastic lymphoma (Richter's syndrome). As expected, the CLL was of B-cell lineage. The neoplasm expressed low-density monotypic IgM lambda, the pan-B-cell antigens CD19, CD20, and CDw75, and the CD5 and CD43 antigens. The large cell immunoblastic lymphoma was of T-cell lineage, positive for the CD45RB, CD3, CD45RO, and CD43 antigens, and negative for the CD20 and CDw75 antigens. Both neoplastic components were negative for Epstein-Barr virus RNA and latent membrane protein. Although 3% to 5% of patients with B-cell CLL may develop higher-grade lymphoma, usually the lymphoma is of B-cell lineage and often represents a histologic manifestation of clonal evolution. Less commonly, B-CLL patients may develop transformation to a higher grade tumor that resembles Hodgkin's disease. Both the usual form of Richter's syndrome and particularly the Hodgkin's variant of Richter's syndrome may be associated with Epstein-Barr virus. Patients with B-cell CLL rarely develop a higher grade lymphoma of T-cell lineage. To our knowledge, only one other example has been reported in the literature. Epstein-Barr virus was not associated with either neoplasm in this case.
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PMID:B-cell chronic lymphocytic leukemia followed by high grade T-cell lymphoma. An unusual variant of Richter's syndrome. 787 59

Two monoclonal antibodies (FB1 and FB21) reactive in formalin-fixed, paraffin-embedded tissue sections are reported in this paper. FB1 and FB21 recognize a cytoplasmic antigen and a surface antigen of B cells, respectively. FB1 reacts with mantle zone (MZ) B cells, germinal centre (GC) cells, and marginal zone (MrZ) B cells, but not with T cells in lymphoid tissues. FB21 reacts with MZ B cells, GC cells in lymphoid tissues, and T cells of peripheral blood, but not with MrZ B cells in the spleen. Neither monoclonal antibody (MoAb) reacts with monocytes, granulocytes, or plasma cells. FB1 reacted with all the B-cell lymphomas tested and with CD20-positive Reed-Sternberg cells in two of five cases of Hodgkin's disease, but not with multiple myelomas or T-cell lymphomas. FB21 reacted with B-cell lymphoma in 20 of 22 cases, but not with multiple myelomas, T-cell lymphomas, or Reed-Sternberg cells of Hodgkin's disease. Immunoprecipitation studies revealed that FB1 recognizes the same two polypeptide chains that are recognized by L26 and is a member of the CD20 antibody cluster. FB21 was thought to recognize a sialic acid-dependent carbohydrate epitope and this was confirmed at the Fifth International Conference on Human Leukocyte Differentiation Antigens (Boston, 1993). FB21 did not react with splenic MrZ B cells and was different from the pan B markers reported previously [CD20 (L26), CD45RA (MB1), and CD74 (LN-2)]. FB21 recognizes a subset of B cells and appears to be closely related to CD75/76 antibodies. FB1 and FB21 are useful MoAbs for the diagnosis and analysis of B-cell lymphomas.
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PMID:Production of two monoclonal antibodies (FB1 and FB21) useful for the identification of human B lymphocytes in formalin-fixed, paraffin-embedded tissues. 796 94

The reactivity of eight preferential B-cell (L26, 4KB5, and KiB3) and T-cell (polyclonal CD3, Leu22, MT-1, UCHL-1, and OPD4) antibodies which detect paraffin-resistant antigens was examined by a three-step immunoperoxidase technique in 111 formalin-fixed, paraffin-embedded diffuse aggressive non-Hodgkin's lymphomas (NHLs) to determine the optimal panel for accurate lineage assignment. L26 (CD20) and polyclonal CD3 (CD3) were the most sensitive (> 95%) and specific (100%) antibodies. They identified the B- or T-cell lineages correctly in 106 (95%) cases. The five L26-negative, polyclonal CD3-negative cases included all three precursor B lymphoblastic NHLs and two (one B and one T) diffuse large-cell NHLs. Immunostaining with the second most sensitive preferential B-cell (4KB5) and T-cell (Leu22) antibodies correctly identified the lineage in two additional NHLs, but one false-positive result occurred. Preferential B-cell antibody KiB3 reacted with two precursor B lymphoblastic NHLs. Use of additional paraffin-reactive antibodies did not increase the number of NHLs assigned to the correct cell lineage. In conclusion, it appears that a two-tiered approach, with a first-line panel consisting of L26 and polyclonal CD3, followed by 4KB5 and Leu22 in nonlymphoblastic NHLs and by KiB3 in lymphoblastic NHLs, represents the most efficient method of correctly identifying the B- or T-cell lineage of diffuse aggressive NHLs by paraffin tissue section immunohistochemistry.
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PMID:Paraffin-resistant antigens detectable by antibodies L26 and polyclonal CD3 predict the B- or T-cell lineage of 95% of diffuse aggressive non-Hodgkin's lymphomas. 808 50


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