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

Lymphoproliferative disorders involving Epstein-Barr virus (EBV) infected natural killer (NK) cells are reported with increasing frequency, but the nature and role of EBV infection in these cells remains undefined. In this study, we have investigated virus-cell interactions in the EBV-positive YTN10 cell line, an NK-like cell line established from a patient with lymphoblastic lymphoma. Low level expression of the EBV receptor CD21 molecule was detected by FACS and reverse transcriptase polymerase chain reaction (RT-PCR) analysis. Immunoblotting and RT-PCR analysis identified a latency II pattern of EBV gene expression, consisting of EBNA-1 transcription from the Qp promoter, in the absence of other EBNA gene expression, and accompanied by LMP-1 and LMP-2A expression. The EBV genome was present in episomal form and there was evidence for lytic viral replication. This latency pattern is typical of EBV gene expression in nasopharyngeal carcinoma and Hodgkin's disease, and differs from the full spectrum of EBV latent gene expression in most posttransplant lymphoproliferative disorders and from the restricted EBNA-1 expression in Burkitt's lymphoma tissues. The interaction between EBV and NK cells described here has important implications for the pathogenesis and treatment of EBV-infected NK malignancies.
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PMID:Virus-cell interactions in a natural killer-like cell line from a patient with lymphoblastic lymphoma. 897 60

To determine whether there might be immunophenotypic differences between nodular lymphocyte predominance Hodgkin's disease (NLPHD) and progressive transformation of germinal centers (PTGC) to aid in the differential diagnosis, we compared 16 cases of NLPHD with 13 cases of florid PTGC and 2 cases of focal PTGC. Paraffin-section immunohistochemistry was performed for CD20, CD45RA, CD45RO, CD3, CD43, CD57, EMA, CD30, and CD21. All PTGC cases showed well-circumscribed nodules of confluent sheets of CD20+ CD45RA+ small cells. T cells were scattered singly or in small groups. In 5 patients with florid PTGC, the T cells in some of the nodules formed rings around a few large transformed lymphocytes. In contrast, the nodules in all NLPHD cases showed an irregular, "broken-up" pattern with CD20 and CD45RA, and there were prominent T cell rosettes around the CD20+ large cells in all nodules. Rosettes of CD57+ cells and staining of large cells for EMA were seen in 3 and 2 cases of NLPHD, respectively, but not in PTGC. There were no differences between NLPHD and PTGC with respect to staining for CD30 or CD21. Three of the eight patients with florid PTGC and a few T cell rosettes had had persistent or recurrent lymphadenopathy; NLPHD developed in 1 of these patients 13 years later. We conclude that a combination of pan-B and pan-T antigens can be a useful adjunct to morphology in distinguishing NLPHD from PTGC. In approximately one-third of florid PTGC cases, T cell rosettes may be present, but they are notably fewer than those in NLPHD. Close follow-up of such patients may be appropriate.
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PMID:Progressive transformation of germinal centers and nodular lymphocyte predominance Hodgkin's disease: a comparative immunohistochemical study. 988 1

Reed-Sternberg (RS) and Hodgkin's (H) cells are considered to be the neoplastic cells in Hodgkin's disease (HD). Although most data suggest their lymphoid origin, the nature of these cells still remains a subject of controversy. Recently, a number of RS cells have been found to express an antigen that is also present on follicular dendritic cells (FDCs), asserting FDCs as the possible progenitor cells of H-RS cells. This prompted us to investigate whether these CD21-positive cases had distinct clinicopathologic characteristics. In a series of 94 examined cases of HD, we identified 9 CD21-positive ones (4 of 37 cases of nodular sclerosis, 1 of 41 mixed cellularity, and 4 of 12 lymphocyte depletion HD) without any other B-cell marker on paraffin sections. The patients varied in age from 16 to 82 years (median, 50 years) and included six men and three women. They had superficial or mesenteric lymphadenopathy without hepatosplenomegaly. Peripheral blood leukocytosis was seen in three patients. The clinical course was indolent, and all patients but one achieved an initial complete response with HD-based treatment regimens, although three of them relapsed. Morphologically, two subgroups could be delineated. Six of the cases were characterized, besides by the classic RS cells, by a varying number of the cells with the distinctive walnutlike or cerebrumlike nuclei and cytologically with cytoplasmic processes. Their fine structural examination also revealed villous processes, but no desmosomes. The other three cases had multinucleated RS cells often with triangular nuclei, but not cytoplasmic processes. The percentage of CD21-positive tumor cells ranged from less than 10% to 60% among the H-RS cells. These RS cells were positive for CD30 (9 of 9), CD15 (7 of 9), CD68 (1 of 8), fascin (8 of 8), S-100 protein (1 of 7), and epithelial membrane antigen (2 of 8) on paraffin sections. Notably, of eight cases examined on frozen sections, two showed immunostaining for DRC1, CD35, R4/23, and Ki-M4p. Only CD35 was also detected in the other two cases. Genotypic investigation showed germline configuration of the T-cell receptor beta and gamma chain genes and the immunoglobulin heavy chain gene in all eight cases examined. In situ hybridization showed Epstein-Barr virus sequences in four cases, three of which were examined by the terminal region analysis and showed the Epstein-Barr virus to be monoclonal. We concluded that in a small proportion (9.6%) of HD, H-RS cells might be derived from FDCs and that they appear to represent a distinct pathologic variant based on morphologic and phenotypic traits within the framework of HD.
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PMID:Hodgkin's disease expressing follicular dendritic cell marker CD21 without any other B-cell marker: a clinicopathologic study of nine cases. 1019 66

Epstein-Barr virus (EBV) was first reported as the causative virus of Burkitt's lymphoma in 1964. Since then, EBV has also been associated with infectious mononucleosis, AIDS and transplant-related B cell lymphomas, and nasopharyngeal cancer. The virus has further been linked with T cell lymphomas, Hodgkin disease, and NK leukemia or LGL leukemia, establishing a concept of a wide spectrum of EBV associated malignant disorders. EBV DNA encodes several proteins such as EBNA1-6, LMP 1, 2 and others. Recent studies have demonstrated that EBNA2, EBNA5, EBNA3A, EBNA 3C are essential for transformation, and that any gene product is not sufficient to transform cells by itself. Further there are different mechanisms of virus-associated transformation or carcinogenesis among EBV-associated malignant disorders. On the other hand, human T lymphotropic virus type I (HTLV-I) is known as a causative virus of adult T cell leukemia (ATL). However, precise molecular mechanisms of leukemogenesis in ATL still remains unclear. Some additional factors to HTLV-I infection are supposed to be involved in complete leukemogenesis. We demonstrated that HTLV-I infected T cells and primary ATL cells express EBV receptor/CD21 on the cell surface. Therefore, it is possible that EBV infection is one of the factors. We further investigated this possibility in 6 HTLV-I infected T cell lines and primary ATL cells from 18 patients with ATL. However, no EBV genome was detected in both T cell lines and primary ATL cells. EBV involved T-cell lymphoma has unique clinical manifestations as compared to non-EBV involved T-cell lymphoma. Therefore, it is still possible that a small group of ATL patients with unique clinical manifestations is associated with EBV.
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PMID:Epstein-Barr virus involvement in T-cell malignancy: significance in adult T-cell leukemia. 1034 73

Large atypical follicular dendritic cells, considered dysplastic by some authors, were first described in association with Castleman's disease in 1991, but until now there has been no cytologic account regarding these cells. We report the cytologic and histologic findings of a case of hyaline-vascular Castleman's disease associated with "dysplastic "follicular dendritic cells which presented as a mediastinal mass in a young man. The presence of giant cells within the preoperative fine-needle aspirate specimen caused initial diagnostic uncertainty and their true nature was only confirmed retrospectively following application of an immunostain for CD21 to direct smears. Awareness of "dysplastic" follicular dendritic cells within aspirates of Castleman's disease will result in less cytological confusion in the future and may help to avoid the possibility of misdiagnosing Hodgkin's lymphoma which has certain cytologic similarities.
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PMID:Cytologic demonstration of "dysplastic" follicular dendritic cells in a case of hyaline-vascular Castleman's disease. 1078 43

Epstein-Barr virus (EBV)-positive T non-Hodgkin lymphomas (T-NHLs) have been described, but it is at present unknown how EBV infects T lymphocytes. It has been postulated that cytotoxic T cells (CTLs) or natural killer (NK) cells can be infected by EBV during the killing of an EBV-infected target cell. The objective of this study was therefore to determine whether the neoplastic cells in EBV-positive T-NHLs (n=221) of various locations have a cytotoxic phenotype. To identify EBV-harbouring cells, combinations were used of EBV-encoded RNA (EBER) in situ hybridization (RISH) and immunohistochemistry for T- and B-cell markers and the cytotoxic proteins TIA-1 and granzyme B. EBV was detected in the neoplastic cells of all nasal T-NHLs (n=9), 5/34 gastrointestinal (GI) T-NHLs, and 2/6 lung T-NHLs, but not in primary cutaneous T-NHLs (n=103). Moreover, EBV was found in the neoplastic cells of 2/48 nodal anaplastic large cell lymphomas (ALCLs), but not in neoplastic T cells of other nodal T-NHLs. However, 5/17 nodal peripheral T-NHLs not otherwise specified (PTCLs NOS) and 1/4 T-prolymphocytic leukaemias did contain EBV-positive non-T cells. Double staining revealed that in EBV-positive extranodal T-NHLs (n=16), the EBER-positive cells had a cytotoxic phenotype (TIA-1- and/or granzyme B-positive). In nodal non-ALCL T-NHLs, the EBER-positive cells were not positive for TIA-1 or granzyme B, nor did they express CD3, CD21 or HECA452. Instead, most of these cells expressed the B-cell marker CD20. These PTCLs NOS with EBER-positive cells showed features of AILD-like T-NHL. It is concluded that neoplastic cells of EBV-positive extranodal T-NHLs always have a cytotoxic phenotype, supporting the view that EBV can infect CTLs. In nodal non-ALCL T-NHL, EBV is only found in T-NHL with AILD-like features and is present in B cells, where it may contribute to the outgrowth of a malignant B-cell clone.
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PMID:Epstein-Barr virus is present in neoplastic cytotoxic T cells in extranodal, and predominantly in B cells in nodal T non-Hodgkin lymphomas. 1091 15

Distinction of lymphocyte predominance Hodgkin's disease (LPHD) from other forms of lymphoma often requires immunohistochemistry (IHC). Most previously published recommended panels include markers to define the large neoplastic cells (for example, CD20, J chain, CD45) as well as the non-neoplastic background cells (CD21, CD45RO, CD57, TiA 1). In the present study we examine the practical use of a double IHC method designed to look simultaneously at two germinal center specific cell types: bcl6+ cells and [bc16+, CD57+] co-positive cells. All 10 nodular LPHD had bcl6+ large cells and numerous CD57+ small background cells, including [bcl6+CD57+] cells in rosettes. One case of LPHD with large cell transformation contained numerous bcl6+ large cells both singly (in areas of typical LPHD) and in sheets (in foci of large cell transformation), many CD57+ small cells but few [bcl6+CD57+] co-positive cells and no rosettes. In none of the five cases of florid progressive transformation of germinal centers were true rosettes seen, although all contained variable numbers of bcl6+ large cells and CD57+ cells. Lymphocyte-rich classic Hodgkin's disease LRCHD cases were notable for bcl6 reactivity in Reed-Sternberg cells in all cases, numerous background small bcl6+ lymphocytes, and rare CD57+ cells. Two phenotypic profiles were associated with the 10 cases of T cell-rich B cell large cell lymphoma (TCRBCL). In the first, group "A," six of six cases had bc16- large cells and few CD57+ small cells, and none had significant numbers of [bcl6+, CD57+] co-positive cells. In the second, group "B," four of four cases had bcl6+ large cells with numerous CD57+ and [bcl6+, CD57+] co-positive cells. These findings not only show that LPHD can be distinguished from its morphologic mimics through identification of specific germinal center cell types, but also identifies a second group of TCRBCL (group "B") whose phenotype suggests it might be an architectural variant of nodular LPHD.
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PMID:Lymphocyte predominance Hodgkin's disease: the use of bcl-6 and CD57 in diagnosis and differential diagnosis. 1093 47

Because previous investigations suggested involvement of the Fas ligand (FasL) in the selection process in the follicular dendritic cell (FDC)-associated cell cluster of the germinal center, we investigated the expression of FasL in Hodgkin lymphoma (HL) on protein and RNA level, while considering the Epstein-Barr virus status of the Hodgkin and Reed-Sternberg (HRS) cells. Tumor tissue from 47 patients with classic HL (32 nodular sclerosis [NS], 11 mixed cellularity [MC], and 4 lymphocyte-rich [LR]) was analyzed by immunohistochemistry for FasL, Fas, CD21, and CD23 and by Western blotting for FasL. FasL mRNA was detected by an exon 4-specific oligonucleotide and Epstein-Barr virus infection by in situ hybridization for Epstein-Barr virus early RNAs (EBER). Western blotting showed soluble and membrane-bound forms of FasL. Immunohistochemistry showed FasL expression in virtually all HRS of 94% of NS cases and 82% of MC cases. FasL expression did not correlate with the Epstein-Barr virus status of the HRS. Low FasL protein expression was found in some HRS of LR cases. FasL mRNA was detected in 39% of NS, 46% of MC, and 33% of LR cases. Seventy percent to 90% of the HRS cells expressed Fas. CD21 immunohistochemistry showed disrupted FDC networks in the tumor tissue with reduced and virtually absent expression of CD23 and FasL. These observations suggest that FasL expression in HRS cells and the absence of FasL in the FDC cluster represent a disturbed microenvironment that may be involved in the pathogenesis of HL.
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PMID:Fas ligand expression in Hodgkin lymphoma. 1122 10

Structural alterations in the meshwork of follicular dendritic cells (FDCs) are frequently found in malignant lymphomas. Formaldehyde fixation and paraffin embedding, however, have long prevented consistent detection of FDCs. Wet heat-induced epitope retrieval in Dako Target Retrieval Solution (TRS) (pH 6.0) enabled the reliable detection of FDCs through CD21, CD23, and CD35 antigens in routinely processed tissues from 11 reactive and 69 neoplastic lymphoproliferations, thus allowing the distribution of the FDCs to be reevaluated. Germinal center FDCs in lymphoid hyperplasias and expanded FDC meshworks in the 8 mantle cell lymphomas, 7 low-grade MALT lymphomas, and 6 low-grade follicular lymphomas were intensely stained with all these markers. In 6 cases of B cell chronic lymphocytic leukemia, tumor cells were CD23+. In four cases of nodular lymphocyte predominance Hodgkin's disease (HD), expanded FDC meshwork's sharply delineating negative tumor cells and their rosetting T cell, were revealed mainly with the CD21 and CD35 antibodies. Follicular dendritic cells were also demonstrated in 11 cases of grade I nodular sclerosing HD, including follicular HD. Striking dendritic cell clusters were revealed with all 3 antibodies in 9 angioimmunoblastic T cell lymphomas. Sparse or no FDC meshworks were detected in the 4 cases of grade II nodular sclerosing HD, 5 follicular lymphomas with high-grade transformation, and 5 T cell-rich B cell lymphomas. CD35 immunostaining showed the most consistent labeling in the four FDC sarcomas studied in the current article. Reproducible demonstration of FDCs in routinely processed paraffin sections with CD21, CD23, and CD35 antibodies, as presented here, provides invaluable pieces of information in the diagnosis of lymphoproliferative disorders.
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PMID:Follicular dendritic cells in reactive and neoplastic lymphoid tissues: a reevaluation of staining patterns of CD21, CD23, and CD35 antibodies in paraffin sections after wet heat-induced epitope retrieval. 1139 28

Flow cytometric analysis is important in the diagnosis, classification, and follow-up of non-Hodgkin lymphoma. It is assumed that the lymphoma phenotype for each patient remains unchanged over time and is consistent from one specimen to another. To determine the variability in expression of lymphoid antigens, we reviewed 211 flow cytometry specimens of malignant lymphoma from 81 patients. Some antigens showed a stable pattern of expression such as CD5, CD10, CD19, CD20, and HLA-DR. In contrast, CD21, CD22, CD23, and CD25 showed more variability from one specimen to another. We believe several factors affect the stability of antigen expression. True differences in expression most probably are related to the biology and function of the different antigens. For instance, CD19 and CD20 are essential in cell maturation and function and, therefore, are present on the majority of cells. In contrast, CD22 has a role during B-cell activation and, therefore, is more variable. Lack of standardization inflow cytometry procedures also is responsible for some variability. Instrument settings for adequate compensation and the criteria used to determine when an antigen is reported as positive are important considerations when evaluating flow cytometry histograms.
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PMID:Immunophenotypic variability of B-cell non-Hodgkin lymphoma: a retrospective study of cases analyzed by flow cytometry. 1193 37


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