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

Both immunophenotypic overlaps between Hodgkin's disease (HD) and non-Hodgkin's lymphoma (NHL), and evolution of one into the other have been reported. However, the underlying assumption that the antigenic expression of Reed-Sternberg (RS) cells is consistent in the same patient has not been evaluated. Such an evaluation was undertaken by immunophenotyping paraffin-embedded lymphoid tissue biopsies with HD from 56 patients in whom multiple specimens were obtained, either simultaneously from different sites or at different times. The panel of antibodies we used included: CD3 polyclonal antiserum, DAKO-M1 (CD15), L26 (CD20), BerH2 (CD30), MT1 (CD43), DAKO-LCA (CD45RB), UCHL1 (CD45R0), LN2 (CD74), and DAKO-EMA. The phenotype of RS cells was identical in simultaneous biopsies in only 11 of 39 patients (28%) and remained constant in consecutive biopsies in only 4 of 21 patients (19%). Major differences (relative to cell lineage specific antigens) were observed in 10 of 39 patients with simultaneous biopsies and in 10 of 21 patients over time; they mainly involved expression of T-cell antigens. Minor differences (relative to any other antigen) were observed in 22 of 39 patients with simultaneous biopsies and in 15 of 21 patients over time; these mainly involved CD15 or CD74. This striking variability of the immunophenotype of RS cells in the same patient may be due to aberrant marker expression, as a result of the neoplastic state, and/or to modulation of antigenic expression in relation to the host environment. This inconsistency suggests caution when interpreting the relationship between HD and NHL by paraffin immunophenotyping alone.
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PMID:Inconsistency of the immunophenotype of Reed-Sternberg cells in simultaneous and consecutive specimens from the same patients. A paraffin section evaluation in 56 patients. 135 42

The most recent sophisticated investigations have provided new and revealing but also contradictory and controversial informaiton on the biological nature and the cellular origin of Hodgkin and Reed-Sternberg (H-RS) cells. Immunophenotypic analyses have shown consistent expression of CD15, CD30, CD74, and HLA-Dr antigens, but generally lack of T- or B cell-associated markers in H-RS cells. The H-RS cells are also devoid of many monocyte/macrophage-associated antigens. Molecular genetic studies have demonstrated heterogeneous findings with respect to rearrangements of T-cell receptor and immunoglobulin genes. Only a small percentage of the cases have rearrangements; this cannot always be attributed to the threshold of sensitivity of the method and/or the scarcity of the malignant cells in tissues examined. The H-RS cells do not express transcription factors such as BSAP, TCF-1, and GATA-3, known to be associated with lymphoid cells. It appears that evidence to support a lymphoid origin for H-RS cells is still lacking. On the contrary, the mechanism responsible for the unique clinical and histopathologic alterations associated with this disease has become clear. The H-RS cells have been shown to secrete IL-1, IL-5, IL-6, IL-9, TNF-a, M-CSF, and TGF-b, and, less frequently, IL-4 and G-CSF. These cytokines are likely to be responsible for the increased cellular reaction and fibrosis observed in tissues involved by HD and for the immunosuppression in patients with HD. Like most lymphomas, the etiology or pathogenesis of HD remains unknown. The Epstein-Barr virus (EBV) genomes are clonally integrated in the H-RS cells of about half the cases. The significance of these findings, whether EBV is a causative agent or an epiphenomenon, remains to be elucidated.
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PMID:The nature of Reed-Sternberg cells: phenotype, genotype, and other properties. 784 86

The nature and frequency of occurrence of monocytoid B-lymphocytes (MBL) was examined in 118 cases of Hodgkin's disease. Monocytoid cells were present in six cases (5%), four nodular sclerosis and two mixed cellularity. These cells were CD20+, CD3-, CD45RO-, KP-1-, PGM1-, with occasional positive reaction for MB-1 and CD74, indicating their B-cell nature, i.e., MBL. The MBL were distributed in the periphery of the nodules of nodular sclerosis accompanying centrally located Reed-Sternberg cells, although Reed-Sternberg cells were observed in some MBL clusters. In the mixed cellularity, MBL were located in the para-follicular area occasionally adjoining the lymph follicles. Because previous studies suggested depressed immune function in autoimmune diseases, acquired immune deficiency syndrome, and older persons to be responsible for the occurrence of MBL, it is possible that in some patients development of foci of MBL under immunodeficient conditions progresses to Hodgkin's disease.
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PMID:Occurrence of monocytoid B-lymphocytes in Hodgkin's disease. 793 19

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

From September 1984 through December 1991, of those with human immunodeficiency virus infection seen at the acquired immune deficiency syndrome unit of the Centro di Riferimento Oncologico, Aviano, Italy, 71 patients had systemic non-Hodgkin's lymphomas. The most frequent histotypes were small noncleaved cell, anaplastic large cell (ALC) CD30/BerH2+, and large cell immunoblastic. In 22 representative cases of these histotypes, including 9 of small noncleaved cell, 9 of ALC CD30/BerH2+, and 4 of immunoblastic non-Hodgkin's lymphomas, Epstein-Barr virus genetic information was assessed by in situ hybridization and correlated with histologic and immunophenotypic findings. Expression of B-cell associated markers, usually including CD19, CD20, CD22, CDw75, and CD74, was found in 17 of the 22 evaluated cases. All small noncleaved cell and immunoblastic cases and four cases of ALC lymphomas expressed B-cell immunophenotypes, whereas the remaining ALC cases were immunologically undetermined. In situ hybridization detected Epstein-Barr virus in 12 of 22 cases (54.5%). Seven of nine ALC lymphomas were positive, as were three of five small noncleaved cell type (Burkitt's lymphoma), one of four small noncleaved cell type (non-Burkitt's variant), and one of four large cell immunoblastic type. The results of this study indicate that Epstein-Barr virus genomes might be identified in more than 50% of the evaluated high grade non-Hodgkin's lymphomas; this association occurred significantly more often in the small noncleaved cell lymphomas resembling endemic Burkitt's lymphoma (60%) and with ALC CD30/BerH2+ lymphomas (77.8%). These findings support the notion that Epstein-Barr virus may play a role in the development of non-Hodgkin's lymphomas in a proportion of human immunodeficiency virus-infected patients.
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PMID:Demonstration of Epstein-Barr viral genomes by in situ hybridization in acquired immune deficiency syndrome-related high grade and anaplastic large cell CD30+ lymphomas. 838 22

This is the second report of histiocyte-rich B-cell lymphoma and the first case analyzed by flow cytometry and cytogenetic study. The immunophenotype determined by flow cytometry was that of a B-cell antigen-positive, surface immunoglobulin-negative B-cell lymphoma with 79% CD11c positive histiocytes. The lymphoid cells were composed of 76% neoplastic B-cells and 24% reactive T-cells. Immunohistochemical staining showed large numbers of histiocytes positive for CD68 and lysozyme in the lymph node and the bone marrow. Neoplastic lymphoid cells were positive for CD20, CD45, CD74 and CDw75. The monoclonality of the tumor cells was established by the evidence of rearrangements of the heavy chain and kappa light chain genes and a complex clonal cytogenetic abnormalities including t(8;14)(q11;q32). The tumor cells were large, pleomorphic lymphoid cells and showed no features resembling those of the L/H cells of Hodgkin's disease as previously reported. The rapidly progressive clinical course in the present case is consistent with the clinical features shown in the original study. The histiocytic component in this tumor is presumably recruited by a lymphokine with the nature of a growth factor from the tumor cells that may also be responsible for the rapid proliferation of the tumor cells and the aggressive clinical course. This entity merits special recognition because it leads to a predictable poor prognosis and because of its potential of being misdiagnosed as true histiocytic lymphoma.
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PMID:Histiocyte-rich B-cell lymphoma. 938 44

The humanized anti-CD74 monoclonal antibody (mAb) hLL1 is under evaluation as a therapeutic agent. The effects of hLL1-at times in comparison with the CD20 mAb rituximab-were assessed on non-Hodgkin lymphoma (NHL) and multiple myeloma (MM) cell lines and in tumor-bearing SCID mice. In vitro, hLL1 caused growth inhibition and induction of apoptosis in B-cell lines when cross-linked with an antihuman immunoglobulin G (IgG) second antibody. The sensitivity profile of the cell lines was different for hLL1 and rituximab, and antiproliferative activity was augmented when the 2 mAbs were combined. Unlike rituximab, hLL1 did not induce antibody-dependent cellular cytotoxicity or complement-mediated cytotoxicity. In xenograft models of NHL and MM, treatment with hLL1 yielded significant survival benefits without cross-linking agents. Efficacy was greater in the MM model, in which median survival time was increased more than 4.5-fold. Thus, hLL1 has therapeutic potential as a naked mAb for B-cell malignancies because of high antigen expression on malignant cells, specifically MM, with limited expression on normal tissue, and because of its antiproliferative activity. Further, hLL1 may be a therapeutic candidate for rituximab-resistant disease because the 2 antibodies apparently act through distinct mechanisms and exhibit different expression and sensitivity profiles, and activity can be augmented when the mAbs are combined.
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PMID:Antiproliferative activity of a humanized anti-CD74 monoclonal antibody, hLL1, on B-cell malignancies. 1529 17

DEV is the only cell line derived from nodular lymphocyte predominance type of Hodgkin's lymphoma (NLPHL); however, a comprehensive report about the genetic and immunophenotypic profile of this unique cell line is lacking. We analyzed DEV with respect to immunophenotype and genetic aberrations. The immunostaining revealed positivity for CD45, CD20, CD22, CD79a, IgA2, CD80, CD86, CD74, and BCL6. Cytogenetically, DEV has complex chromosome 3 translocations involving chromosomes 7, 14, and 22. A detailed analysis of the 3q27 breakpoint of the der(3)t(3;14)(p14;q32)t(3;22)(q27;q11.2) revealed a break in the BCL6 alternative breakpoint region. Using array comparative genomic hybridization, a 3-megabase homozygous deletion at 17q24.1-24.2 was identified. Fluorescence in situ hybridization indicated the presence of 2 chromosome 17 homologues, each of which carried a small interstitial deletion. Eight microsatellite markers flanking the homozygously deleted region all showed a homozygous pattern suggesting loss of one of the parental alleles. D17S1809 and D17S1816 could not be amplified using DEV DNA, in keeping with a location within the homozygously deleted segment. In conclusion, DEV has an immunophenotype that is consistent with the neoplastic cells of NLPHL cases, the lymphocytic and histiocytic cells. We demonstrated involvement of the BCL6 gene based on the presence of a breakpoint in the alternative breakpoint region and nuclear staining for BCL6 protein and identified a homozygously deleted region at 17q24.
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PMID:BCL6 alternative breakpoint region break and homozygous deletion of 17q24 in the nodular lymphocyte predominance type of Hodgkin's lymphoma-derived cell line DEV. 1673 7

Immunophenotypic analysis can identify protein epitopes in non-Hodgkin lymphomas (NHL) that may respond to targeted immunotherapies, such as anti-CD20 and anti-CD52. Recent studies suggest additional targets may provide therapeutic benefits in NHL. This study evaluated protein expression of CD25, CD52, CD74 and CD80 in paediatric NHL to determine possible targets for immune-based therapeutic approaches. Patient samples were derived from paediatric NHL clinical trials sponsored by the Children's Cancer Group (CCG, now the Children's Oncology Group, COG) and included Burkitt lymphoma (BL), diffuse large B-cell lymphoma (DLBCL), disseminated T- and B-cell lymphoblastic lymphoma (T-LBL and B-LBL) and anaplastic large cell (ALCL). Immunophenotypic studies were performed on formalin-fixed, paraffin-embedded diagnostic tissues. CD25 was expressed in 8% of T-LBL and 75% of ALCL cases, but not in BL, DLBCL, or B-LBL. CD52 was expressed in 99% of cases of paediatric NHL of all subtypes. CD74 was expressed in 100% of B-LBL, BL and DLBCL, but was absent in ALCL and T-LBL. CD80 was expressed in 12% of B-LBL, 6% of BL and 10% of DLBCL cases studied, but was not detected in T-cell NHL. These expression patterns suggest that CD25, CD52 and CD74 may represent potential new therapeutic targets in paediatric NHL.
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PMID:Immunophenotypic identification of possible therapeutic targets in paediatric non-Hodgkin lymphomas: a children's oncology group report. 1765 54

The Hodgkin cell line U-HO1 was established from a malignant pleural effusion of a 23-year-old male patient during the end stage of refractory nodular sclerosing classical Hodgkin lymphoma (cHL). Since its establishment in 2005, U-HO1 has maintained stable characteristics in vitro and has a doubling time of about 4 days under standard culture conditions. U-HO1 forms typical Reed-Sternberg cells in suspension, is EBV negative, lacks HLA-A, -B, -C but expresses HLA-D proteins/CD74 and exposes CD15 together with CD30 in the absence of CD19 and CD20 on the cell surface. Karyotype analysis of U-HO1 revealed a hyperdiploid karyotype with multiple clonal aberrations. Most significant is an elongated chromosome 2, der(2)t(2;10)(q35; q16.1)add(2)(p13). CGH analysis revealed the following imbalances: ish cgh dim(1)(p13p31)(p12q21), enh(2)(p13p23), dim(4)(q31.3qter), enh(6)(q22q27), enh(12), enh(18), enh(20) (q13.1pter). FISH analysis showed about six-fold amplification of REL and BCL11A, thus, U-HO1 is prototypical for cHL in every aspect tested so far. As an outstanding feature compared to the existing HL cell lines, U-HO1 has high levels of microRNA transcripts of MIRN216 and MIRN217 located in the amplicon 2p16. Compared to other HL cell lines, U-HO1 proved far less genetically aberrant suggesting that U-HO1's imbalances suffice to cause the full-blown phenotype of primary refractory cHL.
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PMID:U-HO1, a new cell line derived from a primary refractory classical Hodgkin lymphoma. 1825 30


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