Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019829 (Hodgkin's disease)
 30,247 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hodgkin disease (HD) is characterized by the presence of a small number (usually <1% of total tumor mass) of the typical Hodgkin and Reed-Sternberg (H-RS) cells in a hyperplastic background of normal reactive lymphocytes, plasma cells, histiocytes, neutrophils, eosinophils, and stromal cells. HRS cells produce various cytokines, growth factors, and express cytokine receptors and activation antigens, implying a predominant role for these molecules in the pathophysiology of Hodgkin disease. HD may therefore be regarded as a tumor of cytokine producing cells. The CD30 antigen has been characterized as a marker for cultured and primary Hodgkin and Reed-Sternberg cells, and was found to be overexpressed in Hodgkin disease and a subgroup of non-Hodgkin lymphomas including large cell anaplastic lymphomas and Burkitt lymphomas. The molecular cloning of the CD30 antigen revealed that CD30 is a member of the tumor necrosis factor/nerve growth factor receptor superfamily. The cloning of the cognate for CD30, currently termed CD30 ligand, confirmed that the CD30 antigen functions as a cytokine receptor. Recombinant CD30 ligand is a membrane-bound protein with pleiotropic biological activities for different CD30+ lymphoma types, but also for the immune system, mainly T cells. CD30L belongs to the emerging tumor necrosis factor ligand superfamily. The CD30-CD30 ligand interaction could have a critical pathophysiological role in malignant lymphomas, particularly Hodgkin disease, large cell anaplastic lymphomas and Burkitt lymphomas, and is also involved in activation and functioning of the T cell-dependent immune system.
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PMID:CD30 ligand, a member of the TNF ligand superfamily, with growth and activation control CD30+ lymphoid and lymphoma cells. 883 95

Large-cell anaplastic lymphomas (LCAL) are characterized by their distinctive morphology together with expression of the CD30 antigen. In addition, a chromosomal translocation, t(2;5) (p23; q35), can be detected in most cases. A significant proportion of LCALs carry rearrangements of the T-cell receptor-gamma (TCR-gamma) locus and display a T-cell phenotype. In about a third of the cases, another type of non-Hodgkin-lymphoma precedes LCAL. Early transformations of non-Hodgkin's lymphoma into LCAL might escape clinical detection in a significant number of cases. The existence of clonally related lymphoid cells within the lymph node infiltrates must be claimed in these cases. Recently, a small-cell-predominant variant of LCAL was described in which only few large tumor cells expressing the CD30 antigen are found together with numerous small lymphocytes, which are frequently CD30-. This observation in particular prompted us to investigate the clonal relationship of the tumor cell compartment and admixed small lymphocytes in one case of common LCAL with T-cell genotype. For this purpose, we chose to amplify rearranged TCR-gamma sequences from single cells isolated from immunostained frozen sections by using a micromanipulator. A total of 119 cells were investigated. Amplification products were obtained in 17 of 79 CD3+ cells, 12 of 30 CD30+ cells, and three of 10 CD20+ cells. The nucleotide sequences were determined in 28 cells by nonradioactive sequencing. In 11 CD30+ cells, the predominant rearrangement of TCR-gamma was identified. No clonal diversity was observed. The small CD3+ lymphocytes were unrelated to the anaplastic CD30+ tumor cells. This report describes a method to analyze rearrangements of the TCR-gamma in single cells isolated from immunostained frozen sections. Application of this technique revealed an absence of clonal diversity in a case of LCAL and documented the polyclonal nature of admixed small CD3+ lymphocytes.
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PMID:Single-cell analysis of T-cell receptor-gamma rearrangements in large-cell anaplastic lymphoma. 891 40

Fifteen patients with refractory Hodgkin's disease were treated in a phase I/II trial with the natural killer (NK)-cell-activating bispecific monoclonal antibody HRS-3/A9, which is directed against the Fc(gamma)-receptor III (CD16 antigen) and the Hodgkin's-associated CD30 antigen, respectively. Median counts of NK cells and of all lymphocyte subsets were considerably decreased in the patients before therapy. HRS-3/A9 was administered 4 times every 3 to 4 days, starting with 1 mg/m2. The treatment was well tolerated, and the maximum tolerated dose was not reached at 64 mg/m2, the highest dose administered because of the limited amounts of HRS-3/A9 available. Side effects were rare and consisted of fever, pain in involved lymph nodes, and a maculopapulous rash. A total of 9 patients developed human antimouse Ig antibodies, and 4 patients developed an allergic reaction after attempted retreatment. A total of 1 complete and 1 partial remission (lasting 6 and 3 months, respectively) [corrected], 3 minor responses (1 to 11+ months), and 1 mixed response were achieved. There was no clear-cut dose-side effect or dose-response correlation. Our results encourage further clinical trials with this novel immunotherapeutic approach and emphasize the necessity to reduce the immunogenicity of the murine bispecific antibodies.
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PMID:Treatment of refractory Hodgkin's disease with an anti-CD16/CD30 bispecific antibody. 905 26

CD30(Ki-1) positive anaplastic large cell lymphoma (ALCL) is a distinct entity, in which the monoclonal antibody-positivity against the CD30(Ki-1) antigen of tumour cells has a diagnostic value. The histological subtypes of ALCL show also certain clinical differences. Except for some pediatric cases and cutaneous forms clinical outcome is very unfavourable despite of the various treatment methods. In this prospective study (follow-up of 11-60, median 16 months) clinicopathological data and treatment results of fifteen adult patients with ALCL were analysed, Mean age was 46 (16-69) ys with a bimodal tendency and a distinct female: male ratio (3:2) was observed. Early clinical stages (I-II/A-B, eight patients) dominated, and two main groups could be distinguished histologically (Hodgkin-related, ALCL-HR and common type, -CT in eight and seven patients), respectively. In all histological specimens CD30 antigen expression was detected. Additional immunophenotyping was performed in five cases (two 0-variant, two of B-cell and one of T-cell origin), respectively. A bulky disease, mainly in the mediastinum was observed in six cases, and a primary gastrointestinal localization in two other patients. In the treatment of these high grade malignant lymphomas a combination of cobalt irradiation and aggressive chemotherapy was applied (in elder the CHOP-regimen, in younger patients mainly the Pro-MACE-Cyta-BOM-protocol). In one relapsed younger patient autologous bone marrow transplantation was also performed. A complete or partial remission was achieved in thirteen patients (86.6%) but six patients expired after only a short response period to therapy. Overall survival was 19, whilst disease-free survival revealed to be 15 months. Eight of their living nine patients have a durable complete remission. Due to residual mediastinal mass after radiotherapy in three cases a permanent radiological follow-up is needed. Advanced age and clinical stages are considered to be unfavourable, whilst histological subtypes were indifferent prognostic factors, as well. Favourable results in therapy and durable complete remission in younger patients are probably caused by the their better tolerance of third-line aggressive chemotherapy.
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PMID:[Anaplastic large cell lymphoma based on our clinicopathological cases]. 917 73

Reed-Sternberg (R-S) and dendritic interdigitating (DI) cells share many features in nodular sclerosing Hodgkin's disease (NSHD). Such features include commonalities of location (paracortex), histochemistry (paranuclear acid phosphatase and nonspecific esterase activity), and immunohistochemical reactivity (positivity for Mr 70,000 antigen). Because of these similarities, it is hypothesized that there may be a common precursor for R-S and DI cells. To investigate this possibility, paraffin-embedded material from five (5) archival cases of NSHD were reacted in immunohistochemical procedures with antibodies to detect the following antigens: CD15, CD30, S-100 protein, CD68 and IL-9, respectively. Double immunostaining for lysozyme or CD45RB (leukocyte common antigen) or S-100 protein and one of the aforementioned was carried out on representative slides from selected cases. Both relatively large dendriform cells and a population of small mononuclear cells with monocytic karyomorphism showed immunoreactivity for S-100 protein. Similarly, IL-9 antigen which is characteristically found in R-S cells in NSHD was strongly expressed in a population of CD45RB- monocytoid cells. Coexpression of lysozyme antigen in some of the CD30+ R-S cells and Hodgkin's cells is also consistent with a monocytic/histiocytic lineage. Finally, CD30 antigen occasionally could be traced from monocytoid cells, where it was found in a pancytoplasmic distribution to histiocytic cells with a pancytoplasmic and sometimes also paranuclear (Golgizone) pattern of immunoreactivity, to R-S cells with paranuclear and plasmalemmal immunopositivity. In sum, the results of these studies support the contention that there are monocytoid precursors for R-S, Hodgkin's, and DI cells in NSHD and suggest a role for IL-9 in the development of R-S cells from tissue monocytes and monocytoid histiocytes.
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PMID:Histogenesis of Reed-Sternberg and dendritic interdigitating cells in nodular sclerosing Hodgkin's disease. Immunohistochemical evidence for monocytoid precursors. 930 71

The expression pattern of the BCL-6 transcription factor has been assessed in normal and neoplastic B-cell populations and in Hodgkin's disease. However, little is known about BCL-6 expression and its biological significance in T-cell neoplasms. In this study, a series of 59 lymphoma samples, including 27 CD30+ anaplastic large-cell lymphomas (ALCLs), 24 other peripheral T-cell neoplasms, and 8 T-cell lymphoblastic lymphomas (T-LBLs), as well as a panel of t(2;5)-positive lymphoma-derived human cell lines, were evaluated for BCL-6 protein expression by immunohistochemistry on frozen sections and cell smears. To define the relationship between BCL-6 protein and CD30 antigen in CD30+ ALCLs and in non-neoplastic lymph nodes, serial section immunohistochemistry and two-color staining were used in selected CD30+ ALCLs as well as in reactive lymph nodes with non-neoplastic T-cell proliferations. BCL-6 protein was expressed in 12 of 27 (45%) CD30+ ALCL cases, irrespective of their antigenic phenotypes (T-cell or null-cell type), and in the t(2;5)-positive cell lines. In contrast, the remaining 24 peripheral T-cell neoplasms as well as the 8 T-LBLs were considered negative for BCL-6 expression. Coexpression of CD30 and BCL-6, as detected in CD30+ ALCLs, was also found in a subset of non-neoplastic lymphoid elements, namely the large lymphoid cells scattered in the interfollicular areas of reactive lymph nodes. These findings suggest that CD30+ ALCLs may represent the neoplastic transformation of extrafollicular CD30+ cells and that BCL-6 may provide an additional marker for characterizing CD30+ ALCLs.
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PMID:BCL-6 protein expression in human peripheral T-cell neoplasms is restricted to CD30+ anaplastic large-cell lymphomas. 931 Apr 96

A group of 15 patients with refractory Hodgkin's disease were treated in a phase I/II trial with the natural-killer (NK)-cell-activating bispecific monoclonal antibody HRS-3/A9, which is directed against the Fc gamma receptor III (CD16 antigen) and the Hodgkin's associated CD30 antigen. The antibody was given four times every 3-4 days, starting with 1 mg/m2. The treatment was well tolerated and the maximum tolerated dose was not reached at 64 mg/m2. Side-effects were rare and consisted of fever, pain in involved lymph nodes and a maculopapulous rash. Nine patients developed human anti-(mouse immunoglobulin) antibodies. One complete and one partial remission (lasting 5 and 3 months, respectively), three minor responses (1 to 11+ months), and one mixed response were achieved. There was no clear-cut dose side-effect or dose/response correlation. NK cell activity increased in most of the patients treated with 4 mg/m2 or higher doses but lasted no longer than 6 weeks after therapy. Our results encourage further clinical trials with this novel immunotherapeutic approach and emphasize the necessity to reduce the immunogenicity of the antibody to allow retreatment of responding patients.
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PMID:Treatment of refractory Hodgkin's disease with an anti-CD16/CD30 bispecific antibody. 943 69

Cutaneous lymphadenoma is an uncommon epithelial neoplasm with a controverted adnexal differentiation. We report a typical case of cutaneous lymphadenoma that developed on the left cheek of a 18-year-old woman. Histologically, the neoplasm consisted of lobules of basaloid cells with a peripheral palisading array and filled with a lymphocyte-predmoninant mixed cellular population. Numerous intralobular cells with ample amphopilic cytoplasm, large vesicular nuclei, and prominent nucleoli also were noticed. Immunohistochemical study showed labeling of these Reed-Sternberg-like large cells by antibodies against CD30 antigen. Our findings suggest that cutaneous lymphadenoma is a poorly differentiated adnexal neoplasm, probably trichoblastoma-related, where a singular interaction with several immune cells is established, including activated large lymphocytes analogous to those malignantly proliferating in Hodgkin's disease.
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PMID:Cutaneous lymphadenoma: an adnexal neoplasm with intralobular activated lymphoid cells. 950 75

A 62-year-old woman presented with loss of memory and a mild hemiparesis. Neuroradiology demonstrated a left frontoparietal tumour. Biopsy specimens of this lesion revealed intracerebral Hodgkin's lymphoma, a diagnosis supported by immunohistochemical reactions of the tumour cells for the CD30 antigen. Additional cell cycle studies revealed a high proliferative activity of the tumour cells in association with absence of apoptosis. There was no evidence that overexpression of bcl-2 or Epstein-Barr virus infection was involved in the pathogenesis of this neoplasm. Lymphomas in the lung were detected 3 months later. Following neurosurgical excision, radiotherapy, and chemotherapy, the patient had no evidence of Hodgkin's disease after 13 months of follow-up.
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PMID:Primary manifestation of Hodgkin's disease in the central nervous system. 964 50

Fifteen patients with refractory Hodgkin's disease were treated in a phase I/II dose escalation trial with the NK-cell activating bispecific monoclonal antibody HRS-3/A9 which is directed against the Fcgamma-receptor III (CD16 antigen) and the Hodgkin's associated CD30 antigen, respectively. HRS-3/A9 was given four times every 3-4 days starting with 1 mg/m2. The treatment was well tolerated and the maximum tolerated dose was not reached at 64 mg/m2, the highest dose given due to limited amounts of HRS-3/A9 available. Mild to moderate side effects occured in six patients and consisted of fever, pain in involved lymph nodes, and a maculopapulous rash. Median counts of NK-cells and of all lymphocyte subsets were considerably decreased in the patients before therapy and showed no consistent changes under therapy. Eight patients developed human anti-mouse immunoglobulin antibodies, and five patients showed an allergic reaction after attempted retreatment. One complete and one partial remission (lasting 6 and 3 months, respectively), three minor responses (lasting 1 to 15 months), two disease stabilizations (for 2 and 17 months, respectively), and one mixed response were achieved. There was no clearcut dose-side effect or dose-response correlation. Our results encourage further clinical trials with this novel immunotherapeutic approach and emphasize the necessity to reduce the immunogenicity of the murine bispecific antibodies.
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PMID:Anti-CD16/CD30 bispecific antibodies as possible treatment for refractory Hodgkin's disease. 986 3


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