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)

In a study of 157 patients with lymphoid malignancy, the phenotype of the tumour cells was correlated with the histological classification of the tumour using the Rappaport and the Kiel classifications. The markers used included E, Fc gamma, Fc micron (IgM) and C3d rosetting, estimation of SIg and CyIg, and tests for the expression of HTLA, Ia and ALL. Repeat biopsy specimens were studied in 23 of these patients. The phenotypic features of lymphoblastic malignancy indicated B-cell, T-cell and ALL-positive null-cell tumours in this group. Immunoblastic lymphomas were predominantly of non-capping B-cell type, but T-cell immunoblastic lymphoma occurred in 2 patients. Immunoblastic lymphomas of receptor-silent cells occur, and are ALL- and HTLA-negative. In the category of diffuse, poorly differentiated lymphocytic lymphomas, most cases are of centroblastic and centrocytic tumour of diffuse type, but pure centrocytic tumours and centroblastic tumours occur. The dominant phenotype in this group is of B cells expressing C3d receptors. Nodular poorly differentiated lymphocytic lymphomas (Rappaport) are classified as centroblastic and centrocytic follicular (Kiel) and most express SIg+ C3d+ phenotype. The frequency of this phenotype appeared the same in both diffuse and nodular poorly differentiated lymphocytic neoplasms. The Rappaport group of diffuse well-differentiated lymphocytic lymphoma includes 2 Kiel categories, malignant lymphoma lymphocytic, and malignant lymphoma lymphoplasmacytoid. Cells of the former tumour were considered to be immature B cells resembling those seen in CLL, and characteristically expressing SIg weakly, with a high frequency of single kappa light chain. Cells of the latter tumour are by contrast mature, and are related to the centroblastic and centrocytic follicular tumour by their histogenesis and phenotypic features. Repeat biopsy examinations indicate that T-cell predominance occurs in the prodromal phase of B-cell-predominant tumours of SIg+ C3d+ phenotype. It is concluded that non-Hodgkin lymphoma can be divided into 2 categories: (1) tumours of immature immunologically incompetent cells of lymphoblastic histology and with phenotypic features akin to T, B and Null-cell ALL, and (2) tumours of differentiated lymphocytes expressing the phenotypic features of B lymphocytes, with maturation arrested at one of several stages of an antigen-dependent immune response.
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PMID:Surface phenotyping, histology and the nature of non-Hodgkin lymphoma in 157 patients. 31

Fresh tumor cells from pleural effusion of a patient with Hodgkin's disease were analyzed cytogenetically, immunologically and enzymocytochemically. They were characterized by the presence of alpha-naphthyl butyrate esterase activity, Fc gamma-receptor, HLA-DR antigen and No. 9 antigen which has been shown to be present in Hodgkin's cells and granulocytes, and the absence of definite T-, B- and myeloid cell markers. The karyotype analysis of these tumor cells revealed chromosome instability, but the clonality was confirmed by the many common abnormalities such as -4, -6, -10, -12, -13, -14, +21, del(X) (q22,q26), del(7) (q32q36), and +der(19)t(19;?). In addition, there were more duplicated tetraploid clones than near-diploid clones. The karyotype of the near-diploid clone was interpreted as: 48, X, del(X) (q22q26), -4, -6, -10, -12, -13, -14, +20, +21, +der(4)t(4;?) (p16;?), del(7) (q32q36), +der(19)t(19;?) (p13;?), +mar1, +mar2, +mar3. The karyotype abnormalities characteristic of lymphomas or leukemias were not found. These results indicate that the tumor cells are not of lymphoid or myeloid lineage. Further studies are needed to determine the cellular origin of the tumor cells of Hodgkin's disease.
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PMID:Karyotype aberrations and surface marker analyses of the tumor cells of Hodgkin's disease: a case report and review of literature. 243 93

The antibody-coated human erythrocyte and the antibody-coated ox erythrocyte rosette assays (EAHu and EAOx) were compared to detect Fc gamma receptors on human peripheral blood lymphocytes. Two incubation conditions were examined: 1 h at room temperature and overnight at 4 degrees C. In healthy persons, in patients with Hodgkin's disease and in patients with non-Hodgkin lymphoma (NHL) the mean percentage of EAHu-rosette-forming cells (EAHu-RFC) increased significantly when the incubation was carried out overnight at 4 degrees C instead of 1 h at room temperature. This increase was caused by Fc gamma receptor-bearing T cells. In the case of EAOx-RFC only a slight increase was found. The percentage of EAHu-RFC and EAOx-RFC differed significantly in the healthy group after the overnight incubation and in the NHL group after the 1-hour incubation. When comparing the mean percentage of EA-RFC in the patient groups with that of the healthy persons significant increases were observed: EAHu-RFC in patients with Hodgkin's disease in the overnight incubation and EAOx-RFC in patients with Hodgkin's disease and NHL in both incubation conditions. In patients with chronic lymphocytic leukemia (CLL, B-cell type) the mean percentage of EAHu-RFC was very low, however that of EAOx-RFC was moderate to high. It is concluded that in the two rosette assays the antigen-antibody complexes may have different avidities to different lymphocyte subpopulations, and that incubation conditions may have an influence on this avidity.
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PMID:Fc gamma receptors on lymphocytes from normal donors and patients with lymphoproliferative diseases. Influence of incubation conditions. 622 79

T-cell subpopulations have been implicated in the regulation of normal human B-cell reactivity. As the non-Hodgkin lymphomas (NHL) represent predominantly clonal B-cell malignancies, we examined the relationship of total T-cell [Sheep Red Blood Cell (SRBC) binding] and Fc gamma bearing T-cell populations in these disorders. Peripheral blood from seven low-grade (Rai stage 0), six high-grade (Rai stage 3 or 4) CLL patients, lymph node specimens from five patients with WDLL, seven patients with PDLL-D, three patients with MC-D, and eight patients with DHL were studied. All values were compared to normal controls. The percentage of total T cells in each disease category was decreased compared to controls. In addition, there was a reproducible correlation between the percentage of Fc gamma bearing T cells and the histopathologic diagnosis. The percentage of Fc gamma bearing T cells was highest in low-grade CLL and decreased incremently from high-grade CLL and WDLL, to MC-D, and PDLL-D. In DHL, we found no Fc gamma bearing T cells. Finally, the percentage of Fc gamma bearing T cells in each disease category was decreased compared to controls. These findings suggest a correlation between Fc gamma bearing T cells and the clinical aggressiveness of disease in NHL. In addition, they may raise important questions about therapy. Finally, they may offer a useful clinical test as an adjunct to histopathology although this will need to be confirmed in larger series.
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PMID:Fc gamma bearing T cells in non-Hodgkin lymphoma. 623 46

Five samples of tonsil, 10 reactive lymph nodes and 65 consecutive cases of non-Hodgkin lymphoma (NHL) were evaluated in suspension phenotyping with the monoclonal antibodies alpha Leu-I, alpha Leu-2a, alpha Leu-3a, OKT1, OKT3, OKT4, OKT6, OKT8, W6/32, 26/114, DA-2, 2DI, J5, AN51 and OKT9 together with conventional surface marking by rosetting (E, Fc gamma, Fc mu, C3b, C3d) and staining for surface and cytoplasmic immunoglobulin (SIg, CyIg) heavy and light chain classes. The results confirm the reproductability and specificity of staining with monoclonal antibodies against T cells and T cells subsets. Evidence is presented for reactivity of alpha Leu-I antibody with SIg positive and Ia positive cells in some lymphomas (centroblastic centrocytic, lymphocytic and immunoblastic), and 2 cases showed evidence of marking with OKT3 on SIg positive cells in T cell predominant immunoblastic lymphoma. Lymphoblastic lymphomas of T cell type expressed the marker OKT6. On the basis of these results criteria for the diagnosis of T cell lymphoma are suggested. The monoclonal antibody J5, reactive with C-ALL antigen, showed variable positivity, occasionally strong in B cells in cases of centroblastic and centrocytic follicular lymphoma. Proportions of cells staining with the monoclonal antibody OKT9 showed a correlation between levels of cellular expression of transferrin (trf) receptor and the histological grade of malignancy, OKT9+ cells being elevated in high grade lymphomas, and in some cases of transforming lymphoma of low grade histological class. These results are discussed and indicate the advantage of employing a wide range of defined monoclonal reagents in the phenotypic evaluation of NHL.
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PMID:The cellular content of non Hodgkin lymphomas: a comprehensive analysis using monoclonal antibodies and other surface marker techniques. 633 96

The relationship between immunological markers and histology according to the Kiel classification was studied in 40 adult non-Hodgkin lymphoma patients of Rappaport unfavourable histology. The membrane-associated and cytoplasmic Ig as well as receptors for sheep erythrocytes, Fc gamma and C3d receptors were analyzed on cryostate sections and in suspension. In some cases, a more precise immunophenotype was achieved by the use of monoclonal antibodies detecting different T and B cell antigens. Eighty-eight per cent of the lymphomas had B-cell, five per cent T cell and 7 per cent non-B/non-T cell phenotypes. All CBCC and CC lymphomas expressed monotypic Ig, but only 66 per cent of the CB lymphomas. Thus, morphology alone did not consistently predict immunophenotype in large-cell lymphomas. A simultaneous expression of multiple heavy chains and cytoplasmic Ig was found in some lymphomas, suggesting an intratumoral differentiation. The nodular or irregular tissue distribution patterns for Ig and C3d receptors found in histologically diffuse follicle derived lymphomas also suggest intratumoral variations in the marker expression, probably related to differentiation. The results suggest that lymphoma immunophenotype is important in obtaining a definite diagnosis in large-cell lymphomas and that it may lead to a better understanding of the differentiation of lymphomas of low-grade malignancy.
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PMID:Correlation of immunophenotype to morphology in unfavourable non-Hodgkin lymphoma. 636 91

We studied a variant CD5- B cell chronic lymphocytic leukemia (CLL) cell population that produces pathologic IgM kappa rheumatoid factor autoantibodies. In contrast to common CD5+ B cell CLL, this variant leukemia cell population displays intraclonal diversity in its expressed Ig V genes, similar to that noted for follicular B cell non-Hodgkin's lymphomas. Also, in contrast to common B cell CLL, these leukemia cells rapidly undergo cell death hours after being placed in tissue culture. We find that addition of Ag (aggregated human IgG) enhances significantly the survival of these cells in vitro. Leukemia cell survival also could be enhanced by exogenous IFN-gamma or anti-CD40 presented on Fc gamma RII (CDw32)-expressing L cells, but not by exogenous IL-4, IL-6, or monomeric human IgG. We find that Ag acts directly on the leukemia B cells to inhibit apoptosis. This effect could be mimicked by cross-linking the leukemia cells' surface IgM receptors with immobilized murine mAb specific for human Ig mu-chains, but not by immobilized mAb of irrelevant specificity. In contrast to most follicular NHL, this leukemia B cell population does not have evidence of bcl-2 gene rearrangement. Also, in contrast to non-Hodgkin's lymphomas and most B cell CLL, these cells do not express detectable amounts of bcl-2. Finally, although capable of inhibiting apoptosis, surface Ig receptor cross-linking does not induce expression of bcl-2 in these variant leukemia cells. We hypothesize that the lack of bcl-2 expression may render these leukemia cells particularly dependent upon the survival signal(s) derived from surface Ig receptor cross-linking. This state may represent an early stage in leukemia/lymphomagenesis, possibly accounting for the intraclonal diversity observed in the Ig V genes expressed by certain CD5- B cell leukemias and lymphomas.
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PMID:Autoantigen inhibits apoptosis of a human B cell leukemia that produces pathogenic rheumatoid factor. 750 24

In order to target NK cells against the Hodgkin's-derived cell line L540, we developed bispecific monoclonal antibodies (Bi-MAbs) by somatic hybridization of the 2 mouse hybridoma cell line HRS-3 and A9 which produce monoclonal antibodies (MAbs) with reactivity against the Hodgkin and Reed-Sternberg cell-associated CD30 antigen and the CD16 antigen (Fc gamma III receptor), respectively. The CD16 MAb-producing cell line A9 was selected as a partner for HRS-3 because of its efficiency in inducing lysis of the A9 hybridoma cells by resting NK cells. The hybrid hybridoma cell line HRS-3/A9 produced the supernatant with the strongest bispecific reactivity and was repeatedly subcloned and used for ascites production. Crude supernatant and purified HRS-3/A9 Bi-MAb triggered specific lysis of the CD30+ Hodgkin's-derived cell line L540, but not of the CD30- cell line HPB-ALL by unstimulated peripheral-blood lymphocytes and NK-cell-enriched populations. Moreover, treatment of SCID mice bearing heterotransplanted human Hodgkin's tumors with HRS-3/A9 and human peripheral blood lymphocytes induced specific complete tumor regression in 10/10 animals. We thus report successful tumor treatment in an in vivo model using NK-cell-associated Bi-MAbs and show that the Bi-MAb HRS-3/A9 is an efficient promoter of the anti-tumor effects of NK cells in vitro and in vivo.
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PMID:A CD16/CD30 bispecific monoclonal antibody induces lysis of Hodgkin's cells by unstimulated natural killer cells in vitro and in vivo. 824 80

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

Fifteen patients with refractory Hodgkin's disease were treated in a dose-escalation trial with the bispecific monoclonal antibody (bi-mAb) HRS-3/A9, which is directed against the Fc gamma receptor III (CD16 antigen) and the Hodgkin's-associated CD30 antigen. Treatment consisted of four cycles of four bi-mAb infusions given over 1 h every 3-4 days at different dose levels ranging from 1 mg/m2 to 64 mg/m2. Measurable serum levels (above 0.1 microgram/ml) of circulating bi-mAb could be detected in patients treated with doses above 4 mg/m2, reaching peak levels of 9.5 micrograms/ml immediately after the end of antibody infusion on the highest dose level. Bi-mAb elimination corresponded to second-order kinetics with a terminal half-life time (t1/2, beta) of 28-32 h. Bi-mAb treatment induced the occurrence of human anti-(mouse Ig) antibodies (HAMA) in 6 out of 13 patients initially testing negative. All 6 patients not only developed anti-isotypic anti-(mouse Ig) but also anti-idiotypic and anti-anti-idiotypic antibodies. While no consistent changes of peripheral blood cell counts, or of any lymphocyte subpopulation including natural killer (NK) cells, has been observed, 4 out of 6 evaluable patients treated with doses of at least 4 mg/m2 showed an increase of NK cell activity within 2 weeks after treatment, which lasted for a maximum of 12 weeks. Circulating amounts of soluble CD30 antigen could be detected in the serum of 6 patients. However, like the results and time courses of all the other immunological parameters evaluated, this was not predictive for treatment outcome.
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PMID:Initiation of humoral and cellular immune responses in patients with refractory Hodgkin's disease by treatment with an anti-CD16/CD30 bispecific antibody. 1088 97


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