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)

We treated two patients with rare variants of Hodgkin's disease of the thymus. One was a 17-year-old girl with a thymoma-like shadow on the chest X-rays, an increased erythrocyte sedimentation rate and an elevated eosinophil count. Pathologically, a mixed cellularity variant of thymus Hodgkin's disease was evident. The other patient was 22-year-old girl with evidence of mediastinal tumor on the chest X-rays. Pathological examination revealed Hodgkin's disease of the lymphocyte predominance variety. She also had Von der Haeve syndrome. In both cases, Hodgkin's disease was suspected by scintiscanning, using three kinds of radioisotope, 201Thallium-chloride, 67Garium-citrate and 75Selenomethionine. Radical excision of the lesion plus preoperative and postoperative irradiations were carried out. Both are well 6 and 5 years after the treatment, respectively. We propose a new diagnostic procedure and a method of treatment for such patients.
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PMID:Rare variants of Hodgkin's disease of the thymus: report of two cases and proposal for effective clinical management. 379 31

A case of thymic Hodgkin's disease presenting with an anterior mediastinal mass is reported. The mass progressively expanded in size on plain chest radiography during and following a mantle radiation therapy. A repeat computed tomographic (CT) scan of the chest in this patient revealed a cystic component to the mass, and thin-needle aspiration of the cyst led to a shrinkage of the mass. An experience in this case and review of literature suggest Hodgkin's disease involving the thymus gland frequently predisposes to cystic degeneration especially following radiotherapy, leaving a stable or progressively enlarging residual mass. A precise diagnosis of such a progressively expanding mass despite the adequate radiation therapy is crucial. CT scan of the chest in such cases and a thin-needle aspiration of the cystic mass offer precise diagnosis and may obviate the need for an open thoracotomy procedure.
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PMID:Cystic degeneration of thymic Hodgkin's disease following radiation therapy. 383 82

Malignant lymphomas and leukemias are related to maturation stages of distinct subpopulations of hematopoietic or lymphoid cells as defined by immunocytological methods. We first describe various monoclonal antibodies, and the methodology employed in our investigations and report on recent developments in the standardization of these reagents (part 1). The maturation sequence of normal lymphoid cells and their precursors in the bone marrow, thymus and the peripheral lymphoid organs are discussed in part 2. Typical immunomorphological findings in Non Hodgkin Lymphomas (NHL) are summarized in respect to lymphocytic NHL (CLL, lymphoplasmocytoid NHL, hairy cell and prolymphocytic leukemia, some lymphomas of peripheral T-lymphocytes), to NHL of follicular center cells (centroblastic-centrocytic, centrocytic NHL), to "large cell" NHL (centroblastic, immunoblastic NHL, large cell NHL derived from T-lymphocytes or "lymphomas" of macrophage origin) and to lymphoblastic NHL (derived from T-lymphocytes, pre-B lymphocytes and Burkitt-type). Findings in multiple myeloma are also summarized in part 3. Immunocytological features of the normal Myelo-, Mono-, Erythro- and Thrombopoieses are discussed in part 4. The reactivity of some monoclonal antibodies with precursor cells of these cells (CFU-GM, BFU-e and CFU-e, CFU-M) are also described. Finally we summarized the immune phenotype of acute leukemias (part 5) in respect to acute lymphoid leukemias (cALL, T-ALL, O-ALL, B-ALL), to acute non lymphoid leukemias (M1-M6 type according to the FAB-Classification) and to blastic stages of chronic leukemias.
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PMID:[Immunocytologic diagnosis of leukemia and lymphoma: monoclonal antibodies in the differential diagnosis of hematologic neoplasms]. 391 83

Lymphoid cells from peripheral blood, thymus, malignant and non-malignant lymph nodes were analysed for ferritin content using radioimmunoassays specific for the 'acidic' H-subunit-rich and for 'basic' L-subunit-rich isoferritins, and the data were compared with the immunological characteristics of the cells. All tissues with high proportion of T or 'null' cells contained the lowest concentration of L-subunit-rich isoferritins, while the H-subunit-rich forms increased from low levels in the quiescent peripheral blood lymphocytes (PBL), to higher values in the immature and proliferating thymocytes and lymphoblasts, malignant or not. B-cell lymphomas contained concentrations of both ferritin types higher than those found in PBL. No significant difference was found in the isoferritin concentrations between non-malignant lymph nodes and tissues involved in Hodgkin's disease. These findings indicate that maturation stage, proliferative status and anatomical localization affect isoferritin expression in lymphoid cells.
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PMID:Ferritins in malignant and non-malignant lymphoid cells. 394 91

An antiserum was prepared in rabbits against an antigen obtained by density gradient sedimentation of centrifuged medium from monolayer cultures of spleens involved by Hodgkin's disease. The antiserum was tested by isotopic antibody techniques with cells from each of eight cultures derived from spleens involved by Hodgkin's disease, four cultures derived from normal adult spleen, and one culture each of fetal spleen and thymus. By an indirect radioiodine-labeled antibody assay, anti-Hodgkin's disease globulin reacted with an antigen on the surface of cells from the Hodgkin's disease cultures, the quantity of which was related to the number of target cells and the amount of antibody used. This Hodgkin's disease tissue-culture antigen did not react with a rabbit antiserum against fractionated medium from a normal spleen culture, nor against noncultured Hodgkin's disease tumor tissue. The tumor specificity of the Hodgkin's disease tissue-culture antigen was assessed by a direct technique using (125)I-labeled anti-Hodgkin's disease globulin absorbed with either cultured Hodgkin's disease cells or with cultured normal cells. By this method the quantity of antigen on cells from Hodgkin's disease cultures was 15- to 30-fold greater than that on cells from normal cultures. The Hodgkin's disease tissue-culture antigen is intimately associated with the propagation of the tumor in monolayer cultures, but its identity has not been established: it could be a viral component, a tumor or fetal antigen, or a normal tissue constituent.
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PMID:An antigen in Hodgkin's disease tissue cultures: radioiodine-labeled antibody studies. 413 20

Pellets obtained from supernatant fluids of monolayer cultures of cells from patients with Hodgkin's disease were fractionated by isopycnic density sedimentation. Material in a peak of specific gravity 1.15-1.21 g/ml from two Hodgkin's disease cultures was used to immunize rabbits, and the antisera obtained in this manner were reacted by agar-gel diffusion and immunoelectrophoresis with antigens from the purified peaks and the unfractionated pellets of centrifuged culture medium from all the cultures. The antisera reacted with material from 9 of 10 lines derived from spleens of patients with Hodgkin's disease, 2 of 8 cell lines from histologically negative spleens from patients with Hodgkin's disease and with 3 of 6 lymphoma cell lines not diagnosed as Hodgkin's disease. The antisera did not react with 12 cell cultures prepared from normal adult and fetal spleen and thymus. The antigen from cultures from patients with Hodgkin's disease was not found in material sedimenting at lower specific gravities; it resisted Tweenether solubilization, and migrated as a single band by immunoelectrophoresis. The antigen was not found in disrupted, noncultured tumor cells from patients with Hodgkin's disease, and an antiserum against noncultured, minced tumor tissue did not react with the Hodgkin's disease tissue-culture material. No immunological relationship was found between the tissue culture antigen and Epstein-Barr, RD-114, or Rauscher murine leukemia viruses. The Hodgkin's disease antigen may be a tumorrelated antigen or a component of an oncogenic virus.
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PMID:A tumor antigen in tissue cultures derived from patients with Hodgkin's disease. 435 Nov 81

The kinetics of lymphocyte transformation induced by phytohemagglutinin (PHA) and pokeweed mitogen (PWM) were studied daily, with blood lymphocytes from normal individuals and from untreated patients in all stages of Hodgkin's disease (HD). In addition, spleen lymphocytes and lymph node lymphocytes were studied with similar techniques.Peripheral blood lymphocyte transformation stimulated by PHA was found to be depressed in all patients with HD (including those with localized disease and no symptoms) when small numbers of lymphocytes were cultured and studied during a 7-day period. Most patients with HD had an increased number of cells circulating in their blood which were actively synthesizing DNA. HD lymphocytes which demonstrated the highest initial rate of spontaneous DNA synthesis usually did not respond to PHA stimulation. Blood lymphocytes from normal individuals responded equally well to PHA and PWM in our system. HD blood lymphocytes consistently responded better to PWM than to PHA, with the response to PWM frequently within the normal range. Unless the spleen was extensively infiltrated with HD, spleen lymphocytes from patients with HD responded to PHA, even though the blood lymphocyte response was severely reduced. Lymph node lymphocyte response to PHA from patients with HD was variable, but correlated roughly with the blood lymphocyte response. It is hypothesized from the data presented that in HD, circulating thymus-dependent (T-)lymphocytes are stimulated by the presence of active disease. This stimulation of T-lymphocytes leads to a circulating T-cell depletion and to an increase in the number of cells circulating that are active in DNA synthesis. The degree of impairment of cell-mediated immunity would then depend upon the degree of T-lymphocyte depletion.
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PMID:Impaired lymphocyte transformation in Hodgkin's disease. Evidence for depletion of circulating t-lymphocytes. 454 73

Rabbits were immunized with an antigen of specific gravity, 1.15-1.21 isolated by density gradient sedimentation of the centrifuged medium of long-term monolayer cultures derived from spleens involved by Hodgkin's disease. The globulin fraction of the antiserum was absorbed to reduce reactivity with normal cellular antigens and tissue culture components, and was tested by the indirect fluorescent antibody technique with cells from 18 different Hodgkin's disease cultures, and 16 normal cultures derived from adult spleen and fetal spleen and thymus. With anti-Hodgkin's disease globulin diluted 1:40 and 1:80, positive surface staining was observed in 48% and 41%, respectively, of viable cells from Hodgkin's disease cultures, and in less than 5% of cells cells from normal cultures. Fluorescent staining of the cytoplasm without nuclear staining was observed in 51% of acetone-fixed cells from the Hodgkin's disease cultures and in 4-8% of cells from normal cultures. Reactivity of the antiserum with Hodgkin's disease target cells could be removed by absorption of the antibody with additional antigen of density 1.15-1.21 obtained from other Hodgkin's disease cultures. Antisera to fractionated medium from a normal spleen culture and to noncultured Hodgkin's disease tumor tissue were used as controls: 2-10% of viable and acetone-fixed target cells reacted and no difference was observed between Hodgkin's disease and normal cell cultures. In vitro propagation of tumor cells from patients with Hodgkin's disease is needed for detection of the Hodgkin's disease tissue culture antigen; the antigen could not be demonstrated in noncultured Hodgkin's disease tissue.
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PMID:An antigen in Hodgkin's disease tissue cultures: fluorescent antibody studies. 460 85

In patients with Hodgkin's disease, the impaired immune reactivity, especially of the thymus dependent system, is well established. This decreased immune response of the lymphocytes from the peripheral blood contrast to an increased lymphocytopoiesis in the the lymphatic organs with a hyperplasia of these tissues. We studied the reactivity of peripheral T lymphocytes from 20 patients with Hodgkin's disease and 26 healthy control persons against autologous and allogeneic non T cells respectively in the mixed lymphocyte culture (MLC). Our experiments show an extremely depressed autologous mixed lymphocyte reactivity (MLR) of T lymphocytes from patients with Hodgkin's disease compared to those from normal donors. In the allogeneic MLC, the proliferation of the patients' T cells was stronger than in the autologous MLC, but significant lower than the proliferation of normal T lymphocytes when stimulated by normal non T cells. Patients' non T cells stimulated T lymphocytes from healthy donors as well as non T lymphocytes from normals did. Finally, the autologous MLR of normal lymphocytes was significantly suppressed by 18 of 23 sera from Hodgkin's patients when these sera were substituted for normal AB serum in the cultures. These results demonstrate an impaired function of T lymphocytes from patients with Hodgkin's disease in the autologous MLC and the presence of one or more factors in their serum which inhibit the proliferation of normal lymphocytes in the autologous MLC. The role of suppressor cells and their factors will be discussed.
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PMID:Impaired autologous mixed lymphocyte reactivity in Hodgkin's disease. 621 Jul 97

Abnormalities of T lymphocytes in B cell chronic lymphocytic leukemia (B-CLL) have been extensively documented by several immunologic investigations. Following recent studies pointing to the favorable effect of TP-1, a partially purified extract of calf thymus, on the T cell-mediated immunity of several diseases, including Hodgkin's disease, we have used monoclonal antibodies and the enriched T lymphocytes of 16 untreated B-CLL patients to evaluate the proportion of T cell subsets before and after the administration of TP-1. In addition, the proliferative response to phytohemagglutinin (PHA) and the helper function in a pokeweed mitogen (PWM) system were assessed. In ten cases, the effect of TP-1 was also studied in vitro by evaluating the same parameters before and after incubation of B-CLL T cells with the drug. The study demonstrated that in vivo administration of TP-1 increases significantly (P less than .001) the proportion of the defective helper/inducer T cell population (OKT4-positive cells) in B-CLL, leading to a near normal OKT4/OKT8 ratio. Furthermore, the improved phenotypic profile was accompanied by an increased proliferative response to PHA and, in particular, by a significant increase (P less than .01) of T helper capacity; this increase was, however, insufficient to enable the normalization of the serum immunoglobulin levels. The in vitro incubation of B-CLL T lymphocytes did not succeed in producing significant modifications in distribution and function.
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PMID:Effect of a thymic factor on T lymphocytes in B cell chronic lymphocytic leukemia: in vitro and in vivo studies. 623 69


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