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)

Adriamycin is now firmly established as a drug with a very broad spectrum of antitumor activity. It has had a major impact on the therapy of sarcomas. The dose response effect in this tumor is steep and combinations which compromise the dose of adriamycin too greatly are showing inferior results. In lung and breast cancer combinations with adriamycin have been extensively tried. The FAC Regimen in breast cancer has given excellent results at the M.D. Anderson Hospital. The inclusion of adriamycin in combinations has had an impact in the poor prognosis histologies of non-Hodgkin's lymphomas. The CHOP regimen is one of the best developed to date for diffuse histiocytic lymphomas. In the leukemias adriamycin is probably equivalent to daunorubicin which has been more extensively used in this country. A new analog called Rubidazone has shown good activity in AML with a smooth induction and its incorporation into combination with Ara-C, vincristine and prednisone in a regimen called ROAP is being investigated. Adriamycin in complex with DNA has been clinically evaluated, but at this time, no advantage for this approach can be demonstrated.
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PMID:Adriamycin and other anthracycline antibiotics under study in the United States. 36 Mar 30

Although the term thymic hyperplasia is used most commonly to indicate the occurrence of germinal centers in the thymus, cognizance must be taken of the fact that such centers may occur in apparently normal thymuses in both children and adults. A concept of thymic compartmentalization is proposed with origin of germinal centers in the perivascular space (extraparenchymal compartment) of the thymus. These germinal centers contain a high percentage of B lymphocytes in contrast to the true thymic parenchyma. Although the significance of germinal centers in the thymus parenchyma. Although the significance of germinal centers in the thymus in myasthenia gravis remains controversial, removal of nonneoplastic thymus in this condition is of proven therapeutic value. A variety of neoplasms originating in the thymus have previously been lumped together under the single term "thymoma." It is apparent, however, that thymoma, thymic carcinoid, various lymphomas, and germ cell tumors that arise in the thymus differ not only pathologically but also in their clinical behavior. Thymoma is regarded as an epithelial neoplasm and ultrastucturally is characterized by many desmosomes and tonofilaments. The lymphocytes do not behave in a malignant manner, and lymphomas of the thymus should be sharply separated from true thymoma. Poorly differentiated thymic carcinoma and histiocytic lymphoma may be distinguishable only by the electron microscopic demonstration of desmosomes and filaments in the thymic carcinoma. The evidence that Hodgkin's disease of the thymus ("granulomatous thymoma") is not a variant of thymoma appears overwhelming. Lymphoblastic lymphoma of the thymus is a distinctive neoplasm that is especially prevalent in teenage males. High levels of terminal transferase characterize the lymphoblasts and there is a striking tendency for leukemia to occur. Thymic carcinoid is usually nonfunctional, although one-third of the reported cases are associated with Cushing's syndrome. On light microscopy a ribbon pattern and punctate necroses are characteristic of thymic carcinoids. Electron microscopic demonstration of many dense core granules is invaluable in establishing this diagnosis. An important clue to the diagnosis of thymic seminoma (a neoplasm that shows the same radiosensitivity as its testicular counterpart) is the frequent presence of epithelioid and giant cell granulomas and germinal centers. Separation of the various thymic neoplasms described not only is justifiable on pathologic grounds but is often essential for appropriate patient investigation and treatment.
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PMID:Thymic hyperplasia and neoplasia: a review of current concepts. 36 41

The clinical, pathologic, and immunologic features unique to Hodgkin's disease can be explained by the following hypothesis. A viral transformation of a lymph node cell leads to proliferation of tumor cells and the generation of an immune response consisting of lymphokine production, B cell activation and concomitant suppression of further T cell activation, but ineffective cellular cytotoxicity against the tumor cells. The result of this interaction would be chronic infiltration around the transformed cells, increased immunoglobulin synthesis, and anergy. Failure to destroy the target cells would result in chronicity of these features and progressive disease.
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PMID:Hodgkin's disease and anergy. 36 74

We studied the clinical and pathological features of six cases of non-Hodgkin's lymphoma (diffuse undifferentiated in four cases and diffuse histiocytic in two cases) occuring in patients treated for Hodgkin's disease. All six patients had received both radiation and chemotherapy. Abdominal or gastrointestinal involvement was present in five of the six cases. None of the patients had evidence of Hodgkin's disease when the diagnosis of non-Hodgkin's lymphoma was made. Five of the six patients were among a study group of 579 patients with Hodgkin's disease, prospectively followed since diagnosis. At 10 years the actuarial risk of development of non-Hodgkin's lymphoma in this study group is 4.4 per cent (1.2 to 15.0) (per cent probability with 95 per cent confidence limits) and is similar to that of developing acute leukemia: 2.0 per cent (0.3 to 12.9). Non-Hodgkin's lymphoma is a second tumor that may occur late in the course of patients treated for Hodgkin's disease--particularly in patients who have received both radiation therapy and chemotherapy. Like acute leukemia, non-Hodgkin's lymphoma may be another cancer that represents a substantial late risk of combined-modality therapy.
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PMID:Occurrence of non-Hodgkin's lymphoma after therapy for Hodgkin's disease. 36 18

Combined application of morphologic, immunochemical, and immunologic methods has led to a reinterpretation of non-Hodgkin's lymphomas and to the establishment of the Kiel classification. In the present paper, the main Ig-producing entities are considered. These are: 1. Chronic lymphocytic leukemia of the B-type (B-CLL)--a proliferation of lymphocytes and a few so-called prolymphocytes and lymphoblasts. The mean tissue IgM value is slightly increased; the serum IgM level is normal or reduced. The tumor cells bear SIg, and a majority of them have a receptor for C3d but always lack CIg and are usually devoid of receptors for C3b. 2. Lymphoplasmacytoid immunocytoma--a mixed proliferation of lymphocytes and centrocytes, blast cells, plasma cells, or plasmacytoid cells. The tissue Ig content is most often (91%) and most highly increased in this group, whereas the serum Ig level is increased in only 20% of the cases. The tissue IgM of 17 cases was shown to be monoclonal by IEF. Most tumor cells have SIg and a variable numbear CIg. The tumor cells bear both complement receptor subtypes, only a receptor for C3b, or no complement receptors at all. 3. Centroblastic/centrocytic lymphoma--usually a follicular proliferation of abundant small germinal center cells (centrocytes) and some large germinal center cells (centroblasts). The tumor cells bear SIg and both complement receptor subtypes. The C3b- and C3d-positive cells are located in the follicles, as in nonneoplastic lymphatic tissue. 4. Centrocytic lymphoma--a purebred, diffuse proliferation of the small germinal center cells (centrocytes). These cells bear SIg and receptors for C3b and C3d but usually lack CIg. 5. Centroblastic lymphoma--a proliferation of the large germinal center cells (centroblasts). 6. Lymphoblastic lymphoma of Burkitt's type. 7. Immunoblastic lymphoma--a diffuse proliferation of large basophillic cells resembling immunoblasts. The tissue IgM content is increased in 60% of the cases. It proved to be monoclonal with IEF in all five cases studied. The cells of five cases with increased tissue Ig content bore SIg. Nearly half of the cases studied showed CIg. Besides non-Hodgkin's lymphomas, paraffin sections of 87 biopsies from Hodgkin's disease were investigated for CIg in Hodgkin's and Sternberg-Reed cells. These cells stained positively in 68 cases, most often for IgG, followed by IgD. In five cases of the lymphocyte-depleted type, the staining of the Hodgkin's and Sternberg-Reed cells was restricted to one light chain type.
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PMID:Demonstration of immunoglobulin production by tumor cells in non-Hodgkin's and Hodgkin's malignant lymphomas and its significance for their classification. 36 94

Fifteen primary intracranial reticulum cell sarcomas and five cases with an additional solitary extracranial tumor mass have been studied. For comparison, seven extracranial malignant non-Hodgkin lymphomas and normal lymphoid tissue were included. The methods used on formalin-fixed paraffin-embedded tissue sections were an immunoperoxidase technique for the demonstration of intracellular immunoglobulins, microglial staining, Gomori's reticulin, methylgreen-pyronin, Giemsa, diastase resistant PAS, Mallory's PTAH and H&E. Electron microscopy was performed in one primary brain tumor. According to histopathologic criteria all tumors could be classified as malignant non-Hodgkin lymphomas, predominantly of the pleomorphic immunocytic or of the immunoblastic type; follicular lymphomas were notably absent. In all cases intracellular immunoglobulins were demonstrable in tumor cells and in a majority of the tumors these were monoclonal. Thus, all malignant lymphomas proved to be of B cell origin with demonstrable cytoplasmic immunoglobulin production. Based on the microglial staining more than half of the malignant lymphomas could also be classified as microgliomas. As a comparable staining was present in non-Hodgkin lymphomas outside the CNS, microglioma characteristics are not associated with intracranial growth.
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PMID:Intracranial malignant lymphomas. A morphologic and immunocytologic study of twenty cases. 36 44

This paper reviews the changes of blood and peripheral lymph lymphocytes induced by therapeutic irradiation as given for a variety of lymphoid and nonlymphoid neoplastic diseases. The irradiation brings about an abrupt reduction of the numbers of blood B and T lymphocytes. The number of lymphocytes seems to be restored within a few months after irradiation, while at least 3-5 years appear to pass before the number of blood T lymphocytes is restored. The pattern of recovery seems to be the same whether the thymus has been included in the fields of irradiation or not. In the adult organism, considerable differences apparently exist between the capacities for reproduction of B and T lymphocytes. The number of lymphocytes in peripheral lymph is also much reduced in the irradiated patient and remains so for a long period. This is compatible with the concept that migration from blood to peripheral lymph is a feature quite specific for T lymphocytes. These results are discussed in relation to the immune defense against infection and autologous tumor, and also in relation to the influence of radiotherapy on the immune defect in Hodgkin's disease.
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PMID:The influence of therapeutic irradiation of blood and peripheral lymph lymphocytes. 36 38

Thirty-six patients with stage III and IV Hodgkin's disease and non-Hodgkin's lymphoma, who had become refractory to conventional chemotherapy, were treated with VM-26. Complete remissions were documented in two patients with diffuse histiocytic lymphoma. Six patients (four with non-Hodgkin's lymphomas and two with Hodgkin's disease) had partial remissions. The overall response rate was 22% (eight of 36 patients). Hematologic toxicity was the most frequent dose-limiting toxicity. Nonhematologic toxic effects were mild and acceptable. This study demonstrates that VM-26 can produce tumor responses in refractory lymphomas. The Eastern Cooperative Oncology Group is currently planning two new phase II studies to incorporate VM-26 with other active new agents, one involving hexamethylmelamine and the other involving cis-dichlorodiammineplatinum(II).
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PMID:VM-26, a new anticancer drug with effectiveness in malignant lymphoma: an Eastern Cooperative Oncology Group Study (EST 1474). 36 93

Lymphogranulomatosis (Hodgkin's disease) is a rare neoplasm in the G.D.R.: incidence (standardized for "Europe-population") male 3.2--3.5, female 1.8--2.1 per 10 000 per year. Geographical differences in incidence and mortality are remarkable, but firm conclusions cannot be drawn. Epidemiological research has demonstrated: familial aggregation; association with HLA-antigen; space-temporal clusters which are considered as suspicious for infectious aetiology; association with occupational factors; higher incidence after tonsillectomy and appendectomy as an index of social factors; no influence of ionizing radiation. Multiple primary malignant neoplasms are strikingly often found in patients with Hodgkin's disease. It may be that Hodgkin's disease is no nosological entity but clinical and morphological manifestation of two diseases, namely infectious granuloma in youth and true neoplasm in the elderly.
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PMID:[Epidemiology of lymphogranulomatosis (M. Hodgkin) (author's transl)]. 37 79

We examined the binding of soluble immune complexes in sera from patients with Hodgkin's disease to established tissue cultures derived from the tumor. Circulating immune complex levels were determined by the Raji cell assay, and the reaction of serum with cultured cells was examined with a radioimmune assay and by immunoferritin electron microscopy. Serum with elevated immune complexes was found to react with cells of Hodgkin's disease monolayers when tested with radioiodine-labeled antisera against human IgG heavy and light chains and the complement 3 (C3) component. When examined with the electron microscope, monolayers incubated with Hodgkin's disease serum containing immune complex and labeled with ferritin-conjugated antiserum to C3 contained surface-bound ferritin particles with a uniform but discontinuous pattern. Absorption of Hodgkin's disease serum with monolayer cells reduced immune complexes and decreased reactivity of the sample with cultured cells by radioimmune assay. Sera of patients with other disorders and aggregated gamma-globulin with complement, despite markedly elevated immune complex levels, did not react positively with monolayers derived from Hodgkin's disease tumors, and none of the sera reacted with normal cultured spleen. The approximate size of serum components reacting with Hodgkin's disease monolayers was estimated by sucrose density gradient centrifugation. Sedimentation fractions in the 19S region reacted with monolayer cells when tested with 125I-labeled antisera to both IgG and C3 and contained immunoglobulin-complement complexes by gel diffusion and immunoabsorption. A component sedimenting at 7-9S contained immunoglobulin not complexed with complement; this component reacted with monolayer cells when tested with anti-IgG antiserum but did not react when tested with antibody to C3. The reaction of Hodgkin's disease monolayers with serum containing immune complexes differed from that of two suspension culture lines composed of cells with surface complement and IgG Fc receptors. Inasmuch as cells of our long-term Hodgkin's disease monolayers do not contain these surface receptors, possibly the antibody component of the immune complex reacts with antigens on the surface of cultured cells.
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PMID:Reaction of immune complexes with Hodgkin's disease tissue cultures: radioimmune assay and immunoferritin electron microscopy. 37 54


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