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)

The detection of an increasing number of cytokines and the demonstration of autocrine and paracrine mechanisms perpetuating tumor growth prompted the investigation of the expression of the cytokines IL-2, IL-3, IL-4, IL-5, IL-6, IFN gamma, Tac, and GMCSF in primary lymph-node biopsies of patients with peripheral T-cell lymphoma (n = 11), Hodgkin's disease (n = 13), and large-cell anaplastic lymphoma (n = 6) by means of Northern blot analysis and in situ hybridization (ISH); 15 of 28 cases had IL-6 message, predominantly in cases of Hodgkin's disease (HD) and large-cell anaplastic lymphomas (LCAL). Interferon gamma was found in about 50% of the cases among all entities. Other cytokine expression was rare except two cases of HD with high amounts of IL-4 mRNA. These results indicate that large amounts of growth factor transcripts are present in a variety of malignant lymphomas. The meaning of this expression is still unclear. It may be a loss of physiologic regulation within the cytokine network which may thus influence neoplastic cell growth as some cases have a quantity of cytokine expression which is similar or even above that of stimulated T cells. ISH demonstrates in individual cases that the expression is at least in part due to malignant cells.
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PMID:Cytokine expression in T-cell lymphomas and Hodgkin's disease. Its possible implication in autocrine or paracrine production as a potential basis for neoplastic growth. 195 32

In this study we investigated the pattern of T lymphocyte changes in 16 adult patients with acute myeloid leukaemia (8), non-Hodgkin's lymphoma (4) and Hodgkin's disease (4) treated with continuous infusion of recombinant interleukin-2 (rIL-2). Effects indicative of lymphocyte activation occurred even prior to any rIL-2 therapy in these patients, being most prominent in patients with active diseases. Following each course of cytokine therapy, there were further changes in these parameters. Significant rebound lymphocytoses occurred with a concomitant increase in the cytotoxic functions and induction of the cytotoxicity-linked cytoplasmic serine esterase. Hence, both the natural killer and lectin-dependent cellular cytotoxicity activities were up-regulated. There were also increases in the serum sIL-2 receptor, sCD4 and sCD8 levels. More CD3+ lymphocytes, especially cells bearing CD4, were also recruited to the pool of potential effector cells, as demonstrated by the greater proportion of cells expressing the cytoplasmic serine esterase.
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PMID:Lymphocyte activation and serine-esterase induction following recombinant interleukin-2 infusion for lymphomas and acute leukaemias. 203 61

The typical histological picture seen in Hodgkin's disease is consistent with the release of cytokines and other active mediators by the malignant cells, i.e., Hodgkin and Sternberg-Reed cells. Since interferon-gamma is regarded as an important regulator of the cytokine cascade, we have undertaken an immunohistological assessment of this mediator in Hodgkin's disease tissue biopsies. In approximately 50% of the cases investigated we found Hodgkin and Sternberg-Reed cells to be positive with antibodies against interferon-gamma. These in situ findings were substantiated by immunostaining of Hodgkin's disease-derived cell lines L428 and L540. L540 was consistently positive, whereas L428 was negative. It is noteworthy that L428 exhibit a B-cell pheno- and genotype, whereas L540 is of T-cell origin. These data are consistent with theories that propose that cytokine production by tumour cells is central to the pathogenesis of Hodgkin's lymphoma.
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PMID:Immunoenzymatic assessment of interferon-gamma in Hodgkin and Sternberg-Reed cells. 212 5

It is likely that the characteristic histologic features of Hodgkin's disease reflect cytokine production by the tumor cell population. Tumor necrosis factor alpha (TNF-alpha) and lymphotoxin (tumor necrosis factor beta [TNF-beta]) are important inflammatory mediators with wide-ranging effects within the lymphoreticular system. The aim of the present study was to investigate TNF-alpha and lymphotoxin production in the Hodgkin's disease-derived cell lines L428 and L540. At the product level, both cytokines could be demonstrated by immunostaining with specific monoclonal antibodies. TNF-alpha could be demonstrated by means of an enzyme-linked immunosorbent assay in culture supernatants from both cell lines as well as in cell lysates of L428 and L540 cells. Cytotoxic activity could be achieved only in L428 supernatants. This cytotoxic activity could not be blocked by the addition of a polyclonal antibody against TNF-alpha, but was partially inhibited with the monoclonal antibody against lymphotoxin. Synthesis of TNF-alpha and lymphotoxin in both L428 and L540 was confirmed by demonstrating the intracellular-specific messenger RNA (mRNA) using specific cDNA clones in Northern blot analysis. In situ hybridization studies with the TNF-alpha cDNA probe gave positive hybridization signals in L428 and in L540. These results demonstrate the transcription, translation, and export of TNF-alpha and lymphotoxin in cultured Hodgkin's disease-derived cell lines. In addition, results of preliminary experiments are presented in which we demonstrate Reed-Sternberg cells positive for TNF-alpha protein and mRNA in different Hodgkin's disease tissue biopsies, indicating that, at least for TNF-alpha, our cell line data are relevant to the neoplastic population present in Hodgkin's disease tissue.
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PMID:Tumor necrosis factor alpha and lymphotoxin production in Hodgkin's disease. 238

Twenty-one cases of large, B-cell lymphoma with an unusually high content of reactive T lymphocytes are described in this report. Fifteen patients presented with lymphoma in nodal sites and six patients presented with lymphoma in extranodal sites. With two exceptions, all patients were more than 50 years of age. The male to female ratio was 1:2. Histologically, isolated to small groups of large lymphoid cells were intermingled with many small lymphocytes. The large cells were neoplastic and exhibited B-lineage markers; immunoglobulin light chain restriction could be demonstrated in two thirds of the cases. There was a rich infiltrate of immunophenotypically mature T lymphocytes that comprised more than 50% of the cellular population. The T lymphocytes ranged from small cells with dark, round nuclei to slightly larger cells with elongated, irregular nuclei. There were occasional medium-sized blastic cells. There was also a variable infiltrate of histiocytes with or without epithelioid features, eosinophils and plasma cells, and increased vascularity. The peculiar morphologic features were also reproduced in other sites in the four patients for whom additional histologic materials were available for examination. We postulate that the abundance of T cells results either from a florid host reaction or from cytokine secretion by the neoplastic B cells, attracting T cells to the vicinity. The morphologic and immunologic features mimic those of a variety of benign lymphoproliferative diseases, angioimmunoblastic lymphadenopathy and lymphomas arising in angioimmunoblastic lymphadenopathy, peripheral T-cell lymphoma, secondary B-immunoblastic lymphoma, and Hodgkin's disease. Careful morphologic evaluation and immunophenotypic studies using leukocyte antibodies reactive in paraffin-embedded sections are of great assistance in determining a diagnosis.
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PMID:Large B-cell lymphomas with a high content of reactive T cells. 259 44

Quantitative and functional abnormalities of T and B lymphocytes and monocytes have been described in Hodgkin's disease (HD) and non-Hodgkin's lymphomas (NHL), thus making both diseases suitable models to study the interactions between lymphoid and myeloid systems. We evaluated the growth of colony-forming units of granulocytes and monocytes/macrophages (CFU-GM), as well as the colony-stimulating activity (GM-CSA) produced by monocytes and the colony-inhibiting activity (GM-CIA) released by autologous rosette-forming T-cells (Tar cells), a postthymic precursor subpopulation, in peripheral blood samples from 7 patients with HD and 5 with NHL. CFU-GM growth in HD and NHL patients was similar to that observed in controls. However, GM-CSA and GM-CIA were significantly decreased in both HD (p = 0.002 and p = 0.012, respectively) and NHL (p = 0.003 and p = 0.017, respectively) patients as compared to controls. These data suggest that cytokine-dependent mechanisms regulating normal CFU-GM proliferation are impaired in HD and NHL.
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PMID:Granulomonopoiesis and production of granulomonopoietic regulating factors in Hodgkin's disease and non-Hodgkin's lymphomas. 266 Jun 76

The cytokine, interleukin-6 (IL-6), has emerged as a likely mediator of many of the systemic alterations observed in patients with cancer (fever, increased erythrocyte sedimentation rate, and alterations in plasma protein composition) and may also mediate local effects such as alteration in proliferation of tumor cells, increased tumor cell motility, and decreased intercellular adhesions between tumor cells. The distribution of IL-6 immunoreactivity in different human tumors was studied. IL-6 immunoreactivity was detected by the avidin-biotin-complex (ABC) procedure using a polyclonal rabbit antiserum raised against an E coli-derived human IL-6 (rIL-6). Preimmune rabbit serum used as a control did not yield specific staining and preadsorption of the IL-6 antiserum with rIL-6 abolished specific staining. Strong-to-moderate IL-6 immunoreactivity was observed in the neoplastic elements present in primary squamous cell carcinomas, in adenocarcinomas of mammary, colonic, ovarian, and endometrial origin, in various adenocarcinomas metastatic to lymph nodes, and in soft tissue tumors including leiomyosarcoma and neurofibrosarcoma. Weak-to-moderate IL-6 immunostaining was observed in Hodgkin's and non-Hodgkin's lymphomas. This study demonstrates that most human tumors stain positively for IL-6, adding weight to the hypothesis that IL-6 is a key cytokine that participates in the host-tumor interaction.
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PMID:Interleukin-6 immunoreactivity in human tumors. 267 20

In cases of hairy cell leukemia, chronic myelogenous leukemia, and in benign larynx papilloma, interferon alpha has proved to be a valuable therapeutic principle. Regarding most malignant diseases, however, we are still at the beginning of the therapeutic application of cytokines. New therapeutic strategies include the combination of cytokines together with cytotoxic substances, the combination of in vitro activated T-lymphocytes and natural killer (NK) cells together with cytokines, and, finally, the application of cytokine cocktails. Based on presently performed clinical studies, a slight optimism might be justified with regard to the development of new therapeutic modalities for Hodgkin's disease as well as non-Hodgkin's lymphomas and solid tumors.
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PMID:[Cytokines in tumor therapy]. 311 82

Hodgkin's disease (HD) is an aggressive human lymphoproliferative disease that displays a curious pleomorphic histopathologic appearance unlike that of any of the common non-Hodgkin's lymphomas (NHL). Although the bizarre giant cells of the HD lesion, the Reed-Sternberg cells (RSC) and mononuclear variant Hodgkin's cells (HC), have been considered to be malignant cells, little objective evidence supports this conclusion. We have studied the proliferative characteristics of T cell as well as RSC and HC-enriched populations from HD lesions, and found the majority of the proliferative activity in the T cell populations. RSC-enriched populations not only showed little spontaneous proliferation, but also did not respond to a variety of cytokine growth factors in vitro, suggesting that these cell populations are not actively growing cells. Further molecular studies to identify possible monoclonal T or B cell populations in HD lesions, using a TCR beta chain probe and IgH probes respectively on Southern blot analysis, revealed no evidence of monoclonal lymphoid cell populations. Additional studies on the characteristic T cell immunodeficiency in HD were also undertaken. Our previous studies had associated a decrement in IL-2 production with this defect. Our studies now show that an intrinsic T cell abnormality exists when HD patients' T cells are stimulated with agonistic MAb that can optimally activate and stimulate IL-2 production in normal control T cells.
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PMID:In vitro analysis of cell populations involved in Hodgkin's disease lesions and in the characteristic T cell immunodeficiency. 326 Dec 71

Recently, the presence of a soluble form of IL-2 receptor (IL-2RS) in human sera and in supernatants of PHA-stimulated lymphocytes has been demonstrated. It has been suggested that autoimmune diseases could be characterized by a defect in production of IL-2RS, unlike immunoproliferative disorders which are characterized by overproduction. Our aim was to investigate serum IL-2RS levels in 35 newly diagnosed Type 1 diabetic patients, in 25 age-matched healthy blood donors and in five patients with Hodgkin's disease. We found that newly diagnosed diabetic patients have higher IL-2RS levels (424.8 +/- 203 U/ml) than normal controls (252.4 +/- 38.4 U/ml) (p less than 0.005). In 22 out of 35 patients (62.8%) the IL-2RS values were above the higher 95% tolerance limit of controls. Furthermore, the persistence of high IL-2RS levels was observed in 18/35 diabetic patients six months after diagnosis (470 +/- 195.6 U/ml). The increased levels were not correlated with glycaemic and HbA1c levels and patients' age. Our findings suggest a potentially significant role for the released IL-2R in the regulation of IL-2 dependent lymphocyte functions in Type 1 diabetes. The study of IL-2RS in Type 1 diabetes may provide a new tool for the knowledge of cytokine involvement in the disease.
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PMID:Increased soluble interleukin-2 receptor levels in the sera of type 1 diabetic patients. 326 1


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