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)

This study was performed to see if adherent cell-derived toxic oxygen metabolites contribute to the suppression of mononuclear cell blastogenic responses in Hodgkin's disease. Peripheral blood mononuclear cells from 10 patients with Hodgkin's disease were stimulated in culture with the mitogen PHA in the presence of the prostaglandin inhibitor indomethacin and the antioxidants catalase or vitamin E. Patient lymphocytes showed significant increases in PHA-induced proliferation at all PHA doses when cultured with indomethacin. Further augmentation of lymphocyte proliferation was achieved with the addition of catalase or vitamin E to indomethacin in the culture system. The increases in proliferation seen on culture with these agents were greatest in patients with more depressed initial PHA responses. When adherent cells were removed before culture, the agents no longer facilitated increases in proliferation. These data suggest that abnormal lymphocyte proliferative responses seen in Hodgkin's disease may result in part from the excessive production of toxic oxygen metabolites as well as prostaglandins by adherent cell populations.
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PMID:Evidence for the involvement of monocyte-derived toxic oxygen metabolites in the lymphocyte dysfunction of Hodgkin's disease. 733 72

The clinical course of 38 patients with Hodgkin's disease in the stage of remission was evaluated. The material consisted of two groups of patients: 1. submitted to immunotherapy and 2. control group. In 16 cases immunostimulation was performed with BCG vaccine, including four cases treated with BCG vaccine and levamisole and 3 patients were given levamisole only. In some patients, immunotherapy restored normal immunologic reactivity, as shown by the reversion of negative tests of delayed hypersensitivity. In all patients treated with levamisole caused normal blastic transformation of PHA-stimulated lymphocytes. In the group of patients treated with immunotherapy relapses of malignant lymphogranulomatosis were observed in 10.6% of cases, and in the control group--in 15.7%. The patients of both groups remain under continuous clinical surveillance.
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PMID:Preliminary evaluation of immunotherapy in patients with Hodgkin's disease. 734 93

Adherent mononuclear cells may have suppressor functions mediated by prostaglandins (PG). In the present study we tested a large number of normal donors and patients with Hodgkin's disease (HD) using PHA and the prostaglandin inhibitor indomethacin (IM). Stimulation of mononuclear cells from 24 healthy volunteers with PHA led to a mean response of 27 833 cpm; addition of IM caused a 32% increase of 3H-thymidine incorporation. The corresponding values for 30 patients with HD stages IIA-IVB were 14,064 cpm and 70% increase with IM. The effect of the drug was much more pronounced during relapse or progression than in untreated patients. There was an inverse relationship between PHA-response and per cent increase both in normal donors and Hodgkin patients. Depletion of adherent cells using Sephadex G-10 columns abolished the effect of IM completely, but PHA-stimulation was also slightly depressed. Our failure to observe an increase of the mitogen response after removal of monocytes may be related to the technique employed. However, an additional defect of Hodgkin lymphocytes must be considered.
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PMID:[The influence on PHA-stimulation by inhibition of prostaglandin synthesis in vitro in patients with Hodgkin's disease (author's transl)]. 737 Apr 37

Blood lymphocytes from 10 untreated patients with active Hodgkin's disease were compared with those of 10 cured patients with regard to the responsiveness of the cells to PHA and Con A following in vitro irradiation. Lymphocytes of patients remaining in long-term remission exhibited the same pattern of radiosensitivity as those of healthy donors: there was one relatively radiosensitive cell population and one relatively resistant. The latter cell population was undetectable in patients with an active disease. Reappearance of the radioresistant PHA and Con A reactive cell fractions might thus be associated with remission.
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PMID:The effect of in vitro irradiation on mitogenic responsiveness of peripheral blood lymphocytes from patients with untreated and cured Hodgkin's disease. 741 35

Forty-three previously untreated Egyptian patients with Hodgkin's disease and thirty-five patients with non-Hodgkin lymphoma were studied with several readily available tests of immune function, number of peripheral blood lymphocytes, delayed hypersensitivity to two recall antigens, in vitro blastoid transformation by PHA, the capacity of E-rosette formation and surface marker criteria. The results were correlated to the histology, stage of disease and to the presence of general symptoms and signs.
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PMID:Immune deficiency in Hodgkin and non-Hodgkin lymphoma. 744 22

The present study investigated the peripheral blood mononuclear cells (PBMC) blastic responses to PHA, PHA plus recombinant IL-2 (rIL-2) and rIL-2 alone; the expression of membrane-bound IL-2R on PHA-stimulated PBMC; and the levels of IL-1 alpha, IL-2, IL-6, and sIL-2R in serum and in culture supernatants from PHA-stimulated PBMC in 17 patients with with non-Hodgkin's lymphoma (NHL), 4 with Hodgkin's lymphoma (HL), 5 with Hairy cell leukemia, 1 with chronic myelogenous leukemia, and 1 with chronic lymphocytic leukemia. The patients with HL and NHL with active disease (AD) were separated from those in clinical remission. The patients with AD were studied at diagnosis (obviously before therapy) and the patients in clinical remission were out of therapy since at least 6 mo. The lymphocyte blastogenic response to PHA was significantly lower in patients with HL and NHL with AD than in the control group. The response to rIL-2 alone was in the same range in the control group and in HL and NHL AD patients. By adding rIL-2 to PHA there was an increase of the blastogenic response of the same patients. The percentage of CD25 expressed on PHA-stimulated lymphocytes from patients with HL and NHL AD and from normal subjects is in the same range. Serum levels of IL-2, IL-6, and sIL-2R were significantly higher in HL and NHL AD patients than in controls as well as in all other hematological malignancies. Supernatants derived from PHA-stimulated PBMC were assessed for the presence of cytokines and sIL-2R by ELISA. The levels of IL-2, IL-6, and sIL-2R were significantly lower in HL and NHL AD patients than in controls as well as in all other hematological malignancies.
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PMID:Membrane-bound/soluble IL-2 receptor (IL-2R) and levels of IL-1 alpha, IL-2, and IL-6 in the serum and in the PBMC culture supernatants from 17 patients with hematological malignancies. 749 95

Bcl-2 protein was analysed in cell cultures derived from non-Hodgkin lymphomas and chronic lymphocytic leukaemia patients. The presence of bcl-2 proto-oncogene protein product has been demonstrated on cytospin preparations utilising immunochemical methods. The correlation between the expression of the bcl-2 protein and the appearance of proliferation- or differentiation related figures was studied. The reported bcl-2 up regulation in malignant lymphoid cells was confirmed in haemo- and lymphopoietic progenitor cells as well as in TPA/PHA activated peripheral blood lymphocytes. In comparison to neoplastic cells lower intensity of bcl-2 positive staining in freshly isolated cells from non-leukaemic tissue was observed.
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PMID:Studies on bcl-2 protein in cultured lymphoid cells. 801 87

CD30 has been extensively studied as a cell surface marker expressed by Reed-Sternberg cells of Hodgkin's disease and other hematologic malignancies, although little is known about its expression by normal lymphoid cells. We therefore characterized the requirements for the induction of CD30 expression and identified the subsets of T cells that express CD30. CD30 is inducible on approximately 15% of normal PBMC stimulated with any of a variety of nonspecific T cell activators, including PHA, Con A, anti-T11(2) + T11(3), and anti-CD3; ionomycin alone induced lower percentages of CD30+ T cells (3 +/- 2%) compared to other stimuli. Maximal numbers of CD30+ cells were observed at 48 to 72 h of activation and the addition of rIL-2 did not affect these kinetics. However, CD30 expression was enhanced by the addition of exogenous rIL-2 to any of the stimuli tested, although rIL-2 alone did not lead to CD30 expression. The induction of CD30 during anti-CD3 mitogenesis was completely inhibitable by anti-IL-2 antibodies and partially inhibitable by rIL-4, indicating a requirement for both TCR triggering and IL-2 for its expression. Dual immunofluorescence analysis revealed that CD30+ cells were confined to CD3+ T cells that coexpressed higher levels of the p55 IL-2 receptor (CD25) than the CD30- population. Furthermore, CD30 expression was restricted to a subset of cells derived from CD45RO+ T cell precursors. Cell cycle analysis showed that CD30+ expression was not cell cycle dependent. Cross-linking of membrane CD30 induced Ca2+ in TCR+, but not TCR- Jurkat T cells. These results demonstrate that CD30 can serve as a T cell signal-transducing molecule and expressed by a unique subset of activated CD45RO+ T cells.
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PMID:CD30 is a signal-transducing molecule that defines a subset of human activated CD45RO+ T cells. 810 64

We have isolated a novel 667-bp cDNA clone, designated epag, from a Hodgkin's-disease cell line-derived library that is expressed in association with T cell activation and which is not related to any known gene family. By using reverse transcription/PCR, we have demonstrated that epag mRNA is expressed as early as 1 h after stimulation of normal PBMCs with anti-CD3. The levels of mRNA peaked by 4 h, and no expression was detectable by 12 h postactivation or in resting cells incubated in culture without activation. Expression of epag was also detected in PMA- and PHA-stimulated, but not in nonstimulated Jurkat cells, and overall its expression in transformed cell lines of hemopoietic origin is highly restricted. Sequence analysis of multiple independent cDNA clones showed that epag expressed in the Hodgkin's-disease cell line L428 is identical to the gene expressed in normal activated PBMC. Epag expression was detected by reverse transcription/PCR in RNA preparations made from various normal nonlymphoid tissues. Computer analysis of the sequence identified an open reading frame encoding a putative protein of 13.2 kDa initiating at a CUG translational codon. In vitro translation and Western blot analysis with anti-peptide serum supported this analysis. We hypothesize that epag functions as an early signal that helps mediate the activation of T cells.
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PMID:Properties of a novel gene isolated from a Hodgkin's disease cell line that is expressed early during lymphoid cell activation. 813 36

This re-evaluation of a pilot study conducted nearly three decades ago (1965-1970), in which serendipity played a central role in favorable responses of hematologic malignancies to the administration of adoptive lymphocytes from both parents, has been motivated by clearer understanding. Temporary remissions marking LAK cell-driven graft-versus-leukemia (GvL) responses were observed in four of seven acute leukemia patients associated with unique self-limited graft-versus-host (GvH) reactions that were NK cell and cytokine related. Retinopathy not previously reported in a GvH setting was a consistent manifestation in these patients. Cure was achieved in an eighth patient with acute lymphoblastic leukemia after she had been given effective chemotherapy, an active role for the adoptive therapy indicated by the occurrence of a week of fever suggesting an abortive GvH reaction. Two of five patients with Hodgkin's disease also experienced favorable responses to parental leukocyte therapy, one exhibiting GvH manifestations almost identical to those seen in the acute leukemia patients when given the adoptive therapy successfully to spur recovery from severe herpes zoster that had interrupted curative radiation therapy. The GvH in the other patient was a more typical one, the key effect being an increase in circulating lymphocytes that may have contributed indirectly to cure with subsequent therapy. These and other attempts to apply GvL responses therapeutically, including those currently in favor, exemplify the shortcomings of partial mitogenic responses to alloactivation, which are dependent on engraftment, limited in scope, excessively toxic, and difficult to control. Treatment with mitogens such as PHA would be a superior alternative because of the abilities of these agents to regulate immune responses by simple modulations of dosage, scheduling, and modes of application.
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PMID:Haplotype donor-generated graft-versus-leukemia responses: serendipity revisited. 854 57


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