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 search for a rationale for the use of interferons (IFNs) in treatment of non-Hodgkin lymphoma (NHL), we have investigated the IFN system of 13 patients with low-grade NHL, 15 patients with high-grade NHL, and 20 patients with chronic lymphocytic leukemia or leukemic immunocytoma (CLL/IC). Production of IFN induced by phytohemagglutinin (PHA), concanavalin A (Con A), pokeweed mitogen (PWM), Corynebacterium parvum, Herpes simplex virus (HSV), Newcastle disease virus (NDV), and interleukin 2 (IL-2) were studied in the peripheral leukocytes from the patients and from 21 control persons by means of a whole blood technique. All three groups of patients with NHL had significantly reduced production upon stimulation by NDV (p ranged between 0.0038 and less than 0.0001) compared to controls. Similarly, C. parvum also induced lower titers of IFN in the leukocytes of patients with non-leukemic NHL (p = 0.0015 for low-grade NHL and p = 0.0038 for high-grade NHL). When stimulated by PHA, the IFN response of all groups of patients was within normal range. With the exception in low-grade NHL, Con A also induced normal titers of IFN in the patients with NHL. The levels of IFN induced by PWM, HSV, and IL-2 were very low and no differences between controls and patients could be found. As NDV and C. parvum induce mainly IFN-alpha and the mitogens PHA and Con A mainly IFN-gamma, our results suggest that there is a deficiency in the IFN-alpha response in the patients with NHL but normal response in IFN-gamma.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Deficiency in interferon production of peripheral blood leukocytes from patients with non-Hodgkin lymphoma. 137 88

The prognosis of patients with advanced refractory lymphoma remains poor. We have carried out a Phase II study of continuous high dose intravenous recombinant interleukin 2 alone without LAK cells in this group of patients. Eight patients have so far been treated, 4 with non-Hodgkins lymphoma and 4 with Hodgkins disease. Of the 7 evaluable patients, the maximum response observed was stable disease in 2 patients (1 with NHL and 1 with HD). The other patients' diseases progressed in the face of immune activation following the rIL-2 infusion. Adverse reactions were common but no life-threatening occurred. These results are disappointing. Whether or not lymphokine-activated killer (LAK) cells are needed to improve response rate deserve further investigations.
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PMID:Continuous intravenous infusion of high dose recombinant interleukin 2 for advanced lymphomas--a phase II study. 186 30

In search for a rationale for the use of interferons (IFNs) in treatment of non-Hodgkin lymphoma (NHL), we have investigated the IFN system of 13 patients with low-grade NHL, 15 patients with high-grade NHL, and 20 patients with chronic lymphocytic leukemia or leukemic immunocytoma (CLL/IC). Production of IFN induced by phytohemagglutinin (PHA), concanavalin A (Con A), pokeweed mitogen (PWM), Corynebacterium parvum, Herpes simplex virus (HSV), Newcastle disease virus (NDV), and interleukin 2 (IL-2) were studied in the peripheral leukocytes from the patients and from 21 control persons by means of a whole blood technique. All three groups of patients with NHL had significantly reduced production upon stimulation by NDV (p ranged between 0.0038 and less than 0.0001) compared to controls. Similarly, C. parvum also induced lower titers of IFN in the leukocytes of patients with non-leukemic NHL (p = 0.0015 for low-grade NHL and p = 0.0038 for high-grade NHL). When stimulated by PHA, the IFN response of all groups of patients was within normal range. With the exception in low-grade NHL, Con A also induced normal titers of IFN in the patients with NHL. The levels of IFN induced by PWM, HSV, and IL-2 were very low and no differences between controls and patients could be found. As NDV and C. parvum induce mainly IFN-alpha and the mitogens PHA and Con A mainly IFN-gamma, our results suggest that there is a deficiency in the IFN-alpha response in the patients with NHL but normal response in IFN-gamma. This deficiency may have implications for the choice of subtypes of IFN in the treatment of NHL.
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PMID:Deficiency in interferon production of peripheral blood leukocytes from patients with non-Hodgkin lymphoma. 245 68

The role of interleukin 2 (IL-2) for growth and differentiation of normal and malignant B cells still remains controversial. We assessed normal peripheral blood B cells and cell lines derived from patients with B non-Hodgkin's lymphomas (NHLs) with respect to their responsiveness to recombinant human IL-2 (rIL-2). The NHL cell lines used in our experiments expressed the Tac antigen (CD25)--a compound of the IL-2 receptor (IL-2R)--in a percentage ranging from 28 to 57%. As measured in a [3H]thymidine uptake assay, the normal peripheral blood B cells demonstrated a dose-dependent proliferative response to rIL-2, whereas the NHL cells did not show any responsiveness to rIL-2. In a clonogenic culture assay we evaluated the colony formation of the NHL cells and found a decrease of 28 to 41% on average in the presence of rIL-2 (10-50 U/ml). This moderate inhibitory effect on the clonal growth of the NHL cells was not due to a differentiation inducing effect of rIL-2, as studied by measuring the Ig production under increasing doses of rIL-2 (1 to 100 U/ml). Thus, malignant NHL B cells may express the CD25 compound of the IL-2 receptor on their surface, demonstrating a different functional responsiveness to rIL-2 compared to normal peripheral blood B cells.
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PMID:Effect of recombinant human interleukin 2 (rIL-2) on normal peripheral blood B cells and B lymphoblastoid cell lines. 268 Sep 16

One of 4 siblings affected by hereditary spinocerebellar ataxia (HSCA) of Marie's type developed Hodgkin's disease (HD): the stage was IV B, the patient was submitted to conventional chemo- and radiotherapy and achieved complete remission. An accurate clinical, genetic and immunological study was carried out on all his family, including a complete HLA typing, a chromosome study, the immunophenotyping of peripheral blood mononuclear cells (PBMC), the PBMC response to polyclonal mitogens, to interleukin 2 (IL-2), to the association of PHA + IL-2 and the evaluation of the IL-2 receptor expression. No association was clearly demonstrable between an HLA haplotype and HSCA, while the patient with HSCA and HD was HLA-B18- and DQw3-positive (the last at homozygous level), two antigens known to be strongly associated with HD, mainly among the Sardinian ethnic group. The mode of inheritance of HD susceptibility is however completely different from that of Marie's HSCA. The chromosome study did not show any characteristic pattern of the karyotype, neither of the HSCA affected nor of the unaffected members. The immunological investigations did not elucidate any characteristic behavior of the family members, apart from the typical findings of HD seen on patients with HSCA and HD. Our study could not demonstrate any genetic and/or immunologic common background shared by the two diseases, HSCA and HD. Their coexistence in our patient, although the statistic probability is very low, seems to be a fortuitous coincidence more than the result of a common genetic and pathogenetic mechanism.
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PMID:Hodgkin's disease presenting in 1 of 4 siblings affected by hereditary spinocerebellar ataxia: clinical, immunological and genetic study. 278 67

Three Hodgkin's disease-derived cell lines were analysed for the organization of immunoglobulin and T cell receptor genes, for the expression of the interleukin 2 (IL-2) receptor gene, and for the cellular oncogene c-myc. All three cell lines have characteristic genotypic markers of lymphoid cells and can be classified as immature lymphoid cells with respect to the incomplete expression of their antigen receptor genes. This immature genotype is in contrast to the expression of activation antigens Ki-1 (CD 30), IL-2 receptor (CD 25), and HLA-DR. The results obtained are in agreement with studies obtained from primary Hodgkin's lymphomas, which are activated by as yet unknown mechanisms.
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PMID:Molecular analysis of Hodgkin's disease-derived cell lines. 313 69

Peripheral blood T-colony-forming cells (T-CFC) from most patients with T-cell acute lymphoblastic leukaemias (T-ALL) and T-cell non-Hodgkin's lymphomas (T-NHL), can proliferate in vitro in methylcellulose in the absence of added growth factors or mitogens. We now report that spontaneous T-cell colonies could also be obtained during complete remission of 13 out of 21 patients with T-ALL and T-NHL, but none of eight patients with common (pre-B) ALL (cALL). Colony cells were mainly E+T3+, with a variable expression of other T cell markers. Spontaneous T-CFC did not possess self-renewal capacity in the absence of added growth factors. Moreover, incubation of spontaneous colonies with colchicine yielded mitoses in only two out of seven patients, with one normal and one abnormal karyotype. In five patients tested, recombinant interleukin 2 (IL2) could also induce the proliferation of some T-CFC. Both spontaneous and IL2-induced colonies were inhibited by an anti-IL2 receptor monoclonal antibody, suggesting that interaction of IL2 with its receptor may be involved in the proliferation of some T-CFC from these patients. A study of 14 T-ALL patients tested during their first remission indicated that patients who developed no or few spontaneous colonies during their first remission (less than 20 colonies/10(5) mononuclear cells) seemed to relapse later and to have a significantly longer survival than patients with a high number of spontaneous colonies. These data suggest that the spontaneous proliferation capacity of T-CFC might be of prognostic value in the clinical evaluation of T-ALL.
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PMID:Abnormal proliferation of T-colony-forming cells from peripheral blood of patients with T-cell acute lymphoblastic leukaemias and lymphomas in complete remission: potential prognostic value. 349 88

13 patients with Hodgkin's disease (HD) previously treated, 9 of whom were long-time (more than 2 yr) off-therapy, were studied for peripheral blood lymphocyte response to interleukin 2 and for lymphocyte subpopulations by means of in vitro cultures and monoclonal antibodies. The aim of the study was to ascertain the role played by interleukin 2 in the impaired cell-mediated immunity of HD patients. The results show a response of peripheral blood mononuclear cells of HD patients to either the T cell-specific polyclonal mitogens PHA and Con A or to the T cell-dependent, although B cell-specific, PWM, most significantly decreased compared to the normal response. As far as the interleukin 2 involvement in HD is concerned, our study suggests: an impaired endogenous interleukin 2 production by T lymphocytes, a most probable deficiency of the interleukin 2 receptor (Tac) expression and 3) a decrease of the number and/or of the function of NK cells no longer responsive in vitro to interleukin 2. The phenotypic analysis of peripheral blood mononuclear cells showed a slight decrease of total T cells (T3+), of the helper/inducer subset (T4+) and of the T4+/T8+ cells ratio. Our data seem to support the rationale for a therapeutical approach with interleukin 2 in controlled clinical trials also in HD patients, according to the experiments in progress in solid tumor patients.
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PMID:Peripheral blood lymphocyte response to recombinant and non-recombinant interleukin 2 in previously treated patients with Hodgkin's disease, long-time off-therapy. 349 36

A killing defect of natural killer (NK) cells in the absence of NK cytotoxic factors (NKCF) was first demonstrated in a child with Hodgkin's disease. The patient lacked detectable NK cell activity in every phase of the disease as measured by a four-hour 51Cr-release assay using K562 cells as a target. The percent lysis at a 40:1 effector:target ratio by the patient's lymphocytes was persistently below 0.3% as compared with the normal lymphocyte value of 46.2% +/- 5.8% (mean +/- SD). NK cell activity was not detectable at effector:target ratios of 10:1 to 80:1 and by prolongation of the incubation time, and the NK cell defect was not restored or improved by lymphocyte stimulation with polyinosinic-polycytidilic acid, interferon (IFN)-alpha, or interleukin 2 (IL 2). The numbers of Leu-7+ cells and Leu-11+ cells were normal as counted by flow cytometry. A single cell-in-agarose assay demonstrated normal numbers of target binding cells (TBCs), and they showed the morphology of "large granular lymphocytes." However, there were no TBCs with dead targets. These results indicated that the patient's lymphocytes contained normal numbers of NK cells that were capable of recognizing and binding to a target but were incapable of killing the bound target cell. The patient's lymphocytes were then studied for their release of NKCF upon interaction with K562 cells. The patient's cells did not release NKCF, and the NK cell defect was not restored or improved by stimulation of the cells with IFN or IL 2. It is suggested that the deficient release of NKCF may have been related to the killing defect of the NK cells in this patient.
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PMID:A killing defect of natural killer cells with the absence of natural killer cytotoxic factors in a child with Hodgkin's disease. 358 May 73

Ki-1 is a monoclonal antibody (raised against a Hodgkin's disease-derived cell line) that, in biopsy tissue affected by Hodgkin's disease, reacts selectively with Reed-Sternberg cells. The expression of Ki-1 antigen has been analyzed by immunocytochemical techniques in a wide range of human tissue and cell samples, including fetal tissue, malignant lymphomas (290 cases), and mitogen- and virus-transformed peripheral blood lymphocytes. The antigen was detectable on a variable proportion of cells in all cases of lymphomatoid papulosis and angio-immunoblastic lymphadenopathy and in 28% of the cases of peripheral T cell lymphomas (including lympho-epithelioid lymphomas). It was also expressed (more strongly) on tumor cells in 45 cases of diffuse large-cell lymphoma, most of which had originally been diagnosed as malignant histiocytosis or anaplastic carcinoma, because of their bizarre morphology. However, all of these cases lacked macrophage and epithelial antigens. Thirty-five cases expressed T cell-related antigens (associated in nine cases with the coexpression of B cell-related antigens), seven bore B cell-related antigens alone, and three were devoid of T and B cell markers. DNA hybridization with a JH specific probe showed a germline configuration in 11 cases of T cell phenotype, in two cases lacking T and B cell antigens, and in one case of mixed T/B phenotype, while rearrangement was found in two cases of clear B cell type and in one mixed T/B case. Expression of the Ki-1 antigen could be induced, together with interleukin 2 (IL 2) receptor, on normal lymphoid cells of both T and B cell type by exposure to phytohemagglutinin, human T leukemia viruses, Epstein-Barr virus, or Staphylococcus aureus. The results obtained indicate that Ki-1 antigen is an inducible lymphoid-associated molecule that identifies a group of hitherto poorly characterized normal and neoplastic large lymphoid cells. Tumors comprised solely of these cells show both morphological and immunological similarities to the neoplastic cells in Hodgkin's disease. This suggests that both disorders represent the neoplastic proliferation of activated lymphoid cells of either T cell or, less commonly, B cell origin. Disorders in which only a minority of cells express Ki-1 antigen (lymphomatoid papulosis, angio-immunoblastic lymphadenopathy, and certain T cell lymphomas) probably represent lesions in which only some of the abnormal cells have transformed into an "activation state." In direct support of this view is the finding that the Ki-1 expression in these lesions is accompanied by the expression of HLA-DR and IL 2 receptors.
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PMID:The expression of the Hodgkin's disease associated antigen Ki-1 in reactive and neoplastic lymphoid tissue: evidence that Reed-Sternberg cells and histiocytic malignancies are derived from activated lymphoid cells. 387 24


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