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)

Evidence has recently been presented for an infection with a simian type D retrovirus in a patient with AIDS and lymphoma. We tested for simian type D infection in three groups of subjects: 375 patients with lymphoproliferative diseases (255 non-Hodgkin's, 88 Hodgkin's, and 32 chronic lymphoproliferative disease), of whom 75 were human immunodeficiency virus (HIV)-1 infected; seven persons with unexplained low CD4 lymphocyte counts with clinical conditions; and 45 blood donors, of whom 37 were human T-lymphocyte virus (HTLV)-I/II seroindeterminate and eight were HTLV-I/II and HIV-1 seronegative. Serum samples were screened for antibodies against simian type D retroviruses by an enzyme immunoassay, and reactive samples were analyzed by Western blotting. None of the samples were seropositive, but eight (five from non-Hodgkin's and three from Hodgkin's lymphoma patients) were seroindeterminate. Polymerase chain reaction analysis of genomic DNA from peripheral blood lymphocytes of all eight of these patients was carried out using simian type D gag generic primers with generic internal oligoprobing. All samples were negative. We conclude that simian type D infection is rare among HIV-infected and noninfected lymphoma patients, persons with unexplained low CD4 counts, and persons with HTLV-seroindeterminate test results.
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PMID:The search for human infection with simian type D retroviruses. 839 88

We analyzed the stimulating capacities of malignant B cells from non-Hodgkin's lymphomas (NHL) to induce an allogeneic response in primary mixed lymphocyte reaction (MLR). T cells purified from a single healthy donor (KS) were used to compare the responses induced by either malignant or hyperplastic cells. Malignant B cells induced strong proliferation of KS cells independently of their level of expression of adhesion molecules. The KS cells after MLR were predominantly CD3+, CD25+, HLA-DR+, Ki67+ and CD45RO+ T cells, and the CD4/CD8 ratio was heterogeneous (from 0.8 to 2.7). To investigate the role of co-stimulatory molecules CD80 and CD86 for the stimulatory capacities of B cells, the expression of both molecules was analyzed before and during the MLR. Most fresh malignant B cells were negative for CD80 and CD86, whereas co-cultured B cells expressed high levels of both molecules. This expression was crucial for T cell proliferation, since monoclonal antibodies directed against CD80 and CD86 completely abrogated the MLR. We also report that KS responding cells at the end of co-culture were able to lyse fresh B cells used as stimulator cells to different extents (from 10 to 51%), and the level of lysis was enhanced after PMA activation of the target cells. Inhibition experiments using CD8 and CD4 mAb showed that effector cells were mainly CD8+. This report is the first to describe the accessory function of human malignant B cells from NHL and their sensitivity to lysis mediated by CD8+ T cells, and suggests new strategies for the development of antitumor immunity in NHL.
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PMID:Malignant B lymphocytes from non-Hodgkin's lymphoma induce allogeneic proliferative and cytotoxic T cell responses in primary mixed lymphocyte cultures: an important role of co-stimulatory molecules CD80 (B7-1) and CD86 (B7-2) in stimulation by tumor cells. 856 20

The immunologic attributes of cytokine mobilized peripheral blood stem cell (PSC) products (n = 52) and the resulting reconstitution of the hematopoietic and immunologic system following autologous transplantation were examined in a consecutive population of non-Hodgkin lymphoma (NHL), or solid tumor patients at the University of Nebraska Medical Center. Granulocyte-monocyte colony stimulating factor (GM-CSF)-mobilized PSC products had a high frequency of monocytes (31%) and bands (15%) as compared to normal peripheral blood (PB) cells. The phenotypic analysis of the mobilized PSC product revealed that they had normal levels of CD4+ cells, an increased frequency of CD8+ cells and a corresponding decrease in the CD4+:CD8+ cell ratio as compared to the peripheral blood leukocytes (PBL) of normal individuals. PSC products also had an increase in CD34+ cells as compared to PB. Natural killer (NK) and T cell activity in the PSC products were also lower than that observed in PB. Post-transplantation there was an accelerated reconstitution of NK-cell function in the PB as compared to T cell function (PHA (phytohemagglutinin) mitogenesis) which did not return to normal by day 100 post-transplantation. We also report for the first time high levels of an irradiation resistant suppressor cell activity in the PSC product and in the PB post-transplantation. There was also a concomitant increase in CD4-, CD8-, TCR alpha/beta+ cells (phenotypic homolog of 'natural suppressor' (NS) cells) in the PB post-transplantation. The number of months of prior chemotherapy correlated with PHA response but the NS activity and frequency of CD4-, CD8- and TCR alpha/beta+ cells did not. Further, cytokine mobilization and apheresis appears to contribute to the loss of PHA responsiveness and the increased levels of suppressor cell activity.
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PMID:Immunologic attributes of cytokine mobilized peripheral blood stem cells and recovery following transplantation. 867 41

Expression of the Epstein-Barr virus (EBV) gene product LMP1 is found in tumour cells in varying proportions of Hodgkin's disease (HD) cases. It is not clear which cellular genes are influenced by EBV in HD. A total of 387 HD cases were tested for differences among LMP1-positive and -negative cases with respect to age, sex, histotype and immunophenotypic parameters (CD2, CD3, CD4, CD15, CD19, CD20, CD21, CD22, CD23, CD25, CD30, CD43, CD45RA, CD45R0, CD70, HLA-DR, T-cell receptor beta-chain, and p53 expression). Comparison of patient age and sex as well as distribution of histotype and tumour cell immunophenotype with published data suggests that the cases in this study are representative of the spectrum of HD in developed countries. LMP1 expression was found in 131/387 HD cases (36.4 per cent) with non-homogeneous distribution among HD histotypes, the mixed cellularity type (HDmc) being most frequently EBV-associated (71/129 cases, 55 percent). No relationship was found to age and sex. Significant phenotypic differences were restricted to the HDmc histotype, where the tumour cells expressed the activation marker CD30 in a larger proportion, and CD20 in a smaller proportion, when harbouring EBV. These results suggest that EBV may influence the tumour cell phenotype in HD.
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PMID:Phenotypic modulation of Hodgkin and Reed-Sternberg cells by Epstein-Barr virus. 869 46

A 33-year-old, homosexual, cat-owning, African-American man with human immunodeficiency virus infection by positive serologic tests and acquired immunodeficiency syndrome by CD4 lymphocyte count alone (39 cells/mL) presented with a one-year history of intermittent fever, weight loss, and generalized lymphadenopathy. A malignant lymphoma was suspected clinically. Light microscopic study of a left inguinal lymph node biopsy specimen revealed effacement of the lymph node architecture by a diffuse infiltrate of large, atypical reticulum cells, loose, patchy granulomatous inflammation, diffuse hyaline fibrosis, diffusely proliferated blood vessels, and multifocal degeneration and necrosis. Lymph follicles were absent and lymphocytes were moderately depleted. Microorganisms were not seen in lymph node sections stained with special histochemical stains (including the Warthin-Starry stain). These light microscopic changes were considered suggestive of a malignant lymphoma, especially Hodgkin's disease. The diagnosis of cat scratch disease (CSD) became apparent only after transmission electron microscopic study of the lymph node revealed clusters of small, pleomorphic bacteria in degenerated collagenous tissue and in blood vessel walls. This case illustrates the value of transmission electron microscopy in making the diagnosis of CSD, especially when light microscopic changes are superimposed on those of late human immunodeficiency virus infection of the lymph node.
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PMID:Cat scratch disease and acquired immunodeficiency disease: diagnosis by transmission electron microscopy. 872 61

Considerable evidence has been accumulating in favor of a possible involvement of viral agents in the pathogenesis of human lymphomas. The most recent proposal for a lymphoma classification, the Revised European-American Classification, emphasized for the first time the pathogenetic importance of two viruses, namely Epstein-Barr virus (EBV) and human T lymphotropic virus I (HTLV-I) in the development of certain lymphoid neoplasias. However, in the last ten years new viral agents possibly related to lymphoproliferative activity have been discovered: three herpesviruses [human herpesvirus-6 (HHV-6), -7 (HHV-7) and -8 (HHV-8)] and a flavivirus, HCV. HHV-6 was isolated from the peripheral blood of patients with lymphomas and a possible role for this beta-herpesvirus in Hodgkin's disease and in angioimmunoblastic lymphadenopathy (AILD) has emerged from serological and molecular studies. HHV-7, a beta-herpesvirus genetically close to HHV-6, has not yet been found in a human disease but it utilizes CD4 as a receptor on the lymphocyte surface. Only partial HHV-8 genomic sequences have been identified so far, suggesting a genetic homology with members of the gamma-herpesvirus family, including EBV. HHV-8 sequences have been identified for the first time in all forms of Kaposi's sarcoma as well as in a variety of lymphoid disorders, including body-cavity-based non Hodgkin's lymphomas, Castleman's disease, AILD and a type of HIV-negative reactive lymphadenopathy with peculiar histologic features. Finally, after its identification as the major cause of post-transfusion and sporadic non-A, non-B hepatitis, HCV has revealed a lymphotropism both in vitro and in vivo. A strong association between HCV infection and a benign lymphoproliferative disease, essential mixed cryoglobulinemia type II, has clearly emerged both from serological and molecular studies. A possible role for this viral infection in B-cell non Hodgkin's lymphomas not associated with cryoglobulinemia has also been proposed recently. The present work offers an overview of the huge amount of experimental and clinical observations supporting the possible involvement of these new lymphotropic viruses in human lymphoproliferative diseases.
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PMID:The new lymphotropic herpesviruses (HHV-6, HHV-7, HHV-8) and hepatitis C virus (HCV) in human lymphoproliferative diseases: an overview. 876 34

Lymphocyte predominance Hodgkin's disease (LPHD) is a B-cell lymphoproliferative disorder; patients with LPHD have an increased risk of developing synchronous or metachronous B-cell non-Hodgkin's lymphoma. The synchronous presence of LPHD and B-cell lymphoma in the same lymph node in some cases lends support to the argument that the B-cell lymphoma arises as a consequence of transformation or progression of LPHD. We have recently identified three cases of LPHD occurring simultaneously with T-cell lymphoma in a series of 76 cases of LPHD in the files of the Nebraska Lymphoma Study Group Registry. In large areas of the lymph nodes, atypical T cells with large, irregular, and hyperchromatic nuclei were admixed with Reed-Sternberg variants characteristic of LPHD (L&H cells). However, in all cases, areas of typical nodular LPHD without obvious T-cell lymphoma were also evident. In one case, frozen-section immunohistochemistry demonstrated the absence of expression of CD5, CD4, or CD8 by the T-cell lymphoma. The L&H cells in all cases expressed CD45 and CD20, as expected. In all three cases, clonal T-cell receptor (TCR)-gamma gene and TCR-beta gene rearrangements were documented by polymerase chain reaction analysis and Southern blotting, respectively. No clonally rearranged immunoglobulin genes were detected by either technique. To our knowledge, this represents the first report of the simultaneous occurrence of LPHD and T-cell lymphoma. Although B-cell lymphoma occurring in the setting of LPHD is a well-recognized phenomenon, previous reports of T-cell lymphoma occurring after a diagnosis of LPHD, as well as our cases with synchronous disease, suggest that the association of T-cell lymphoma and LPHD may not be uncommon as well. Furthermore, our cases indicate that T-cell lymphoma occurring in LPHD is not therapy related. However, the underlying mechanisms by which these composite lymphomas occur remain unknown.
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PMID:Concurrent lymphocyte predominance Hodgkin's disease and T-cell lymphoma. A report of three cases. 877 90

Persons with HIV infection are at an increased risk of developing intermediate and high-grade non-Hodgkin's lymphomas. Patients present with wide-spread extranodal disease at the time of initial presentation, with unusual sites of disease common. Factors predictive of a poor prognosis are low performance status, history of AIDS prior to the diagnosis of lymphoma, bone marrow involvement, and low CD4 count. Experience suggests that in some patients, more aggressive chemotherapy may be associated with shortened survival time. Recent clinical trials have demonstrated that the use of either myeloid growth factors or reduced-dosage chemotherapeutic regimens can reduce the morbidity associated with chemotherapy. A number of new and exciting experimental treatments are now in clinical development. These include new chemotherapy-based regimens, immune modulators immunotoxin therapy, and cellular therapy. It is hoped that as we continue to learn more about the biology of the HIV-associated lymphomas, we can develop more rational and effective treatment modlities that take advantage of the unique molecular characteristics of these tumors.
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PMID:Diagnosis and management of systemic non-Hodgkin's lymphoma in HIV disease. 888 Jan 99

Hodgkin's disease is characterized by an immune response in the involved tissues that is predominantly CD4 mediated. The CD4+ T-cells are CD45RO+ and CD45RBdim, they express several activation markers but lack CD26, and in vitro can be stimulated to produce gamma-interferon and IL-4, but not IL-2. This is not the usual immunophenotype and cytokine production pattern of Th1, Th2 or Th0 cells and may be a reflection of anergy. The cause of such an anergic reaction is not clear since RS cells express HLA class II as well as the co-stimulator molecules CD80 and CD86. It is possible that a (hypothetical) super antigen expressed on the RS cells may play a role. The absence of IL-2 production however explains the absence of a CD8 mediated response. In addition to that, RS cells generally do not express HLA class I, which allows them to escape CD8 mediated responses. The link between the ineffective immune response in the tissue and the generalized immune deficiency in Hodgkin's disease may consist of several components. These include the influx of mature T-cells into the affected tissues, the secretion of inhibitory molecules by the neoplastic cells and the spill-over of the anergic T-cell response into the general circulation by either the Hodgkin related antigen or also as a result of an IL-4 dominated response. The latter possibility may also be related to the hyper-gamma-globulinaemia and the frequently observed high IgE levels.
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PMID:Immunology of Hodgkin's disease. 892 39

Six patients with human immunodeficiency virus (HIV)-associated non-Hodgkin lymphoma receiving chemotherapy (CT) with cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) plus granulocyte colony-stimulating factor were sequentially monitored to study the effects of these treatments on their immunologic status (CD4 and CD8 cell counts) and on HIV plasma viremia. We show that mean CD4 cell counts declined significantly after the third cycle of CT (187 +/- 117/microliters before CT versus 92.4 +/- 60/microliters; p = 0.04) and remained significantly reduced 4 months after completion of CT. Modifications of CD8 cell counts were not statistically significant. The effects of CT on plasma viremia, as measured by a competitive polymerase chain reaction technique, were delayed until the fourth cycle, when an increase of viral load ranging from 0.6 to 2 logs (p = 0.027) was observed. After this point, viremia returned to baseline levels, with the exception of two patients who later developed opportunistic infections and one who underwent disease progression. These results suggest that, contrary to CD4 cell counts, plasma viremia could be a faithful surrogate marker for monitoring of HIV disease progression in patients undergoing CT.
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PMID:The effects of antineoplastic chemotherapy on HIV disease. 895 47


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