Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: UMLS:C0019829 (
Hodgkin's disease
)
30,247
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
In order to clarify the mechanisms of the eosinophilia frequently observed in patients with
Hodgkin's disease
(HD), 18 patients and 16 age- and sex-matched controls were studied. Increased eosinophil numbers in peripheral blood and serum IgE, as well as decreased cell-mediated immunity were present in HD patients compared with control individuals. Advanced disease was accompanied by lower eosinophil levels, increased IgE, and lower CD4+ T cell counts in peripheral blood. Eosinophilia correlated with CD4+ T cell counts, suggesting that eosinophil production could be under CD4+ T cell control. GM-CSF production in vitro by Phytohemagglutinin-stimulated mononuclear cells was significantly lower in HD patients with eosinophilia. On the other hand, an eosinophil-survival-enhancing activity was found in sera and culture supernatants from controls and HD patients; this activity was stronger for HD patients and was higher for those with eosinophilia. Furthermore, this activity was completely abolished by preincubation with monoclonal antibodies to IL-5, but not with normal mouse serum. Our results suggest that defects of cell-mediated immunity present in patients with HD are accompanied by a predominant type 2
cytokine
profile. IL-5 is involved in the increased eosinophil production observed in these patients.
...
PMID:Eosinophilia in Hodgkin's disease: a role for interleukin 5. 868 71
We examined paraffin sections for the expression of interleukin-1 alpha, interleukin-1 beta and tumor necrosis factor-alpha, in 40 cases of
Hodgkin's disease
. Our purpose was to study the role of these cytokines in the "inflammatory" histological features and "B" symptoms in this disease. Immunohistochemistry with the avidin-biotin-peroxidase complex method was used. The findings were compared with those of 20 cases of non-
Hodgkin
's lymphomas and of 20 non-neoplastic lymphadenopathies. Evidence for EBV infection and myc and ras oncoproteins expression was also studied in these patients, but no correlation between any of these features and
cytokine
expression was found. We found a significant correlation between the expression of interleukin-1 beta and several "inflammatory" histological features, as well as between the expression of tumor necrosis factor-alpha and B symptoms and tumor bulk. The differential correlations between these major pro-inflammatory cytokines expression and the "inflammatory" manifestations in
Hodgkin's disease
are remarkable, considering the complexity of the cytokines composing the
cytokine
network involved in this disease.
...
PMID:Interleukin-1 and tumor necrosis factor-alpha in the Reed-Sternberg cells of Hodgkin's disease. Correlation with clinical and morphological "inflammatory" features. 870 95
Hodgkin disease
(HD) is characterized by the presence of a small number (usually <1% of total tumor mass) of the typical
Hodgkin
and Reed-Sternberg (H-RS) cells in a hyperplastic background of normal reactive lymphocytes, plasma cells, histiocytes, neutrophils, eosinophils, and stromal cells. HRS cells produce various cytokines, growth factors, and express
cytokine
receptors and activation antigens, implying a predominant role for these molecules in the pathophysiology of
Hodgkin disease
. HD may therefore be regarded as a tumor of
cytokine
producing cells. The CD30 antigen has been characterized as a marker for cultured and primary
Hodgkin
and Reed-Sternberg cells, and was found to be overexpressed in
Hodgkin disease
and a subgroup of non-
Hodgkin
lymphomas including large cell anaplastic lymphomas and Burkitt lymphomas. The molecular cloning of the CD30 antigen revealed that CD30 is a member of the tumor necrosis factor/nerve growth factor receptor superfamily. The cloning of the cognate for CD30, currently termed CD30 ligand, confirmed that the CD30 antigen functions as a cytokine receptor. Recombinant CD30 ligand is a membrane-bound protein with pleiotropic biological activities for different CD30+ lymphoma types, but also for the immune system, mainly T cells. CD30L belongs to the emerging tumor necrosis factor ligand superfamily. The CD30-CD30 ligand interaction could have a critical pathophysiological role in malignant lymphomas, particularly
Hodgkin disease
, large cell anaplastic lymphomas and Burkitt lymphomas, and is also involved in activation and functioning of the T cell-dependent immune system.
...
PMID:CD30 ligand, a member of the TNF ligand superfamily, with growth and activation control CD30+ lymphoid and lymphoma cells. 883 95
Hodgkin's disease
represents a phenotypically and genotypically heterogeneous lymphoma of CD30-positive tumour cells. Infection of the putative tumour cell population with Epstein-Barr virus (EBV) represents the most common genetic abnormality detectable in HD, yet the role of EBV in the pathogenesis of HD is only poorly understood. In virus-associated HD cases, monoclonal EBV genomes are detectable in all
Hodgkin
and Reed-Sternberg (HRS) cells, indicating that EBV infection takes place before expansion of the HRS cell population and, by implication, supporting the concept of a monoclonal origin of HRS cells. EBV infection does not define a distinct subgroup of HD but is detectable in different histotypes and in HRS cells expressing lymphocyte differentiation antigens of different cell lineages. Through the EBV-encoded protein, LMP1, the virus may superimpose an activated phenotype on genotypically immature lymphocytes. EBV-induced modulation of the
cytokine
expression pattern of HRS cells may contribute to the local inhibition of EBV-specific immunity observed in EBV-positive cases.
...
PMID:The role of Epstein-Barr virus in the pathogenesis of Hodgkin's disease. 883 3
Micromanipulation of single
Hodgkin
-Reed/Sternberg cells and subsequent nucleic acid amplification (H-RS single cell PCR) has now been established as a new and powerful method for specific genetic analysis of the tumor cells in
Hodgkin's disease
(HD). Although there are still some discrepancies in the results presented by different groups, most probably due to methodological problems, H-RS cells, at least in a substantial proportion of cases, seem to be B-lymphoid cells of monoclonal origin. In addition, new data were presented on the
cytokine
/cytokine receptor interaction in HD, on transcription factors in HD-derived cell lines and on a promising approach for identification of tumor associated antigens in HD.
...
PMID:Report on the workshop biology of the Third International Symposium on Hodgkin's Lymphoma in Cologne 1995. 883 9
The presence of a prominent tissue eosinophilia represents a typical histopathologic hallmark of
Hodgkin's disease
(HD). To evaluate the putative role of eosinophils on tumor cell regulation in HD, we have analyzed these cells for the functional expression of CD30 ligand (CD30L), a surface molecule able to transduce CD30-mediated proliferation signals on
Hodgkin
's (H) and Reed-Sternberg (RS) cells. The results demonstrate that circulating and tissue eosinophils from normal donors and patients with HD or hypereosinophilic syndrome (HES), display CD30L mRNA and express CD30L protein, as shown by immunostaining with a specific monoclonal antibody (M80) and with a biotinylated soluble CD30-Fc fusion protein. The surface density of CD30L on eosinophils from HD and HES patients was remarkably higher compared with healthy donors, probably reflecting a
cytokine
-mediated upregulation in these pathologic conditions. Accordingly, we provide evidence that cytokines regulating eosinophils proliferation and activation, ie, interleukin-5 (IL-5), IL-3, and granulocyte-macrophage colony-stimulating factor (GM-CSF), are able to enhance the cellular density of CD30L on purified eosinophils from normal subjects. Finally, we show that native CD30L on human eosinophils is a functionally active surface structure able to transduce proliferative signals on CD30+ target cells, including cultured H-RS cells. Our data suggest that eosinophils may not merely represent innocent bystanders, but rather act as important elements in the pathology of HD by contributing to the deregulated network of CD30/CD30L-mediated interactive signals between H-RS cells and surrounding reactive cells.
...
PMID:Human eosinophils express functional CD30 ligand and stimulate proliferation of a Hodgkin's disease cell line. 889 93
Hodgkin's disease
is an oncogenic core disorder characterized by both mitotic and amitotic neoplastic multiplication, and is associated with collateral disorders such as lacunar formation and leukocytic infiltration. Research has demonstrated that
Hodgkin's disease
progresses stepwise, beginning with a reversible, biological stage during which
Hodgkin
and Reed-Sternberg cells are formed, followed by constitutive, but reversible Hodgkinogenic medical stage that leads to an irreversible, systemic and fatal proto-oncogenic stage. This disease results from collateral activation of
cytokine
and archaic oncogenes, suppression of DNA repair genes in multiple chromosomes. The variability of
Hodgkin's disease
manifestations has required antisynthetic (antimetabolites, radiotherapy), anti-viral (acyclovir) and anti-mitotic (vincristine, vinblastine) for different loci minores of treatment. Continued molecular biological research of the ancestral and prokaryotic oncogenes is recommended.
...
PMID:Evolution of Hodgkin's disease. 889 21
We investigated the in vitro antitumor activity of monocytes derived from autologous bone marrow transplanted (ABMT) patients treated in vivo with granulocyte-macrophage colony-stimulating factor (GM-CSF). Thirty-four patients (17 female, 17 male), median age 42 (range 3-57) years, were enrolled in the study. Fourteen patients were diagnosed with non-Hodgkin's lymphoma (NHL), eight with
Hodgkin's disease
(HD), nine with breast cancer and three with neuroblastoma. Six patients who did not receive GM-CSF post-ABMT served as controls. We assessed cytotoxicity, antibody-dependent cellular cytotoxicity (ADCC), expression of the activation antigen CD16, and
cytokine
production by an enriched population of monocytes (> 90% CD+14) pre-, during and post-GM-CSF administration. Within the group of patients receiving treatment, ADCC was significantly higher during in vivo GM-CSF administration than post-therapy (P < 0.05) and in 50% of these patients, ADCC increased during in vivo GM-CSF administration over pretreatment values. In addition, in vivo GM-CSF administration caused the monocytes to secrete elevated levels of tumor necrosis factor-alpha (TNF-alpha) and GM-CSF (P < 0.05). We conclude that GM-CSF augments monocyte-mediated cytotoxicity post-ABMT, and therefore may have a role in controlling minimal residual disease post-transplant.
...
PMID:Granulocyte-macrophage colony-stimulating factor dependent monocyte-mediated cytotoxicity post-autologous bone marrow transplantation. 891 16
Hodgkin's disease
(HD) is characterized by the presence of the typical, clonal malignant
Hodgkin
and Reed-Sternberg (H-RS) cells in a hyperplastic background of normal reactive lymphocytes, plasma cells, histiocytes, neutrophils, eosinophils and stromal cells. The neoplastic nature of HD is based on aggressive clinical progression, presence of the proliferating and atypical H-RS cells, aneuploidy and cellular clonality. Immunophenotypical studies have demonstrated frequent expression of lymphoid "activation markers' including CD15, CD25, CD30, CD40, CD54, CD70, CD71, CD80, CD86 and MHC class II and less frequent expression of T- or B-cell-associated antigens by the neoplastic H-RS cells. The clonality of H-RS cells is demonstrated by clonal EBV integration, clonal cytogenetic abnormalities including p53 mutations and clonal immunoglobulin rearrangements in some HD cases. There is involvement of diverse molecules with oncogenic potential, including presence of viruses (Epstein-Barr virus and human herpes virus-6) and/or oncogenes/tumour suppressor genes (bcl-2/bcl-x, p53/MDM-2, c-myc, c-fms, N-ras, lck). The histopathological presentation and characteristic clinical features of HD correlate with an unbalanced production of multiple cytokines and define HD as a tumour of
cytokine
-producing cells. The proportion of malignant H-RS cells to reactive cellular components and fibrosis is dependent on the production of particular cytokines and allows subtyping of HD cases. The combined use of immunohistochemical, biochemical and molecular techniques has thus allowed recognition that HD represents more than one clinico-pathological entity with different types of H-RS cells. The defined mechanism for the biological nature, origin and oncogenesis of H-RS cells remains not fully understood, but is susceptible to further analysis using modern technology.
...
PMID:Pathophysiology of Hodgkin's disease: functional and molecular aspects. 892 38
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.
...
PMID:Immunology of Hodgkin's disease. 892 39
<< Previous
1
2
3
4
5
6
7
8
9
10
Next >>