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)

A cluster of cases of Hodgkin's disease was observed in a small town which contained a large navy bean elevator. In previous investigations a lectin was isolated from the navy beans and lymphocytes from town residents were shown to be sensitized to this lectin. Mice were exposed to 15 weekly injections of navy bean lectin. Splenic lymphocytes from injected mice incorporated greater amounts of thymidine than did controls when incubated with the lectin. Cell-mediated immunity as measured by a Concanavalin A dose-response curve was significantly suppressed (p < 0.01) in the injected mice. Long term studies are needed to see if the decreased Concanavalin A response in the mice chronically stimulated with navy bean lectin will predispose to lymphoreticular malignancies.
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PMID:Suppression of immune response in mice by navy bean lectin. 742 Apr 7

Jacalin is a lectin which reacts with D-galactose. We have tested jacalin on 75 samples of different formalin- and alcohol-fixed tissues. A consistent cytoplasmic stain of the histiocytes was observed in paraffin-embedded tissues in all cases studied of reactive sinus histiocytosis, macrophages in clear centres of follicular hyperplasia, in tuberculosis granulomas and in osteoclast-like giant cells in a breast carcinoma. We failed to find any clear binding of jacalin to the cells of eosinophilic granulomas, giant cell tumors of tendon sheath, pleomorphic malignant fibrous histiocytomas, Hodgkin's disease, melanomas, nevi or signet ring cell carcinomas of the breast and stomach. It seems that jacalin is a good marker for free histiocytes/macrophages, not for fixed histiocytes and tumors related to them. This lectin might play a role in differential diagnosis with histiocyte mimicking processes.
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PMID:Jacalin, another marker for histiocytes in paraffin-embedded tissues. 757 7

Forty-four cases of Hodgkin's disease (HD), mostly of the nodular sclerosing type, were investigated for the presence of Epstein-Barr virus (EBV) by polymerase chain reaction (PCR) and DNA and RNA in situ hybridization (DISH, RISH), as well as by immunohistochemistry for the detection of latent membrane protein-1 (LMP-1) of EBV. In situ hybridization (ISH) was combined with immunohistochemistry to correlate the presence and activity of the virus at the cellular level. In 18/34 (53 per cent) cases, EBV-DNA sequences could be detected with the PCR method. In 12/18 positive cases, DISH and RISH were also positive. In the remaining six EBV-PCR positive cases, two were also positive with RISH and LMP-1, whereas no positive signal with DISH could be obtained. All DISH and/or RISH positive cases were also positive for LMP-1. With RISH, not only the Reed-Sternberg cells and their mononuclear variants (RS cells) stained positive, but also small and intermediate cells frequently reacted with the EBV-specific probes (EBER-1 and -2). Double staining with cellular markers (CD3, CD20, CD45, CD45RO, CD68, and the lectin PNA) revealed that most of the smaller EBER-positive cells frequently did not express T, B, or histiocytic markers, but that they, as well as the RS cells, showed cytoplasmic and membranous staining with PNA. These smaller EBER-positive cells were not found in EBV-PCR negative HD. EBER-positive RS cells were almost always LMP-1 positive, as well as a substantial proportion of the intermediate-sized cells, whereas the majority of the small EBER-positive cells remained LMP-1 negative.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Presence of Epstein-Barr virus harbouring small and intermediate-sized cells in Hodgkin's disease. Is there a relationship with Reed-Sternberg cells? 839 21

Using autologous serum for the immunoscreening of a cDNA expression library derived from tissue involved by Hodgkin's disease, a new 36-kDa protein with the characteristics of galectins (S-type lectins) was detected. Sequence analysis of the cDNA clone HOM-HD-21 revealed two homologous motifs known as lectin domains with galactoside binding capacity. The two domains are linked by a stretch of about 30 amino acid residues and share a sequence homology of 39%. While the N-terminal lectin domain shows merely moderate homologies with known galectins, the C-terminal lectin domain is highly homologous to rat galectin-5 with an amino acid sequence identity of 70%. We ruled out mutations of the tumor-derived transcript by sequence comparison with the respective cDNA cloned from normal peripheral blood leukocytes. Recombinant protein expressed in Chinese hamster ovary cells was purified from lysates by lactose and galactose affinity chromatography, proving the galactoside binding capacity of this new galectin. Northern blot analysis revealed an expression spectrum restricted to peripheral blood leukocytes and lymphatic tissues. In accordance with the nomenclature of known galectins, we suggest to designate this novel galactoside binding protein galectin-9.
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PMID:Molecular definition of a novel human galectin which is immunogenic in patients with Hodgkin's disease. 904 65

Interleukin (IL)-18 was identified as a molecule that induces IFN-gamma production and enhances NK cell cytotoxicity. In this paper, we report upon the purification and characterization of human IL-18 receptor (hIL-18R). We selected the Hodgkin's disease cell line, L428, as the most strongly hIL-18R-expressing cell line based on the results of binding assays. This binding was inhibited by IL-18 but not by IL-1beta. The dissociation constant (Kd) of 125I-IL-18 binding to L428 cells was about 18.5 nM, with 18,000 binding sites/cell. After immunizing mice with L428 cells and cloning, a single monoclonal antibody (mAb) against hIL-18R was obtained (mAb 117-10C). Sequentially, hIL-18R was purified from 3-[(3-cholamidopropyl)dimethylammonio]-1-propanesulfonic acid (CHAPS)-extracted L428 cells by wheat germ lectin-Sepharose 4B chromatography and mAb 117-10C-Sepharose chromatography. The internal amino acid sequences of hIL-18R all matched those of human IL-1 receptor-related protein (IL-1Rrp), the ligand of which was unknown to date. When expressed in COS-1 cells, the cDNA of IL-1Rrp conferred IL-18 binding properties on the cells and the capacity for signal transduction. From these results, we conclude that a functional IL-18 receptor component is IL-1Rrp.
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PMID:Purification and characterization of the human interleukin-18 receptor. 932

A novel probe, a 9-O-acetylated sialic acid binding lectin, namely achatininH (ATNH) has been used for the detection of changes on the cell surface during acute lymphoblastic leukemia (ALL). ATNH does not agglutinate normal human erythrocytes, however it is capable of agglutinating erythrocytes and peripheral blood mononuclear cells (PBMC) of patients suffering from ALL. The differential expression of a key receptor, 9-O-acetylated sialo glyco conjugate (9-O-AcSG), on PBMC was observed using a simple lymphoproliferative assay (LA). The extent of expression of 9-O-AcSG was used as an index to distinguish ALL patients of different clinical stages and assess the probability of relapse. The amount of ATNH needed for maximum stimulation served as a tool to indirectly measure the extent of expression of 9-O-AcSG on PBMC surface. The acetylated sialo glycoconjugate was expressed at a very high concentration during acute phase of the disease. Subsequently it decreased during treatment persisted during maintenance therapy and reappeared with relapse. PBMC of normal human donors required 80 times more ATNH in comparison to the untreated acute phase ALL patients. No cross reactivity was found in non Hodgkin's lymphoma, chronic myelogenous leukemia and thalassaemia patients.
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PMID:O-acetyl sialic acid binding lectin as a probe for detection of subtle change on cell surface induced during acute lymphoblastic leukemia (ALL) and its clinical application. 934 33

The growth of a transplantable murine non-Hodgkin lymphoma tumour, developing either intraperitoneally as an ascites tumour or subcutaneously as a solid tumour, has been shown to be markedly diminished by including phytohaemagglutinin (PHA), a lectin present in raw kidney bean (Phaseolus vulgaris) in the diet. In NMRI mice fed PHA within the range 0.45-7.0 mg/g diet, tumours which developed during a 10 day period after subcutaneous injection of cells were about 35% of the dry weight of those in lactalbumin-fed (control) animals. The reduced rate of growth occurred in a dose-dependent manner within the range 0.45-3.5 mg/g diet. Based on these observations it has been suggested that a competition between the gut epithelium undergoing hyperplasia and the developing tumour may occur for nutrients from a common body pool, and this may be an important factor with regard to the observed initial low level of tumour growth following the feeding of a PHA-containing diet. Observations which showed that the level of hyperplasia of the small bowel in response to feeding the PHA diets was higher in non-injected mice compared to those which had been injected with tumour cells substantiated the concept of competition between gut and tumour for nutrients etc. required for growth. Experiments with a second murine tumour cell line (a plasmacytoma) in Balb/c mice gave similar results indicating that the effect of PHA was not restricted to a single tumour system.
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PMID:The induction of gut hyperplasia by phytohaemagglutinin in the diet and limitation of tumour growth. 958 10

The results presented in this study show that a switch from a non-protein diet (NPD) to one of a normal protein content (LA) on the day of subcutaneous injection of non-Hodgkin lymphoma tumour cells greatly favoured the development and growth of the tumour. Interestingly, however, inclusion of the plant lectin phytohaemagglutinin (PHA) in the LA diet appeared to compete with the effect of switch to the protein-rich diet, resulting in decreased tumour size and an increased incidence of necrosis. PHA was shown to induce hyperplasia of the gut even in the presence of the growing tumour. This observation together with the fact that gut hyperplasia also occurred in animals which were fed NPD supplemented with PHA, indicated the strength of PHA as a growth signal. It would seem likely that this 'normal' growth is able to compete with the tumour for important growth factors and nutrients, including polyamines, effectively starving the tumour for these molecules and resulting in its decreased rate of proliferation.
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PMID:A combination of dietary protein depletion and PHA-induced gut growth reduce the mass of a murine non-Hodgkin lymphoma. 1039 71

The growth of a non-Hodgkin lymphoma, developing subcutaneously as a solid tumour in NMRI mice, is markedly diminished by including phytohaemagglutinin (PHA), a lectin present in raw kidney bean (Phaseolus vulgaris), in the diet. In the experiment described in this communication the effect of first allowing tumours to develop for 5 days before switching the mice to a diet containing PHA at different concentrations was tested to establish whether or not feeding the lectin at late times also resulted in reducing tumour growth. This switch of diet indeed proved to be effective in slowing down growth of the lymphoma tumour. The reduced rate of growth occurs in a dose-dependent manner. We have suggested that a competition between the gut epithelium undergoing PHA-stimulated hyperplasia and the developing tumour may occur for polyamines and other nutrients from a common body pool and this could be an important contributory factor with regard to the observed low level of tumour growth following the feeding of PHA-containing diet. Recent data which showed that the level of hyperplasia of the small bowel in response to feeding the PHA diets was higher in non-injected mice compared to those which had been injected with tumour cells substantiated the concept of competition between gut and tumour for nutrients and other requirements for growth.
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PMID:The growth of an established murine non-Hodgkin lymphoma tumour is limited by switching to a phytohaemagglutinin-containing diet. 1065 13

Midkine (MK) was originally cloned as a product of a retinoic acid-responsive gene. The rationale for studying MK expression is based on previous reports showing that it transforms 3T3 cells, and that it acts as an autocrine growth factor in Wilm's tumors, and that its overexpression has been associated with worse outcome in bladder carcinoma. Besides bladder carcinoma, its expression was reported in various solid tumors. We investigated the expression of MK protein and/or MK gene in biopsied specimens from 40 patients with primary malignant lymphoma, 21 with Hodgkin's disease (HD) and 19 with non-Hodgkin's lymphoma (NHL). Reed-Sternberg (R-S) cells were stained positive in 10 of 16 HD cases evaluated by immunohistochemical method, whereas 18 of 19 NHL cases did not stain, and one B-cell NHL stained weakly positive. Immunostaining analysis was extended to established cell lines and to normal lymphocytes with or without lectin stimulation or with EB virus transformation. Among hematopoietic cells examined, erythro- or megakaryoblastic leukemia cell lines (K562, MEG-01 and UT7) were positive, while normal lymphocytes (except the EB virus-transformed one) and most myeloid and lymphoid cell lines (except Raji cells) were negative. On the contrary, solid tumor cell lines showed high and strongly positive staining including cell lines derived from of lung gastric, colon, and a pancreatic cancer. Using semi-quantitative reverse transcription polymerase chain reaction (RT-PCR), which is suitable for the detection of weakly expressed mRNA, the relative ratio of MK mRNA to beta-actin mRNA of samples was measured and compared in cases where RNA was available. The mean values of relative ratio (MK/beta-actin) of HD were almost twice as those of NHL samples, peripheral blood T cells, and spleen B cells. Our findings showed that MK is expressed in Reed-Sternberg cells of HD, and that MK might play a role in the pathogenesis of HD.
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PMID:Midkine expression in Reed-Sternberg cells of Hodgkin's disease. 1075 93


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