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)

An analysis of red cell membrane proteins in acute and chronic lymphatic leukaemia, Hodgkin's disease, lymphosarcoma, and myeloma was carried out. The electrophoretic pattern after solubilisation in urea or SDS was examined, along with migration on cellulose acetate or acrylamide in different buffers. Protein acid, basic and neutral amino acid percentages were also determined. An increase in low molecular weight and faster anodic migration proteins was noted in the lymphoblastoses, whereas the amino acid spectrum of these proteins showed percent changes in the case of some amino acids, particularly glutamic acid, phosphoserine, lysine and histidine. The alterations observed were compared with those noted previously in other haemoblastoses, congenital haemolytic and anhaemolytic blood diseases, and endoglobular or acquired metabolic defects in a closer assessment of their significance.
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PMID:[Changes in membrane proteins in the erythrocytes of patients with hemolymphoblastosis not directly involving the erythroblastic line]. 106 86

T cell activation process in patients of Hodgkin's disease was studied in terms of cellular protein phosphorylation following interaction of T lymphocytes with mitogen PHA. Peripheral blood lymphocytes from Hodgkin's disease patients and healthy donors, labelled with [32P] were activated with PHA. The cell lysates were subjected to SDS-PAGE, 2-dimensional gel analysis and were autoradiographed. It was observed that lymphocytes from both Hodgkin's disease patients and healthy donors followed similar time kinetics of phosphorylation. Nine of the eleven major protein bands, resolved on SDS-PAGE in the molecular weight range of 15.7-98 kD showed reduced phosphorylation (ratios of densitometric readings taken after and before stimulation) compared to that of healthy donors. Isoelectric focusing of these major protein bands in 2-dimensional gels further resolved them into about 27 proteins. Most of these showed increased phosphorylation in lysates of activated lymphocytes from healthy donors compared to that of Hodgkin's disease patients. The results showed a defect even at an early stage in terms of inadequate cellular protein phosphorylation.
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PMID:Impairment in cellular protein phosphorylation by mitogen activated lymphocytes from patients with Hodgkin's disease. 142 61

The origin of the malignant mononuclear Hodgkin's cell and the classic Reed-Sternberg cell in Hodgkin's disease (HD) remains controversial despite extensive immunohistological and lymphoid gene analysis. Sodium dodecyl sulphate-polyacrylamide gel electrophoresis (SDS-PAGE) in combination with protein staining and radioactive labelling has not been fully exploited in analysing the HD-derived cell lines available. The NP40 solubilised cellular proteins from the three HD cell lines, L428, KM-H2 and HDLM-2 were analysed using these techniques and compared with other haemopoietic cell lines and leucocytes of myeloid and lymphoid origin. The electrophoretic patterns of the three HD cell lines, although clearly different from one another, had many features in common. No major differences between the cell types were detected by Coomassie brilliant blue staining. The HD cell lines were more readily distinguished from the myeloid and to a lesser extent the lymphoid cell lines by silver staining, but HD cell line specific proteins (13, 19, 36, 60, 150 kD) were detected only on one line, L428. Iodination of cell membrane molecules, SDS-PAGE and subsequent autoradiography revealed three molecules (118, 22, 12 kD) which were restricted to the HD cell lines and the B-cell line Mann, and one molecule (144 kD) restricted to the HD cell lines and U937. Molecules unique to HDLM-2 (211 kD) and L428 (46 kD) were also detected by this method. Cell surface labelling with NaB3H4 identified a glycoprotein of 102 kD limited to HDLM-2 and L428, as well as a glycoprotein of 97 kD present on KM-H2 alone and one of 63 kD on L428 alone. Overall the HD cell line protein profiles displayed little similarity to the patterns of the other cell types studied and provide further evidence to support functional and phenotypic studies which identify Hodgkin's cells as a unique cell type. The molecules identified as HD cell line restricted may have potential as markers for this cell type.
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PMID:Cellular protein profiles of the Hodgkin's disease cell lines L428, KM-H2 and HDLM-2: a comparative study. 156 Jun 74

Peanut agglutinin (PNA) binding glycoproteins from four Hodgkin's disease (HD)-derived cell lines and a variety of cell lines/peripheral blood cells representative of the lymphoid and myeloid lineages were identified by probing nitrocellulose membranes of SDS-PAGE separated NP40 solubilized cellular glycoproteins with [125I]-labelled PNA. The two Hodgkin's cell lines Ho and L428 demonstrated the most heterogeneous glycoprotein profiles each expressing 15 PNA binding glycoproteins, respectively. The two remaining Hodgkin's lines Co and L591 expressed only four glycoproteins each and these were all also commonly expressed by Ho and L428. Comparative analysis with all other cell types studied revealed the expression of five glycoproteins restricted to Ho (gp42, gp40, gp38, gp24 and gp22) and six restricted to L428 (gp180, gp75, gp40, gp38, gp24 and gp22). Four of these, gp40, gp38, gp24 and gp22 were commonly expressed by both Ho and L428. Of cell lines of myeloid lineage studied only the erythroleukemia cell line K562 expressed detectable glycoproteins also expressed by some of the Hodgkin's cell lines (gp110, gp96, gp50 and gp45). Only one glycoprotein, gp20 expressed by Ho was also commonly expressed by normal peripheral blood granulocytes. This limited study has thus succeeded in demonstrating for the range of cell types studied, that some glycoproteins with terminal D-galactose beta (1----3) N-acetyl galactosamine oligosaccharide sequences are apparently restricted to two of the HD cell lines. Moreover, the heterogeneous glycoprotein profiles obtained for the HD cell lines Ho and L428 suggests that galactosylation processes in these two cell lines is aberrant.
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PMID:Identification of peanut agglutinin binding glycoproteins restricted to Hodgkin's disease-derived cell lines. 246 95

A polyethylene glycol 6000 (PEG) mediated precipitation procedure was used to estimate the levels of CIC in sera of healthy donors and patients with Hodgkin's disease (HD). In comparison with the normal serum samples, sera from untreated HD patients showed elevated CIC levels scattered over a wider range and a mean which differed significantly. Sera from treated patients who were in clinical remission exhibited decreased CIC levels. However, the mean level in this category was still above the mean found in the normal sera. The analysis of the data showed that the sera from HD patients in Stage I and II, and with LP and MC type histology showed preferential increase in CIC levels. The analysis of these CICs in 2D-SDS-PAGE and a careful scrutiny of the polypeptide patterns obtained revealed significantly elevated amounts of a component with a Mr of 40 kD and a pI of 5.6 in CICs from the untreated HD patients. Congruent peptide maps of this component and its decreased amounts in CICs from sera of patients in remission suggests its quantitative involvement in the disease.
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PMID:Circulating immune complexes (CIC) in Hodgkin's disease. I. Levels and two-dimensional analysis. 271 24

Nodular sclerosing Hodgkin's disease is characterized by dense collagen fibrosis. Although transforming growth factor-beta (TGF-beta) is an important bifunctional growth factor for fibroblasts and is stored and released by many cells, it requires acidification to pH 2.0-3.0 before it becomes a biologically active growth factor. We show here that the L-428 Hodgkin's cell releases a high molecular weight TGF that competes for the TGF-beta cell membrane receptor but not the TGF-alpha receptor. This growth factor is most active at physiologic pH and is 97% inactivated by acidification. Hodgkin's TGF is also inactivated by proteases and can be preserved by protease inhibitors. The Hodgkin's TGF can be separated from an autocrine growth factor using either column chromatography or electroelution from gels and is shown to have a molecular weight of approximately 350,000. Incubation of the Hodgkin's TGF in SDS releases a 25,000-D protein with reduced biological activity but which cross-reacts with anti-TGF-beta IgG. We propose that L-428 nodular sclerosing Hodgkin's disease fibrosis is mediated by a potent high molecular weight TGF-beta which, unlike TGF-beta characterized to date, is secreted in a form most active at physiologic pH.
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PMID:L-428 nodular sclerosing Hodgkin's cell secretes a unique transforming growth factor-beta active at physiologic pH. 290 50

The MLR-3 monoclonal antibody reacts with activated but not with resting lymphocytes. We report that MLR-3 identifies an early activation molecule since its binding is detectable on T cells 1.5-2 hr after in vitro activation. Its expression, therefore, does not require DNA synthesis and precedes, by many hours, that of the receptors for interleukin-2 (IL-2R) and transferrin (TF-R). The MLR-3 antigen is also found on activated thymocytes (including the large early thymic CD3- subset) and B cells. The majority of T- and B-lymphoblastoid cell lines, as well as the myeloid and erythroid cell lines HL60, GM1 and K562, are MLR-3+; conversely, non-haemopoietic cell lines are MLR-3 negative. Seventy percent of B-cell chronic lymphocytic leukaemia and 15% of B non-Hodgkin's lymphomas (B-NHL) are MLR-3+. On tissue sections MLR-3 is reactive with epithelia, sweat glands, hair follicles and Henle's loop but not with vessels, connective, endothelium and many other tissues. In vitro studies show that MLR-3 (1-100 micrograms/ml) significantly alters the thymidine uptake of mitogen-treated lymphocytes:augmentation is found when T and B cells are induced with TPA-Ionomycin and reduction when induced with phytohaemoagglutinin (PHA) or Staphylococcus aureus Cowan strain 1 (SAC), respectively. On SDS-PAGE, MLR-3 immunoprecipitates a disulphide-linked heterodimer of MW 29,000-35,000: both subunits are glycosylated, phosphorylated and exhibit a pI of 4.1 and 5.0, respectively. Our data, particularly the in vitro results, suggest that the MRL-3 molecule could have an important role in the early hours of activation for the progression of resting lymphocytes into mitosis.
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PMID:Early lymphocyte activation molecule defined by the monoclonal antibody MLR-3: biochemical and functional studies. 326 71

Chronic idiopathic thrombocytopenic purpura (ITP) is caused by an antibody reactive with platelet-associated antigens. The present studies provide direct evidence that some patients with chronic ITP have autoantibodies against the platelet glycoprotein (GP) IIb/IIIa complex. Microtiter wells, coated with a monoclonal antibody (2G12) specific for GPIIb/GPIIIa were reacted with GPIIb/GPIIIa contained in a platelet extract. Control wells containing the same antibody were reacted with a cell extract containing no GPIIb/GPIIIa. After washing, the wells were reacted with patient or control plasma, and IgG binding was detected using 125I-Fab2-anti-human IgG. Assay values were expressed as binding ratios (cpm GPIIb/GPIIIa wells/cpm control wells). Plasma from 5 of 56 patients with chronic ITP had ratios (1.36-3.14) greater than 3 standard deviations above the mean (+/- SD) of control plasmas--0.93 +/- 0.12. Elevated values were also noted in two patients with anti-P1A1 antibody (ratios greater than 30) and in one patient with Hodgkin's disease and an ITP-like syndrome (ratio 1.53). Normal values were noted in 34 patients with a variety of immune and nonimmune diseases. Plasma from two of the positive ITP patients was reacted with 125I-surface-labeled platelets and, after solubilization, the IgG and bound antigen were precipitated with Staph-A. Autoradiographs from SDS-PAGE electrophoresis of the Staph-A-bound proteins shows two radioactive bands consistent in size with GPIIb and GPIIIa.
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PMID:Autoantibodies against the platelet glycoprotein IIb/IIIa complex in patients with chronic ITP. 622 97

Immune complexes (IC) present in sera from patients with Hodgkin's disease (HD) were isolated using three different affinity columns: C1q-degalan, anti-C1q sepharose and conglutinin (K)-degalan. The isolated IC were analysed by immunoprecipitation, SDS-PAGE and sucrose density gradients and compared with IC similarly isolated from patients with rheumatoid arthritis (RA), systemic lupus erythematosus (SLE) and in vitro prepared BSA-anti-BSA complexes. Isolated material from each disease, and BSA-anti-BSA complexes contained proteins compatible with true immune complexes--IgM, IgG, C1q and C3 breakdown components. Albumin, fibronectin and CRP, whose affinity for IgM, C1q and C3 are known, were co-isolated along with IC material. The size of isolated IC in HD ranged from 8-40S on sucrose density gradients. Despite the operational difference in detecting and isolating HD complexes via the C1q ligand (C1q-degalan or anti-C1q column) and C3bi (K-degalan), material purified by both methods showed remarkable similarity on SDS-PAGE and immunoprecipitation analysis. Although IC isolated from different diseases showed disparate banding patterns on SDS-PAGE this was attributed to a variation in the relative concentrations of constituent proteins--IgM, IgG and C3 breakdown products. IgM, IgG and C3 bind loosely, and non-specifically, to macromolecular aggregates formed around immune complexes. Using the anti-C1q column, most of this material could be eluted using 0.02M EDTA. Least protein, yet the most specific for antigen and antibody was eluted at pH 3.0.
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PMID:Immune complexes in Hodgkin's disease: isolation, immunochemical and physico-chemical analysis. 641 1

A total of 74 children suffering from acute lymphoblastic leukaemia (ALL) or non-Hodgkin lymphoma (NHL) were involved in a retrospective analysis of their physical growth during and after the therapy. Out of this total number, 54 children were subjected to radiochemotherapy in compliance with the VII/(81) scheme, and another 20 children in compliance with the LSA2L2 scheme. At the beginning of the therapy the average height-standard deviation score (H-SDS) for both groups of patients corresponded with the population average. The patients subjected to the VII/(81) scheme showed, throughout the observation period of five years from the beginning of the therapy, a height normal for their age group. Contrary to this observation, the patients subjected to the LSA2L2 scheme experienced a significantly different growth in the period under observation and continually lost height in comparison to the normal population. The same results were experienced with a smaller group of patients whose growth was followed up for eight years from the beginning of therapy. 16 patients (VII/81 n = 4/LSA2L2 n = 12) reached their final height. For the patients of the VII/(81) scheme the final height showed an average H-SDS of 0.27 and for the patients of the LSA2L2 scheme of -1.22 (p = 0.068). Considering that the same cranial radiotherapy (max. 18 Gy for both schemes) and a comparable intensive induction therapy were applied, it must be concluded that the intensity and duration of the maintenance treatment are the critical factors initiating a different growth behaviour of the two groups subjected to radiochemotherapeutical schemes.
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PMID:[Effect of various therapeutic protocols on growth and final height of children with acute lymphoblastic leukemia or non-Hodgkin's lymphoma]. 750 Jun 1


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