Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0019829 (Hodgkin's disease)
 30,247 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Serum levels of immunosuppressive acidic protein (IAP) in 105 patients with hematopoietic malignancies, there were 12 cases of acute myeloblastic leukemia, 1 acute monocytic leukemia, 13 myelomonocytic leukemia, 4 acute promyelocytic leukemia, 26 chronic myelogenous leukemia, 22 non-Hodgkin's lymphoma, 5 Hodgkin's disease, 6 adult T-cell leukemia, 5 acute lymphoblastic leukemia, 3 chronic lymphocytic leukemia, and 8 multiple myeloma. High levels of serum IAP were detected in all of the patients except chronic phase of CML, malignant lymphoma in stage I and II, and multiple myeloma. In the cases of malignant lymphoma, serum IAP levels in stage III and IV were higher with statistical significance (p less than 0.01) than those in stage I and II. Serum IAP levels in the patients with CML in blastic crisis were higher than in the chronic phase, so serum IAP levels are useful as one diagnostic parameters in blastic crisis. However, in patients with ANLL in relapse, serum IAP levels showed normal values. Serum IAP levels paralleled those of acute phase reactants such as alpha 1-acid glycoprotein , C-reactive protein, alpha 2-globulin, and alpha 1-antitrypsin, and had inverse correlations with PPD and PHA skin test.
 ...
PMID:[Quantitative measurement and clinical analysis of serum levels of immunosuppressive acidic protein (IAP) in hematopoietic malignancies]. 673 51

HLA antigen B12 is in linkage disequilibrium with HLA antigen Cw5. In some way this particular haplotype seems to be associated with a mechanism increasing serum transcortin levels. As shown before, the latter mechanism does not involve elevated estrogen levels or a generalized increase in glycoprotein synthesis. Similar high transcortin levels (more than 2 SDs above the mean) are found frequently in patients with lymphatic leukemia, hairy cell leukemia, or non-Hodgkin lymphoma, as well as in the siblings of these patients. HLA antigen Bw35 is in linkage disequilibrium with HLA antigen Cw4. Transcortin levels in patients with this combination of HLA antigens are significantly lower than in patients who do not carry these two antigens. Relatives of subjects with very low transcortin levels often have the same low levels. These findings together with recent data in the literature suggest that a cluster of genes regulating certain aspects of glucocorticoid metabolism is located in the vicinity of HLA locus B and C.
 ...
PMID:Association of aberrant transcortin levels with HLA antigens of the B and C loci: high transcortin levels are frequently found in patients with lymphatic leukemia, hairy cell leukemia, or non-Hodgkin lymphoma. 693 3

Acidic isoferritins have been identified as leukemia-associated inhibitory activity (LIA), which suppresses colony and cluster formation of colony-forming unit-granulocyte macrophages from normal donors but not from patients with leukemia. LIA was detected in all ferritin preparations tested, including ferritin isolated from normal heart, spleen, liver, and placental tissues, and from the spleens of patients with chronic myelogenous leukemia and Hodgkin's disease. Purified preparations of LIA were composed almost entirely of acidic isoferritins, as determined by immunoassay, radioimmunoassay, and isoelectric focusing. The inhibitory activity in the LIA and ferritin samples was inactivated by a battery of antisera specific for ferritin, including those prepared against acidic isoferritins from normal heart and spleen tissues from patients with Hodgkin's disease, and those previously absorbed with basic isoferritins. Antisera absorbed with acidic isoferritins did not inactivate the inhibitory activity. Separation of LIA and chronic myelogenous leukemia and normal spleen ferritin by sodium dodecyl sulfate-polyacrylamide gel electrophoresis and isoelectric focusing confirmed that the regions of peak inhibitory activity corresponded in each to an apparent molecular weight of approximately 550,000 and to a pI value of 4.7. Similar physicochemical characteristics included inactivation by methods that dissociate ferritin molecules into subunits and by treatment with trypsin, chymotrypsin, pronase, and periodate. The purified preparations were extremely stable to heat treatment. The glycoprotein nature of the inhibitory activity was substantiated because it bound to concanavalin A-Sepharose and was eluted off by alpha-methyl mannose. Inhibitory activity of the activity of the acidic isoferritins was detected at concentrations as low as 10(-17)-10(-19) M and iron saturation did not appear to be necessary for its action. These results implicate acidic isoferritins in the regulation of normal myelopoiesis and suggest a role for them in the progression of leukemia.
 ...
PMID:Identification of leukemia-associated inhibitory activity as acidic isoferritins. A regulatory role for acidic isoferritins in the production of granulocytes and macrophages. 697 99

Normal cross-reacting antigen, a glycoprotein that shares some antigenic determinants with carcinoembryonic antigen, was consistently demonstrated by tissue immunoperoxidase staining in the cytoplasm of both non-neoplastic and neoplastic neutrophilic granulocytes. It was absent in lymphoid cells, but occasional cells of the macrophage/histiocyte series showed variable staining. Malignant cells from patients who had non-Hodgkin or Hodgkin lymphomas were negative for normal cross-reacting antigen. These findings were in contrast to the findings of specific normal cross-reacting antigen positivity in neoplastic granulocytes from three patients who had acute granulocytic leukemia, three who had chronic granulocytic leukemia, and one who had a granulocytic sarcoma. Similar normal cross-reacting antigen positivity was also seen in granulocytes from two patients who had granulocyte dysplasia. It is suggested that direct tissue visualization of normal cross-reacting antigen using immunoperoxidase technics may be of value in the classification and diagnosis of hematologic malignancies, and may provide an additional marker for cells of the granulocytic series.
 ...
PMID:Direct tissue visualization of normal cross-reacting antigen in neoplastic granulocytes. 698 61

Endothelial cell activation and alterations of intravascular coagulation were investigated in 27 cases of Hodgkin's disease (HD), in five cases of anaplastic large cell lymphoma (ALCL), and in ten reactive lymph nodes. Lymph node sections were immunostained for E-selectin, a molecule present on cytokine-activated endothelial cells; for tissue factor (TF), a cellular initiator of the coagulation cascade; for glycoprotein (gp) II/III, a platelet-specific antigen; and for fibrin. In HD, vascular activation was particularly prominent in the nodular sclerosis subtype, as indicated by a larger number of E-selectin-positive blood vessels (72 +/- 49) compared with mixed cellularity (22 +/- 37). High expression of E-selectin was associated with alterations of intravascular coagulation, as indicated by immunostaining of some vascular endothelial cells for TF, by a higher incidence of intravascular thrombi, and by the extensive presence of areas of fibrin exudation and necrosis. In ALCL, the levels of endothelial cell activation and intravascular coagulation were comparable to those of HD nodular sclerosis. In reactive nodes, some E-selectin-positive blood vessels were observed only in 3/10 cases; immunostaining for TF was not detected on endothelial cells; and alterations of intravascular coagulation were rarely observed.
 ...
PMID:Vascular activation in the histopathogenesis of Hodgkin's disease: potential role of endothelial tissue factor in intravascular thrombosis and necrosis. 750 70

The CD30 antigen was originally described as a specific surface marker for Hodgkin's lymphoma. Recent work established CD30 as a member of the tumor necrosis factor/nerve growth factor receptor superfamily whose ligand (CD30L) has also been cloned and expressed; CD30L is active as membrane-bound type II glycoprotein. Here, CD30L mRNA expression was studied in a panel of 102 continuous human leukemia-lymphoma cell lines and was found only in four Burkitt lymphoma, one Burkit-type acute lymphoblastic leukemia and one non-Hodgkin's lymphoma (NHL) cell line. The product of CD30L mRNA is expressed as a membrane protein on the surface of these malignant B-cell lines. Treatment of these cell lines with soluble CD27L, phorbol ester or staphylococcus aureus Cowan antigen resulted in the enhancement of cell surface CD30L protein expression. CD30L mRNA was not detected in normal unstimulated peripheral blood (PB) monocytes, monocyte-derived macrophages, or T-cells, but was detected in primary granulocytes; exposure to activating reagents induced and upregulated CD30L transcription in these different PB populations. While CD40 and CD30L surface protein expression on PB monocytes could be enhanced or induced by treatment with gamma-interferon, these cells remained negative for CD30, both at the mRNA and at the protein level. Similarly, PB monocyte-derived macrophages and granulocytes remained negative for CD30 mRNA and protein expression, regardless of stimulation. Only activated T-cells expressed CD30 mRNA and surface protein. CD30L-transfected cells and cells constitutively expressing CD30L delivered a similar stimulus for proliferation of the CD30+ Hodgkin's disease (HD)-derived cell line HDLM-2, but inhibited proliferation of the CD30+ large cell anaplastic lymphoma cell line KARPAS-299. These data provide strong evidence for the involvement in growth regulation of recombinant and natural CD30L through its interaction with the CD30 receptor. Collectively, these data suggest that the CD30L-CD30 interaction has potent biological activity and might play a critical role in the immune response and pathogenesis of HD and some NHL, in particular Burkitt lymphomas.
 ...
PMID:Expression and regulation of CD30 ligand and CD30 in human leukemia-lymphoma cell lines. 752 56

Intravascular bronchioloalveolar tumor, the pulmonary counterpart of epithelioid hemangioendothelioma, typically presents as bilateral pulmonary nodules in young women. We report a case of intravascular bronchioloalveolar tumor that clinically mimicked acute pulmonary thromboembolic disease initially and was subsequently proven to have pulmonary hypertension with right ventricular dysfunction by angiography. The diagnosis of intravascular bronchioloalveolar tumor was confirmed by immunohistochemical and ultrastructural studies after it was suspected on routine histologic examination. In addition, the tumor cells expressed glycoprotein cell adhesion molecule CD44, which has been implicated in increased tumor invasiveness and metastasis in various carcinomas and several aggressive non-Hodgkin's lymphomas.
 ...
PMID:Intravascular bronchioloalveolar tumor of the lung presenting as pulmonary thromboembolic disease and pulmonary hypertension. 753 58

CD52 is a phosphatidylinositolglycan (PIG)-anchored glycoprotein (PIG-AP) expressed on normal T and B lymphocytes, monocytes, and the majority of B-cell non-Hodgkin lymphomas. We observed the emergence of CD52- T cells in 3 patients after intravenous treatment with the humanized anti-CD52 monoclonal antibody Campath-1H for refractory B-cell lymphoma and could identify the underlaying mechanism. In addition to the absence of CD52, the PIG-AP CD48 and CD59 were not detectable on the CD52- T cells in 2 patients. PIG-AP-deficient T-cell clones from both patients were established. Analysis of the mRNA of the PIG-A gene showed an abnormal size in the T-cell clones from 1 of these patients, suggesting that a mutation in the PIG-A gene was the cause of the expression defect of PIG-AP. An escape from an immune attack directed against PIG-AP+ hematopoiesis has been hypothesized as the cause of the occurrence of PIG-AP-deficient cells in paroxysmal nocturnal hemoglobinuria (PNH) and aplastic anemia. Our results support the hypothesis that an attack against the PIG-AP CD52 might lead to the expansion of a PIG-anchor-deficient cell population with the phenotypic and molecular characteristics of PNH cells.
 ...
PMID:Emergence of CD52-, phosphatidylinositolglycan-anchor-deficient T lymphocytes after in vivo application of Campath-1H for refractory B-cell non-Hodgkin lymphoma. 763 56

Most likely identical to ubiquitin carboxyl-terminal hydrolase isozyme L1 (UCH-L1), protein gene product (PGP) 9.5 is one of the major constituents of cytoplasmic polypeptides in neurons. The antigen seems to be expressed almost exclusively in neuronal and neuroendocrine tissues and their neoplasms. PGP 9.5 is also present in undifferentiated embryonic neoplasms like primitive neuroectodermal tumors (PNETs). However, the significance of PGP 9.5 as a marker in diagnostic (neuro-) oncology has not been systematically evaluated yet. In the present study the sensitivity and specificity of the widely used antiserum against PGP 9.5 has been retrospectively examined on 290 formalin-fixed, paraffin-embedded tumors of the nervous system and small round blue cell tumors. The presence of the antigen in tumors of neuronal (24/24) and neuroendocrine (63/73) differentiation confirm PGP 9.5 as a sensitive marker of these tumor groups, particularly in the diagnosis of pituitary adenomas where the expression was neither related to the staining behavior of the tumors in the PAS-orange G-reaction nor to their degree of polypeptide- and glycoprotein hormone activity. The nearly constant immunostaining of medulloblastomas (18/19) and other PNETs (5/6) demonstrate the role of PGP 9.5 as an additional marker in the detection of these embryonic tumors as this peptide was not or only weakly found in glial (11/58), meningeal (5/29), and nerve sheath neoplasms (1/28). On the other hand, the significance in the differential diagnosis of small round blue cell tumors seems to be limited because of positive immunoreactions in neuroblastomas (7/7) and oat cell carcinomas of the lung (7/7) although rhabdomyosarcomas (1/6) and malignant Non-Hodgkin-lymphomas (0/13) react completely negative in our series.
 ...
PMID:Protein gene product (PGP) 9.5 in diagnostic (neuro-) oncology. An immunomorphological study. 767 53

The depressed cellular immunity observed in patients with Hodgkin's disease (HD) has been attributed to production of transforming growth factor (TGF)-beta or TGF-beta-like substances by Hodgkin's Reed-Sternberg (H-RS) cells. The TGF-beta produced by L-428 cells (an H-RS cell line) is a 130-kd molecular weight glycoprotein that apparently differs from the TGF-beta (molecular weight, 25 kd) produced by most lymphoid and hematopoietic cells. Among several distinct types of TGF-beta that have been purified, only TGF-beta 1 and TGF-beta 2 have thus far been identified in hematopoietic cells. By using monoclonal antibodies (1D11 and 3C7) and oligonucleotide probes specific for TGF-beta 1 and TGF-beta 2, were confirmed that a cultured H-RS cell line, KM-H2, can produce both TGF-beta types, whereas another line, HDLM-1, produces only TGF-beta 1. Despite the abundance of mRNA in both of these cells, only small amounts of TGF-beta activity were detected, probably because of rapid degradation of TGF-beta 1 mRNA by specific nuclease. No degraded TGF-beta 2 RNA products were observed in KM-H2 cells. The TGF-beta produced by both types of H-RS cells had a molecular weight of approximately 25 kd. In tissues expression of TGF-beta was observed in a small portion (30%) of H-RS cells in 16 of 20 cases examined. A large number of small to medium-sized lymphoid cells (T lymphocytes) in tissues involved by HD also were positive for TGF-beta. These results indicate that there is functional heterogeneity among H-RS cells, and that H-RS cells are not the only source of TGF-beta in tissues involved by HD. Hodgkin's Reed-Sternberg cells are known to secrete several other cytokines, including interleukin (IL)-1, IL-6, and tumor necrosis factor-alpha. These cytokines could be responsible for the increased number of T lymphocytes in tissues involved by HD. Furthermore, T lymphocytes can respond to IL-1 and IL-6 secreted by H-RS cells by increasing their production of TGF-beta. Abundant expression of TGF-beta by T lymphocytes was not observed in lymphoid tissues other than those involved by HD.
 ...
PMID:Abundant expression of transforming growth factor-beta 1 and -beta 2 by Hodgkin's Reed-Sternberg cells and by reactive T lymphocytes in Hodgkin's disease. 768 Oct 31


<< Previous 1 2 3 4 5 6 7 8 Next >>