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)

When human marrow cells were cultured in a medium containing alpha-medium, methylcellulose, fetal calf serum, bovine serum albumin, erythropoietin, and leucocyte-conditioned medium, mixed colonies composed of erythrocytic cells and granulocytes were formed. The clonal nature of the mixed colonies was confirmed by the linear relationship between the numbers of cells plated and the number of colonies, and the absence or presence of Y-chromatin in the mixed colonies in a co-culture experiment with male and female cells. Using the methylcellulose cell culture techniques, the pluripotent hemopoietic precursors (CFUMIX) in marrow cells from 15 patients with aplastic anemia were assayed. In the control subjects of patients with iron-deficiency anemia, lymphoadenitis, reactive leucocytosis or Hodgkin's disease, 8 X 10(5) marrow cells in 4 dishes produced 12.7 +/- 6.9 (mean +/- SD) mixed colonies. On the other hand, 8 X 10(5) marrow cells from patients with aplastic anemia formed only 2.1 +/- 5.5 (mean +/- SD) mixed colonies. Furthermore, the marrow cells from 5 patients who were repeatedly receiving transfusions contained no CFUMIX which give rise to mixed colonies. The present results provided the first direct evidence that pancytopenia in most patients with aplastic anemia results from a reduced influx into the compartment of maturing hemopoietic cells from the compartment of pluripotent hemopoietic precursors.
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PMID:Pluripotent hemopoietic precursors in vitro (CFUMIX) in aplastic anemia. 722 71

Fatal graft-versus-host disease (GVHD) developed in a patient with Hodgkin's disease treated with combined chemotherapy and radiotherapy following the transfusion of 2 U of packed red blood cells. Clinical features of the GVHD included the development of exfoliative dermatitis, progressive hepatic dysfunction, aplastic anemia, and finally progressive fatal pneumonia. GVHD was documented by skin biopsy and chimerism by HLA typing. The HLA phenotype of the patient's skin fibroblasts [A3, Bw44 (w4)/A2, B15 (w4)] was appropriate for parental haplotypes and probably represented her true HLA phenotype. Lymphocytes from the patient (peripheral blood and lymph node biopsy) were of a different HLA phenotype (A3; Bw35, w38, w4, w6; Cw4), which was inappropriate for parental HLA haplotypes but identical to the HLA phenotype of one of the blood donors. The HLA-DR typing of the patient's family and of the blood donor demonstrated that the patient and the donor probably were HLA-DR identical (DRw5/DRw6), although no B lymphocytes could be obtained from the patient for direct DR typing. We are currently irradiating all blood products administered to patients with Hodgkin's disease receiving intensive treatment. Further observations will be necessary to determine whether transfusions to other cancer patients with immunodeficiency states should be restricted to irradiated blood products.
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PMID:Fatal graft-versus-host disease following blood transfusion in Hodgkin's disease documented by HLA typing. 736 71

Antiviral humoral immunity was studied in patients with Hodgkin's disease, idiopathic thrombocytopenic purpura (ITP), and aplastic anemia (AA). Insufficiency of antiviral humoral immunity as regards antigenically unrelated viruses and Mycoplasma pneumoniae was characteristic of all these conditions. A remission of Hodgkin's disease and ITP was associated with a reliable increase of the studied parameters in comparison with the acute period of the disease. After splenectomy humoral immunity parameters were virtually unchanged in patients with ITP, whereas in patients with Hodgkin's disease and AA the deficiency of antibody production is 40% increased after the operation.
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PMID:[Humoral antiviral immunity in children with hematologic neoplasms]. 748 71

We developed a sensitive method of measurement of granulocyte colony-stimulating factor (G-CSF) by an enzyme-linked immunosorbent assay, which we applied in the plasma of the bone marrow aspirate in 70 patients with various hematological disorders. The lowest limit of detection by this method is 2 pg/ml. G-CSF was detected in all but two of the patients. Compared to the G-CSF level in normal healthy controls, those in non-Hodgkin's malignant lymphoma, aplastic anemia, agranulocytosis and multiple myeloma were significantly higher, while the level in refractory anemia was not different. The G-CSF level in acute myelogenous leukemia patients was either elevated or decreased regardless of the French-American-British subgroup. The level in acute lymphoblastic leukemia was not different from the normal value, as was that in refractory anemia with an excess of blasts, and that in chronic lymphocytic leukemia. A patient with chronic myelomonocytic leukemia showed initial elevation of G-CSF with normalization after entering complete remission. The G-CSF level in chronic myelogenous leukemia was significantly decreased, although one patient in hematological remission who was under alpha-interferon therapy showed normal levels. The level in polycythemia vera was not significantly different from the normal value. The G-CSF level for the entire group showed an inverse, although not statistically significant, correlation with the percentages of myeloid cells of the bone marrow (r = -0.174, p = 0.1703, n = 80). These results are thought to reflect the regulatory mechanism of granulopoiesis in the bone marrow in various hematological disorders, and it is concluded that this method may be of clinical use in the treatment of patients with these disorders and in the selection of candidates likely to benefit from G-CSF administration.
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PMID:The levels of granulocyte colony-stimulating factor in the plasma of the bone marrow aspirate in various hematological disorders. 872 2

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.
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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

The clinical and microbiological features of 7 cases of bacteremia due to Capnocytophaga (Capnocytophaga ochracea group) are reported. They were diagnosed during 1991-93 at three hospital clinics. Five patients were < 10 years old and all had hematological disorders, 4 acute lymphoblastic leukemia and 1 each had aplastic anemia, non-Hodgkin lymphoma, and myelodysplastic syndrome. All were profoundly granulocytopenic with an absolute granulocyte count < 0.13 x 10(9)/l, and all but 1 had oral lesions as a possible portal of entry. A favourable response to antibiotic therapy was recorded in all patients but one who, being profoundly granulocytopenic, rapidly succumbed to Pseudomonas aeruginosa septicemia. None of the isolates were beta-lactamase producers. In addition to penicillin the isolates were susceptible to broad-spectrum cephalosporins and ciprofloxacin, but resistant to aminoglycosides.
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PMID:Capnocytophaga (Capnocytophaga ochracea group) bacteremia in hematological patients with profound granulocytopenia. 766 80

The status of hemopoietic stem cell transplantation in Australia from January 1, 1993 to December 31, 1993 is reported. A total of 523 hematopoietic stem cell transplants were carried out throughout Australia during this 12 month period: 296 autologous transplants, 223 allogeneic transplants, and 4 syngeneic transplants. These were carried out by transplant programs in 20 hospitals, and the total number of transplants represented a 9.4% increase on the total number performed in 1992 (n = 478). Of the 296 autologous transplants, 133 utilized blood stem cells only, 125 marrow stem cells only, and 38 both. The most common indications for autologous transplant were non-Hodgkin's lymphoma (n = 92), acute myeloid leukemia (n = 53), breast cancer (n = 37), Hodgkin's disease (n = 33), and myeloma (n = 25). The most common indication for allogeneic transplantation was chronic myeloid leukemia (n = 59), acute myeloid leukemia (n = 56), acute lymphoblastic leukemia (n = 43), and severe aplastic anaemia (n = 14). The number of allogenic transplants performed for individual diseases was comparable between 1992 and 1993, but increases in the number of autologous transplants for non-Hodgkin's lymphoma (26%), Hodgkin's disease (45%), breast cancer (48%), and myeloma (20%) were seen.
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PMID:Hematopoietic stem cell transplantation in Australia in 1993. 775

We conclude that the most common secondary cancers which develop after marrow transplantation are lympho-proliferative disorders and solid tumors. The consequences of the secondary malignancies are serious, with more than 90% of the patients with non-Hodgkin lymphomas associated with EBV infection and more than 75% of the patients with solid tumors dying despite treatment. Secondary leukemia developing in donor T-s is rare, but was fatal in all cases. EBV infection plays a major role in leading to the non-Hodgkin lymphomas in a setting of immune dysregulation from ATG or anti-T-cell monoclonal antibody treatment of acute GVHD. Other factors are also important for development of non-Hodgkin lymphoma and include T-cell depletion of donor marrow and HLA-mismatching between donor and recipient, known to lead to dysregulation of T-lymphocyte function. These factors set up an environment of proliferative stimuli which cannot be controlled by the recovering immune system, setting the stage for a secondary cancer. The role of irradiation is becoming more prominent in association with solid tumors, particularly in aplastic anemia patients conditioned with irradiation. The final event of tumor expression is most likely the result of a cascade of events, perhaps initiated with the conditioning regimen or with stimuli to proliferation, which, after later signals, leads to malignant transformation. For lymphoproliferative disorders, the time of latency is shorter than for solid tumors, suggesting a different molecular mechanism. The incidence of oncogene expression or mutation in tumor suppressor genes in these solid tumor patients has not been investigated.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Secondary malignancies after marrow transplantation for leukemia or aplastic anemia. 780 95

We report a case of severe and fatal aplastic anemia during an episode of infectious mononucleosis caused by Epstein-Barr (EB) virus infection. The 13-year-old female patient had shown normal hematological findings and had previously undergone repeated chemotherapy and autologous bone marrow transplantation for refractory non-Hodgkin malignant lymphoma (NHL). She was probably in an immuno-suppressed condition prior to this episode of infection. The possible causal relationship of the EB virus infection in the pathogenesis of aplastic anemia was documented by the clinical course, demonstration of EB virus genome in the bone marrow cells, and an elevated plasma interferon (IFN)-gamma level.
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PMID:Fatal aplastic anemia caused by Epstein-Barr virus infection after autologous bone marrow transplantation for non-Hodgkin malignant lymphoma. 794 35

We describe a patient who had lipothymoma with red cell aplasia, hypogammaglobulinemia, and lichen planus. Parathymic syndromes described in association with lipothymomas also include myasthenia gravis, hyperthyroidism, lymphangioma, aplastic anemia, chronic lymphocytic leukemia, and Hodgkin's disease. The behavior of lipothymoma is generally benign, although local recurrence was noted in 1 patient who had an incomplete resection. Lipothymoma should be considered in the diagnosis of mediastinal tumors and parathymic syndromes, and also in patients with cardiomegaly, phrenic nerve palsy, and a widened mediastinum.
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PMID:Lipothymoma with red cell aplasia, hypogammaglobulinemia, and lichen planus. 797 92


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