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)

Eighty-six consecutive adult patients undergoing ABMT colony-stimulating factor for lymphoma in three (CSF) trials were studied retrospectively to investigate whether the administration of CSFs had a beneficial impact on the incidence of bacteraemia. Forty-nine patients did not receive CSFs and 51% of them developed bacteraemia during the recovery phase. Nineteen patients received M-CSF post-ABMT, 9 G-CSF and 9 GM-CSF; 40%, 33% and 22%, respectively, developed bacteraemia during the recovery phase. Ninety per cent of all infections (Gram +ve and Gram -ve) and 100% of the Gram -ve ones occurred when the absolute neutrophil count (ANC) was < or = 0.1 x 10(9)/l. This period of maximum risk, i.e. the total number of consecutive days with ANC < 0.1 x 10(9)/l, was not shortened by CSFs; however, a decrease in the incidence of bacteraemia was detected in the CSF-treated patients during the above period and this might be a result of enhanced phagocytic function. The incidence of bacteraemia appeared to be related to the type of lymphoma (p < 0.02) regardless of CSF administration: 28 of 59 patients with Hodgkin's disease developed bacteraemia (46.7%) versus 6 of 27 patients (22.2%) with non-Hodgkin's lymphoma.
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PMID:Does treatment with haemopoietic growth factors affect the incidence of bacteraemia in adult lymphoma transplant recipients? 768 1

The effect of rhIL-3 was investigated in 32 patients with newly diagnosed non-Hodgkin lymphoma in a phase I/II trial. All patients received 6 cycles of standard CHOP chemotherapy, and each patient was his own control where rhIL-3 was given as a daily s.c. injection for 14 days (day 2-15) in cycle 2 and 4, while cycle 1 and 3 were control cycles. Five dose levels were examined (0.5 - 1 - 5 - 7.5 - 10 micrograms/kg). Compared to the other more lineage-specific hemopoietic growth factors G- and GM-CSF, the effect of rhIL-3 on the hemopoiesis was less dramatic and more delayed, i.e. the most apparent effect was observed in the 2 weeks of treatment. Thus, the neutrophil counts from days 15 to 22 following CHOP were significantly raised and the duration of neutropenia was shorter (significantly only at 10 micrograms/kg), while the nadir values were unaffected. Platelet recovery from days 12-22 was significantly increased and nadir values occurred earlier compared to control cycles, but were only increased in some subsets. Other cell populations affected moderately in the recovery period were eosinophils and monocytes. Reticulocytes increased, but no effect on hemoglobin or RBC transfusion requirement was noted. Only moderate adverse reactions occurred such as fever, chills, flushing of the face and flu-like symptoms. There was no evidence of stimulation of tumor growth. Most significant, the rhIL-3 treatment at all but the lowest dose levels led to an improved tolerance to chemotherapy, as indicated by a decline in number of delayed cycles. A conclusion concerning the role of rhIL-3 as post-chemotherapy adjuvant should await studies using rhIL-3 in combination with more lineage-restricted hemopoietic growth factors.
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PMID:Effects of interleukin-3 following chemotherapy of non-Hodgkin's lymphoma. A prospective, controlled phase I/II study. 769

Few studies have explored bone marrow findings in patients with graft failure or delayed engraftment after bone marrow transplantation (BMT). The authors retrospectively identified 4 patients of 165 transplant recipients who underwent bone marrow examination after BMT because peripheral blood counts had not recovered to expected levels. All patients were women who were 21- to 49-years old (mean 37 years). Three patients underwent autologous BMT; the fourth received peripheral stem cell infusion. Transplants were performed for treatment of Hodgkin's disease, breast carcinoma, and follicular small cleaved cell lymphoma. Three patients received GM-CSF after marrow infusion. The time between transplant and biopsy ranged from 19 to 40 days (mean 22 days). White cell counts ranged from 0.1 to 0.6 x 10(9)/L, hematocrits from .25 to .41, and platelet counts from 10 x 10(9)/L to 39 x 10(9)/L. Aspirate smears were markedly hypocellular in all cases, and markedly hypocellular, and all contained histiocytes with foamy eosinophilic cytoplasm diffusely throughout the biopsy. Acid-fast and Gomori's methenamine-silver (GMS) stains were negative. Serous fat atrophy and marrow fibrosis were not seen. Delayed engraftment after BMT may be associated with a profuse histiocytic proliferation similar to that seen in immunodeficiency, some hematologic disorders, and storage diseases.
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PMID:Failure to engraft after bone marrow transplantation: bone marrow morphologic findings. 780 81

Expression of the receptor for the urokinase type plasminogen activator (uPAR) has been studied by flow cytometry and immunohistology in normal blood and bone marrow cells, in vitro activated lymphoid cells, and tissue samples from reactive lymph nodes (n = 6), thymus (n = 2) and malignant lymphomas (n = 82), or leukemias (n = 32). HL-60 myeloid precursor cells and CD34-positive normal stem cells also were analyzed. In the normal cells, staining was confined to monocytes, macrophages, neutrophils, and myeloid precursors. No labelling was seen of normal or activated lymphoid cells. Purified CD34-positive hematopoietic progenitors were uPAR negative, but expressed uPAR during differentiation in short-term liquid culture stimulated in vitro by recombinant interleukin (IL)-1, IL-3, IL-6, granulocyte-macrophage colony stimulating factor (CSF), granulocyte-CSF, and stem cell factor. Enhanced uPAR expression was also seen in HL-60 cells after induction of differentiation with dimethyl sulfoxide or 1 alpha,25-dihydroxyvitamin D3. In lymphomas and leukemias, the staining pattern was similar to that seen in the normal cells with labelling of monocytic and myeloid that seen in the normal cells with labelling of monocytic and myeloid malignancies, but not of the neoplastic cells in B-cell or T-cell lymphomas or Hodgkin's disease. In conclusion, uPAR is a differentiation marker for myeloid and monocytic cells, and may act to facilitate migration of these cells in normal and pathologic conditions by cell-associated plasminogen activation. Whether expression of uPAR in myeloid and monocytic malignancies relates to their growth and behavior will be an important topic for investigations in the future.
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PMID:Expression of the receptor for urokinase-type plasminogen activator in normal and neoplastic blood cells and hematopoietic tissue. 780 1

Thirty-seven patients with Hodgkin's disease in sensitive relapse were autografted using blood-derived haematopoietic progenitor cells. At the time of transplantation 22 patients were in complete remission and 15 patients in partial remission. Twenty-six patients were male and 11 female, with a median age of 31 years (range 21-52). The pre-transplant conditioning therapy consisted of cyclophosphamide, BCNU and etoposide (CBV). Five patients died of transplant-related complications and 11 patients relapsed after a median time of four months following autografting. For the remaining 21 patients the probability of event-free survival (EFS) was 45% at 68 months. Blood progenitor cell collection can be integrated into salvage therapy by administering haematopoietic growth factors (HGFs) to enhance the chemotherapy-induced progenitor cell rebound during leucocyte recovery. In a subgroup of 14 patients, seven received recombinant human granulocyte-macrophage colony stimulating factor (rhGM-CSF) (250 micrograms/m2/day) by continuous intravenous infusion following dexamethasone, BCNU, etoposide and melphalan (Dexa-BEAM) as salvage therapy, while seven patients were treated without haematopoietic growth factor (HGF) post-chemotherapy. The yield of total nucleated cells (TNC) and granulocyte-macrophage colonies (CFU-GM) collected per leukapheresis was 2.2- and 2.4-fold higher respectively in the rhGM-CSF-treated patients. Following high-dose conditioning therapy, the seven patients autografted with rhGM-CSF-mobilised stem cells showed a faster leucocyte recovery compared with the control group. Neutrophil recovery (> 1.0 x 10(9)/L) and platelet recovery (> 20 x 10(9)/L) were also accelerated in the rhGM-CSF-treated group.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Autologous blood progenitor cell transplantation in relapsed Hodgkin's disease--the role of haematopoietic growth factors. 810 59

High-dose chemotherapy regimens can cure a number of otherwise incurable diseases, such as Hodgkin's disease, non-Hodgkin's lymphoma, neuroblastoma, acute leukemia (in remission), and breast cancer. Trials of high-dose chemotherapy have generally used autologous bone marrow transplant or peripheral blood stem cell support to ensure hematologic recovery after intensive chemotherapy and/or radiation. This report describes an approach in which high-dose carboplatin chemotherapy was followed initially by granulocyte-macrophage colony-stimulating factor (GM-CSF; Escherichia coli. Sandoz-Schering, East Hanover and Kenilworth, NJ) and in subsequent patients, by both GM-CSF and repeated cycles of peripheral blood progenitor cell (PBPC) collection and administration. The addition of PBPC to this regimen led to significant reductions in the duration of neutropenia and thrombocytopenia, the requirement for erythrocyte and platelet transfusions, the length of hospital stay, and the use of intravenous antibiotics in this group relative to those patients who received GM-CSF alone. In addition, laboratory studies are presented that show a direct correlation between the number of progenitor cells reinfused and the duration of neutropenia and thrombocytopenia. The report also reviews data indicating that circulating progenitor cells are depleted by this approach. This suggests that the number of progenitor cells available for mobilization is finite. Finally, the magnitude of these effects, and their implications for future trials with repetitive cycles of dose-intensive therapy, are discussed.
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PMID:High-dose carboplatin chemotherapy with GM-CSF and peripheral blood progenitor cell support: a model for delivering repeated cycles of dose-intensive therapy. 810 54

The introduction of hematopoietic cytokines into the clinic has been rapid with three currently approved by the Food and Drug Administration and perhaps a dozen more in clinical trials. Combinations of cytokines have been relatively unexplored in the clinics. Knowledge about the use of cytokines with chemotherapy has grown considerably in the past few years. The literature relating to use of cytokines in support of standard chemotherapy, marrow failure syndromes associated with malignant disease, and dose intensification not requiring progenitor cell replacement has been reviewed. This review does not address the use of cytokines to support bone marrow transplantation and collection of progenitor cells. Hematopoietic cytokines shorten the duration of cytopenia and decrease infectious complications when used to support standard chemotherapy regimens. However, several randomized trials have failed to show a benefit of such cytokine-supported treatment programs in terms of antitumor response, palliation, or survival. One exception is granulocyte-macrophage colony stimulating factor used with aggressive but standard chemotherapy for high-risk non-Hodgkin lymphoma. Cytokines decrease the infectious complications of myelodysplastic syndromes and may decrease transfusion requirements. Marked escalations in chemotherapy doses are possible with specific chemotherapy regimens. These increase complete remission rates although no benefit in survival or palliation has yet been proven. Cytokines have not been effective in allowing escalation of doses with certain chemotherapy agents and regimens. Cytokines decrease hematopoietic toxicity with standard or escalated chemotherapy doses. Randomized trials are now beginning to define the true patient benefit of this capability.
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PMID:Hematopoietic cytokines. Current use in cancer therapy. 824 71

The cell line AG-F was isolated from the marrow of a neuroblastoma patient undergoing myeloablative treatment and autologous bone marrow rescue. A year later, the patient developed a Hodgkin's type lymphoma. AG-F cell line demonstrated an unusual phenotype, lacking surface CD2 and CD3, but expressing high levels of CD4, CD5, CD7, CD29, and CD45RO. Markers associated with Hodgkin's lymphoma cells, CD15 and CD30, were also positive. AG-F cells grow in suspension in clusters of 50-200 cells, with a doubling time of 9 h. They can also grow in serum-free medium and form tumors in nude mice. AG-F cells have amplified N-myc and c-myc and high levels of the corresponding mRNA transcripts. Cytogenetic analysis revealed a DNA index by flow cytometry of near tetraploid cells and a karyotype of 85-87 chromosomes, with consistent abnormalities in chromosomes 1, 5, and 9. Gene rearrangement studies revealed rearrangement of the beta gene of the T-cell receptor. AG-F cells secrete high levels of IL-6, IL-8, IL-10, and GM-CSF. Cell adherence and formation of long processes could be induced by fibronectin and were enhanced by exposure to PMA. Cells exposed to phorbol myristate acetate (PMA) had increased expression of CD11a, CD11b, CD18, CD45RO, and HLA-DR, whereas expression of CD15 and CD30 was markedly decreased. Similarly, the level of c-myc and N-myc oncoproteins and the levels of the cytoskeletal proteins, actin, tubulin, and vimentin markedly decreased early after PMA-induced differentiation.
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PMID:Isolation and characterization of an early T-helper/inducer cell line with a unique pattern of surface phenotype, constitutive cytokine secretion and myc oncogene expression. 825 4

Use of growth factors to augment hematopoietic recovery after cytotoxic therapy is a useful method for dose intensification. We wanted to evaluate the clinical and cost-effectiveness of granulocyte-macrophage colony stimulating factor (GM-CSF; Leucomax) in patients undergoing autologous bone marrow transplantation (ABMT) for Hodgkin's disease. Twenty-four patients with Hodgkin's disease were treated with high-dose chemotherapy and ABMT. Patients were then randomized in a double-blind manner to receive GM-CSF intravenously (10 micrograms/kg) over 6 h or placebo until the absolute neutrophil count (ANC) was greater than 1000/mm3 for 3 days. The study medication was stopped after 30 days. Patients treated with GM-CSF (n = 12) had shorter periods of neutropenia (median duration of an ANC of less than 1000 cells/mm3, 16 versus 27 days on placebo; p = 0.23), shorter periods of platelet-transfusion dependency (median duration, 13.5 versus 21 days on placebo; p = 0.03), shorter hospitalizations (median hospital stay, 32 versus 40.5 days on placebo; p = 0.0004). Other clinical outcomes, such as frequency and severity of toxicities, development of pneumonia or infection, in-hospital death, and response rate were similar in the two groups. Actuarial long-term disease free survival was 58% for patients treated with GM-CSF and 50% for patients who received placebo after 38 months of follow up (p = 0.6).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Role of granulocyte-macrophage colony stimulating factor (GM-CSF) after autologous bone marrow transplantation for Hodgkin's disease. 834 51

To a great extent, the risks of autologous bone marrow transplantation are related to neutropenia. Although the efficacy of the recombinant human granulocyte-macrophage colony-stimulating factor (rhu GM-CSF) on neutrophil recovery has appeared in numerous open trials, only a few randomized studies have hitherto been published. Ninety-one patients with non-Hodgkin's malignant lymphoma treated with ablative chemotherapy followed by purged or unpurged bone marrow transplantation were entered in a placebo-controlled, double-blind randomized study; 44 patients received GM-CSF (E. coli) in doses of 250 micrograms/m2/day, and 47 received a placebo. Treatment was administered daily as continuous infusion started on the day of transplantation and pursued until the absolute number of neutrophils reached 0.5 x 10(9)/l during 7 days or, if this failed, during 30 days. The median time of neutrophil recovery was 14 days in patients on rhu GM-CSF and 21 days in patients on placebo (P < 0.0001). Patients who received a mafosfamide-purged bone marrow also had a rapid neutrophil recovery (median: 16 days versus 20.5 days; P = 0.013). The stay in hospital was shorter in the rhu GM-CSF group (median: 23 days versus 28 days; P < 0.05). No significant difference in the number of days with fever, infections, antibiotics administered and overall survival was detected between the two groups. The main toxicity ascribable to rhu GM-CSF was a capillary leakage syndrome found in 3 patients. Thus, after purged or unpurged autologous bone marrow transplantation rhu GM-CSF significantly reduces the duration of both neutropenia and hospital stay.
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PMID:[Hematopoietic growth factor (GM-CSF) after autologous bone marrow transplantation. A randomized, double-blind, multicenter study in 91 cases of non-Hodgkin's malignant lymphomas]. 849 15


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