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)

The purpose of this study was to evaluate the antigenic profile of granulocyte colony-stimulating factor (G-CSF)-mobilized peripheral blood progenitor cells (PBPC) in patients with non-Hodgkin's lymphoma (NHL), Hodgkin's disease (HD), and multiple myeloma (MM). The mobilization regimens consisted of high-dose cytarabine/mitoxantrone for patients with NHL, DexaBEAM for patients with HD, and high-dose cyclophosphamide (4 or 7 g per m2) for patients with MM. Cytotoxic therapy was supported by recombinant human G-CSF (Filgrastim, 300 micrograms/day sc) to shorten the period of neutropenia and to increase the number of circulating hematopoietic progenitor cells. The mean numbers of circulating CD34+ cells/microliters during leukocyte recovery were different between patient groups, 80.5 +/- 9.8 (mean +/- SEM) in low-grade NHL and 51.2 +/- 9.7 in high-grade NHL compared with 31.3 +/- 6.9 in HD and 24.4 +/- 4.1 in patients with MM. As a result, the greatest numbers of CD34+ cells/kg collected per leukapheresis were observed in patients with NHL, whereas the collection efficiency was substantially lower in patients with HD or MM. Patients with MM had also the smallest proportion of CD34+ cells in the mononuclear cell fraction (mean 0.79 +/- 0.10% versus 2.15 +/- 0.19% in low-grade NHL) but the greatest proportion of early CD34+ HLA-DR- progenitor cells (mean 2.38 +/- 0.51 versus 0.84 +/- 14% in low-grade NHL). Patients with MM had a mean proportion of CD34/c-kit+ cells that was twofold greater than that observed in patients with high- or low-grade NHL.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Characterization of peripheral blood progenitor cells mobilized by cytotoxic chemotherapy and recombinant human granulocyte colony-stimulating factor. 753 8

The aim of this study was to evaluate the role and potential benefit of G-CSF administered following standard regimen chemotherapy (CHT) in non-Hodgkin lymphomas. Twenty patients with NHL were given CHOP or CHOP/CVP CHT every 21 days. None was given G-CSF after the first cycle. After each cycle, G-CSF was administered only for: 1) ANC < 1 x 10(9)/L between cycles; or 2) delay in cycle schedule due to ANC < 1 x 10(9)/L on the planned day of treatment; or 3) development of a febrile syndrome or a documented infection, regardless the ANC. Once administered, G-CSF was maintained in the following cycles. Nineteen patients required administration of G-CSF (5 micrograms/Kg B.W.), but for different reasons only 16 were treated (a mean of 10 +/- 3 doses/cycle). Comparing 48 cycles where G-CSF was not administered, with 50 where it was, in this last group we observed: 1) a ANC significantly higher at day 7 (p < 0.0001), day 14 (p < 0.0001) and day 21 (p = 0.0030); 2) a significantly lower (p = 0.0001) incidence of neutropenias (6 vs 29); 3) a trend (p = 0.1040) in favour of lower incidence of febrile neutropenias of infections (1 vs 6); 4) a significantly lower (p < 0.0001) incidence of cycle delays (1 vs 22) with a median of 8 days (1 to 20); and 5) a significantly higher (p < 0.0001) dose intensity (99.5% vs 87.8%).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Granulocyte colony-stimulating factor (G-CSF) allows the delivery of effective doses of CHOP and CVP regimens in non-Hodgkin lymphomas. 754 Apr 61

We report a 54-year-old patient with Hodgkin's disease who achieved a complete remission after combined modality treatment. Three years later the patient developed a severe hemorrhagic syndrome, concomitant with the onset of a factor VIII inhibitor in plasma. The control of very proteiform bleedings was extremely difficult, even with plasmaphereses, as well as with immunosuppressive and substitutive therapies. Two years later, a secondary acute nonlymphocytic leukemia (ANLL) was diagnosed. Two courses of chemotherapy with fludarabine, cytosine arabinoside and G-CSF (FLAG) were able to obtain a complete remission. Hemorrhagic complications were mainly linked to thrombocytopenia and continued until recovery of thrombopoiesis. Factor VIII inhibitor levels and related clinical symptoms decreased progressively. In conclusion, we suggest that FLAG succeeded in inhibiting an abnormal lymphoid clone responsible for factor VIII inhibitor production, suggesting a possible role for intensive chemotherapy in similar situations, which are often refractory to conventional immunosuppressive and depletive therapy.
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PMID:Factor VIII inhibitor prior to and during secondary acute nonlymphocytic leukemia in a patient with cured Hodgkin's disease. 754 Apr 64

Mobilization of peripheral blood stem cells (PBSC) can be accomplished with cytokines or rebound from myelo-suppressive chemotherapy. In this study, patients were mobilized with cyclophosphamide (CY) 4 g/m2 either alone or followed by GM-CSF 250 micrograms/m2 or G-CSF 600 micrograms. Colony-stimulating factors were administered subcutaneously. Eligibility included patients with non-Hodgkin's lymphoma (NHL; n = 29), Hodgkin's disease (n 4) and acute lymphoblastic leukemia (n = 2). One patient died from mobilization-related complications. Admission for neutropenic fevers and other complications occurred in 73% of patients receiving CY alone compared with 32% received CY + G-CSF or GM-CSF (P < 0.05). Apheresis was initiated when the white blood count approached 1 x 10(9)/l and continued until approximately 6 x 10(8) mononuclear cells/kg were collected. Mobilization with CY + GM-CSF led to significantly greater numbers of collected CFU-GM than with CY alone. Colony-stimulating factors were not administered after transplantation. collected progenitor cells correlated with the peak cell counts after mobilization. Following transplantation, an ANC > = 500 x 10(6)/l was achieved at 14.5 days and a platelet count > = 50 x 10(6)/l was achieved on day 20. Days to achieve an ANC > = 500 x 10(6)/l did not correlate with any of the analyzed variables. Platelet engraftment correlated with harvested BFU-E, thawed CD34+ cells and peak counts following mobilization. for patients with NHL, CR was obtained in 82% of evaluable cases. Median time to relapse was 343 days. Twenty five per cent of patients remain disease-free at 900+ days of follow-up.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Cyclophosphamide-mobilized peripheral blood stem cells in patient with lymphoid malignancies. 759 69

Treatment results of Hodgkin's disease have been improved by polychemotherapy. The overall cure rate for adults is about 70%. For advanced stages of Hodgkin's disease (IIIB-IV), the results of treatment are less satisfactory. One approach to improving the cure rates for patients with advanced stages is the intensification of chemotherapy. The German Hodgkin Study Group (GHSG) will apply this treatment strategy by introducing a new protocol (BEACOPP) in combination with growth factor (G-CSF) support to prevent prolonged neutropenia and severe infections. In a currently initiated "run-in"-study the maximal tolerable dose of cyclophosphamide, adriamycin, and etoposide will be defined within a multicenter setting. The subsequent trial will consist of a randomized study of BEACOPP baseline vs. BEACOPP dose-intensified vs. COPP/ABVD standard, in order to evaluate the role of dose intensification for the improvement of treatment outcome.
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PMID:Dose-escalation study for the treatment of Hodgkin's disease. The German Hodgkin Study Group (GHSG). 768 48

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

Forty six patients with lymphoid malignancies receiving autologous transplants using three different sources of hematopoietic stem cells were compared for engraftment parameters. Thirteen patients (five with multiple myeloma, seven with non-Hodgkin's lymphoma and one with Hodgkin's lymphoma) received autologous marrow with post-transplant growth factors (group 1). During the same time interval, 14 patients (five with multiple myeloma, six with non-Hodgkin's lymphoma and three with Hodgkin's lymphoma) were transplanted with autologous marrow plus recombinant granulocyte colony-stimulating factor (rhG-CSF)-mobilized peripheral blood stem cells (PBSC) and post-transplant growth factors (group 2). Nineteen patients (seven with multiple myeloma and 12 with non-Hodgkin's lymphoma) received rhG-CSF mobilized PBSC and post-transplant growth factors (group 3). All PBSC were collected after G-CSF mobilization (16 micrograms/kg/day s.c. for 6 days) without prior chemotherapy. After high-dose myeloablative chemotherapy or chemoradiotherapy, the median days to recovery of neutrophils to levels of 0.5 and 1.0 x 10(9)/l were 12 vs. 9 vs. 9 days (P = 0.0003 (group 1 vs. group 2) and P = 0.53 (group 2 vs. group 3)) and 13 vs. 10 vs. 10 days (P = 0.0003 (group 1 vs. group 2) and 0.92 (group 2 vs. group 3)) for groups 1, 2 and 3, respectively. The median day to platelet transfusion independence was 22 vs. 11 vs. 11 days (P = 0.001 (group 1 vs. group 2) and P = 0.50 (group 2 vs. group 3)) for groups 1, 2 and 3, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Engraftment of patients with lymphoid malignancies transplanted with autologous bone marrow, peripheral blood stem cells or both. 777 13

The most recent sophisticated investigations have provided new and revealing but also contradictory and controversial informaiton on the biological nature and the cellular origin of Hodgkin and Reed-Sternberg (H-RS) cells. Immunophenotypic analyses have shown consistent expression of CD15, CD30, CD74, and HLA-Dr antigens, but generally lack of T- or B cell-associated markers in H-RS cells. The H-RS cells are also devoid of many monocyte/macrophage-associated antigens. Molecular genetic studies have demonstrated heterogeneous findings with respect to rearrangements of T-cell receptor and immunoglobulin genes. Only a small percentage of the cases have rearrangements; this cannot always be attributed to the threshold of sensitivity of the method and/or the scarcity of the malignant cells in tissues examined. The H-RS cells do not express transcription factors such as BSAP, TCF-1, and GATA-3, known to be associated with lymphoid cells. It appears that evidence to support a lymphoid origin for H-RS cells is still lacking. On the contrary, the mechanism responsible for the unique clinical and histopathologic alterations associated with this disease has become clear. The H-RS cells have been shown to secrete IL-1, IL-5, IL-6, IL-9, TNF-a, M-CSF, and TGF-b, and, less frequently, IL-4 and G-CSF. These cytokines are likely to be responsible for the increased cellular reaction and fibrosis observed in tissues involved by HD and for the immunosuppression in patients with HD. Like most lymphomas, the etiology or pathogenesis of HD remains unknown. The Epstein-Barr virus (EBV) genomes are clonally integrated in the H-RS cells of about half the cases. The significance of these findings, whether EBV is a causative agent or an epiphenomenon, remains to be elucidated.
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PMID:The nature of Reed-Sternberg cells: phenotype, genotype, and other properties. 784 86

Cytokines play important roles in the pathogenesis of lymphomas via an autocrine or a paracrine mechanism, or both. The characteristic clinical and histopathological features of malignant lymphomas may be due in part to elevated serum or tissue levels of cytokines. Determination of the effects of cytokines on the growth or differentiation of lymphoma cells is often complicated by the fact that more than one cytokine is responsible, and by the failure of anti-cytokine antibodies or antisense oligonucleotides to block the proliferation in vitro of lymphoma cells. However, it appears that IL-6 and/or IL-9 may play a prominent role in the tumor cell proliferation of Hodgkin's disease (HD), anaplastic large-cell lymphoma, or immunoblastic lymphoma. IL-6 may also be responsible for the plasmacytoid differentiation of lymphoma cells in polymorphic immunocytoma. The histopathological changes as a result of paracrine effects are most noticeable in HD. The malignant (H-RS) cells of HD have been shown to express IL-1, IL-5, IL-6, IL-9, TNF-alpha, M-CSF, TGF-beta, and CD80, and, less frequently, IL-4 and G-CSF. These cytokines may be responsible for the increased cellular reaction and fibrosis observed in tissues involved by HD and for the immunosuppression found in patients with HD. In contrast to H-RS cells, most non-HD lymphoma cells do not produce cytokines in excess amounts and reveal only a minimal cellular reaction. Exceptions include T-cell-rich B-cell lymphoma, angiocentric T-cell lymphoma, and angio-immunoblastic lymphadenopathy (AILD-like T-cell lymphoma. IL-4 is responsible for the T-cell reaction in T-cell-rich B-cell lymphoma, whereas IL-6 accounts for the plasma cell reaction in AILD-type T-cell lymphoma. The authors extensively review the role of cytokines in lymphomas because this may lead to major advances in the understanding of the molecular processes involved in the histopathogenesis of lymphomas.
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PMID:Autocrine and paracrine functions of cytokines in malignant lymphomas. 785 53

We have recently reported that the hematologic recovery of patients with non-Hodgkin's lymphoma (NHL) and Hodgkin's disease (HD) undergoing autologous bone marrow transplantation (BMT) is significantly faster when recombinant human interleukin-3 (rhIL-3) is combined with recombinant human granulocyte colony-stimulating factor (rhG-CSF) in comparison with patients receiving G-CSF alone. In this paper, we studied the kinetic response and concentration of BM progenitor cells of 17 patients with lymphoid malignancies submitted to autologous BMT and treated with the G-CSF/IL-3 combination. The results were compared with those of five lymphoma patients receiving the same pretransplant conditioning regimen followed by G-CSF alone. rhG-CSF was administered as a single subcutaneous (sc) injection at the dose of 5 micrograms/kg/d from day 1 after reinfusion of autologous stem cells; rhIL-3 was added from day 6 at the dose of 10 micrograms/kg/d sc (overlapping schedule). In both groups (G-CSF- and G-CSF/IL-3-treated patients), cytokine administration was discontinued when the absolute neutrophil count (ANC) was >0.5 x 10(9)/L of peripheral blood (PB) for 3 consecutive days. After treatment with the CSF combination, the percentage of marrow colony-forming units-granulocyte/macrophage (CFU-GM) and erythroid progenitors (BFU-E) in S phase of the cell cycle increased from 9.3 +/- 2% to 33.3 +/- 12% and from 14.6 +/- 3% to 35 +/- 6%, respectively (p < 0.05). Similarly, we observed an increased number of actively cycling megakaryocyte progenitors (CFU-MK and BFU-MK). Conversely, G-CSF augmented the proliferative rate of CFU-GM (22.6 +/- 0.6% compared to a baseline value of 11.5 +/- 3%; p < 0.05) but not of BFU-E, CFU-MK, or BFU-MK, and the increase of S-phase CFU-GM was significantly lower than that observed in the posttreatment samples of patients receiving IL-3 in addition to G-CSF. The frequency of hematopoietic precursors in the BM, expressed as the number of colonies formed per number of cells plated, was unchanged or slightly decreased in both groups of patients. Because of the increase in marrow cellularity, however, a significant augmentation of the absolute number of both CFU-GM (3605 +/- 712/mL BM vs. 2213 +/- 580/mL; p < 0.05) and BFU-E (4373 +/- 608/mL vs. 3027 +/- 516/mL; p < 0.05) was reported after treatment with G-CSF/IL-3 but not G-CSF alone. Similarly, administration of the cytokine combination resulted in a higher number of CD34+ cells/mL BM, and their concentration was significantly greater than that observed in the posttreatment samples of G-CSF patients. Finally, we investigated the responsiveness to CSFs, in vitro, of highly enriched CD34+ cells, collected after priming with G-CSF in vivo (i.e., after 5 days of G-CSF administration). Our results demonstrated that pretreatment with G-CSF modified the response of BM cells to subsequent stimulation with additional CSFs. The results presented in this paper indicate that in vivo administration of two cytokines increases the proliferative rate and concentration of BM progenitor cells to a greater degree than G-CSF alone. These results support the role of growth factor combinations for accelerating hematopoietic recovery after high-dose chemotherapy.
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PMID:Proliferative response of human marrow myeloid progenitor cells to in vivo treatment with granulocyte colony-stimulating factor alone and in combination with interleukin-3 after autologous bone marrow transplantation. 854 41


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