Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0026986 (myelodysplastic syndrome)
 14,926 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Pyoderma gangrenosum (PG) is a neutrophilic dermatosis, which may be associated with systemic conditions such as hematologic disorders. We present a patient who had been diagnosed as having myelodysplastic syndrome associated with PG at onset, in whom a febrile ulcerative skin lesion developed following cytosine arabinoside, aclarubicin and granulocyte colony-stimulating factor (G-CSF) combination chemotherapy in the course of the disease. Skin biopsy revealed dense neutrophilic infiltrate in the dermis with central epidermal ulceration, consistent with the diagnosis of PG. Oral prednisolone was effective for the skin lesion. In this case, G-CSF application may participate in the recurrence of PG.
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PMID:Pyoderma gangrenosum following cytosine arabinoside, aclarubicin and granulocyte colony-stimulating factor combination therapy in myelodysplastic syndrome. 961 71

Previous studies of the hematologic effects of granulocyte colony-stimulating factor (G-CSF) and granulocyte-macrophage colony-stimulating factor (GM-CSF) have emphasized the morphologic changes induced by these growth factors, but few have reported increases in blasts. Here, we report six cases in which growth factor treatment resulted in a marked but temporary increase in peripheral and bone marrow blasts that led to diagnostic confusion with acute leukemia and high-grade myelodysplastic syndromes. Five of the six patients were receiving treatment for hematologic malignant neoplasms, and one patient had an optic nerve germinoma. Growth factor treatment included single agent therapy with G-CSF (three patients), GM-CSF (one patient), or simultaneous therapy with G-CSF and GM-CSF (two patients). In two patients, there was a dramatic increase in blasts in the peripheral blood (39% and 20%), whereas four had substantial increases in blasts on the aspirate smear (8%-41%). One patient had a medium-sized blast cluster shown on the core biopsy specimen. The blasts decreased after removal of growth factor in all patients. The findings indicate that growth factor therapy can cause a substantial transient increase in blasts in the bone marrow and peripheral blood that may be confused with relapse of acute leukemia or progression of a myelodysplastic syndrome.
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PMID:Transient increase in blasts mimicking acute leukemia and progressing myelodysplasia in patients receiving growth factor. 1023 Mar 65

Treatment with erythropoietin (epo) may improve the anemia of myelodysplastic syndromes (MDS) in approximately 20% of patients. Previous studies have suggested that treatment with the combination of granulocyte colony-stimulating factor (G-CSF) and epo may increase this response rate. In the present phase II study, patients with MDS and anemia were randomized to treatment with G-CSF + epo according to one of two alternatives; arm A starting with G-CSF for 4 weeks followed by the combination for 12 weeks, and arm B starting with epo for 8 weeks followed by the combination for 10 weeks. Fifty evaluable patients (10 refractory anemia [RA], 13 refractory anemia with ring sideroblasts [RARS], and 27 refractory anemia with excess blasts [RAEB]) were included in the study, three were evaluable only for epo as monotherapy and 47 for the combined treatment. The overall response rate to G-CSF + epo was 38%, which is identical to that in our previous study. The response rates for patients with RA, RARS, and RAEB were 20%, 46%, and 37%, respectively. Response rates were identical in the two treatment groups indicating that an initial treatment with G-CSF was not neccessary for a response to the combination. Nine patients in arm B showed a response to the combined treatment, but only three of these responded to epo alone. This suggests a synergistic effect in vivo by G-CSF + epo. A long-term follow-up was made on 71 evaluable patients from both the present and the preceding Scandinavian study on G-CSF + epo. Median survival was 26 months, and the overall risk of leukemic transformation during a median follow-up of 43 months was 28%. Twenty patients entered long-term maintenance treatment and showed a median duration of response of 24 months. The international prognostic scoring system (IPSS) was effective to predict survival, leukemic transformation, and to a lesser extent, duration of response, but had no impact on primary response rates.
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PMID:Treatment of anemia in myelodysplastic syndromes with granulocyte colony-stimulating factor plus erythropoietin: results from a randomized phase II study and long-term follow-up of 71 patients. 1153 40

Anemia is a frequent complication in hematologic malignancies. In advanced stages of chronic lymphocytic leukemia, non-Hodgkin's lymphoma, and myeloma, anemia usually develops in parallel with marrow involvement. However, anemia may occur in the absence of overt infiltration of bone marrow by malignant cells. When all other causes of anemia (such as chronic bleeding, vitamin deficiency, hemolysis, and pure red blood cell aplasia) are eliminated, anemia can be related to "anemia of chronic disorders." Myelodysplastic syndromes are characterized by cytopenias. Anemia is very frequent, and nearly 90% of patients present with anemia during the evolution of the disease. In this disorder, erythroid progenitors are defective for their proliferation and maturation, as shown by in vitro culture techniques. Moreover, these patients often have a high endogenous serum erythropoietin level. The rationale for treating these patients with epoetin alfa is the possibility of overcoming the defective proliferation by pharmacologic doses of epoetin alfa. The response rate was rather low with epoetin alfa alone. Combinations with earlier-acting cytokines, such as recombinant human granulocyte colony-stimulating factor, have been tested in an attempt to improve response rates.
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PMID:Update on the role of epoetin alfa in hematologic malignancies and myelodysplastic syndromes. 967 24

Epoetin alfa is being used to treat patients with symptomatic anemia of cancer and to prevent or postpone chemotherapy-induced anemia in cancer treatment. As only approximately 50% of unselected anemic cancer patients respond sufficiently to epoetin alfa treatment, careful patient selection according to reliable prediction criteria is of great importance. Predictions of response to epoetin alfa treatment are based either on the degree of blunted erythropoietin response to the anemic condition or on indicators of responsiveness during the early treatment phase. The most accurate predictions of responsiveness, however, are derived from combinations of predictive factors. Combinations of synergistically acting hematopoietic growth factors, particularly epoetin alfa and granulocyte colony-stimulating factor, are beneficial to selected patients with myelodysplastic syndrome and may prolong survival in certain cases. Correction of anemia in cancer patients is particularly important because highly significant correlations have been reported between hemoglobin levels and quality of life in these patients.
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PMID:Anemia of cancer patients: patient selection and patient stratification for epoetin treatment. 967 28

In recent years, many cytokines have been defined and some of them used clinically. In hematological malignancies, cytokines, including granulocyte colony-stimulating factor (G-CSF), have been widely used for leukopenia after chemotherapy. However, in acute myelogenous leukemia (AML), some leukemic cells may be induced to proliferate by these cytokines and they must be used with care. In this study, we have investigated cell reactivity and proliferation with G-CSF, granulocyte-macrophage colony-stimulating factor (GM-CMF), macrophage colony-stimulating factor (M-CSF), stem cell factor (SCF) and thrombopoietin (TPO) in cases of AML. We have also investigated the reactivity of some myeloid leukemia cell lines to TPO. G-CSF, GM-CSF, M-CSF, SCF and TPO caused proliferation of leukemic cells in 25%, 58.3%, 8.3%, 21.1% and 0% of cases, respectively. Because of this result, the use of G-CSF in AML should be regarded as potentially hazardous. TPO did not cause proliferation of leukemic cells in any case of AML, or in cell lines except MO7E, which is a megakaryocytic cell line. This result suggests that TPO might cause proliferation of some megakaryocytic leukemia cells. We cannot conclude that TPO does not cause proliferation of other AML cells, as the number of cases was small and it has been reported elsewhere that leukemia cells may proliferate when exposed to TPO in 50% of AML cases. Reactivity of AM L cells to TPO is an important factor when deciding the indications of TPO in AML and myelodysplastic syndrome.
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PMID:Proliferative reaction of myelogenous leukemia cells with cytokines G-CSF, GM-CSF, M-CSF, SCF and TPO. 967 22

A 34-year-old woman was admitted to our hospital because of pancytopenia. She had been given a diagnosis of idiopathic thrombocytopenic purpura during her first pregnancy about 7 years earlier. The patient received a diagnosis of severe aplastic anemia (AA) and was treated with methylprednisolone, cyclosporin A, and granulocyte colony-stimulating factor (G-CSF), but no hematological improvement was observed. Six months later, myeloblasts appeared in the patient's peripheral blood, and she was given a diagnosis of acute myelocytic leukemia AML (FAB : M2). No chromosomal abnormalities were found. As some dyshematopoietic features had been observed in the bone marrow when the patient was first given a diagnosis of AA, it is conceivable that she already had hypoplastic myelodysplastic syndrome (MDS) then. She was treated according to the JALSG-AML92 protocol and achieved complete remission (CR). In this case, the long-term administration of G-CSF may have played an important role in the transformation of MDS into AML. It may be difficult to strictly distinguish AA from hypoplastic MDS with slight dysplastic features, as in this case, because we have no established criteria. Recently the incidence of MDS/AML in AA patients undergoing G-CSF treatment has become a concern. We should be careful about ruling out hypoplastic MDS when diagnosing a condition as AA, especially when therapy includes G-CSF. The patient is still in CR 26 months after intensive combination chemotherapy.
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PMID:[Hypoplastic myelodysplastic syndrome progressing to acute myelocytic leukemia (M2) after treatment with G-CSF and immunosuppressants]. 969 75

Thrombopoietin (TPO) has been successfully used to stimulate megakaryocyte progenitor proliferation and platelet production both in vitro and in vivo. We and other investigators have found that TPO also stimulates normal marrow colony-forming unit granulocyte-macrophage (CFU-GM) and burst-forming unit-erythroid (BFU-E) growth. In contrast to its effect on normal marrow precursors, TPO stimulates acute myelogenous leukemia (AML) progenitor proliferation in only 25% of the cases. Because the hematopoietic cells in Myelodysplastic syndrome (MDS) originate from both the normal and leukemic clones, we hypothesized that TPO may be a useful therapeutic agent for MDS. To test this hypothesis, we used fresh marrow samples taken from 14 MDS patients. We found that in the presence of fetal calf serum (FCS) and erythropoietin (EPO) TPO (5 to 40 ng/ml) MDS CFU-GM and BFU-E colony-forming cell proliferation were stimulated in a dose-dependent fashion by up to 103% and 93% respectively. This effect was similar to the stimulation obtained with optimal concentrations of granulocyte colony-stimulating factor (G-CSF), granulocyte-macrophage CSF (GM-CSF), or interleukin-3 (IL-3). Furthermore, TPO increased the colony-stimulatory effects of G-CSF, GM-CSF, IL-3, and stem cell factor (SCF) on MDS marrow cells. However, depletion of either T lymphocytes or adherent cells abrogated the effect of TPO, suggesting that the effect is not a direct one but is mediated through interaction with cytokines produced by accessory cells. Taken together, our data suggest that the therapeutic role of TPO in the management of MDS warrants further investigation.
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PMID:Thrombopoietin stimulates myelodysplastic syndrome granulocyte-macrophage and erythroid progenitor proliferation. 971 60

Translocation t(6:9)(p23;q34), resulting in a dek-can gene fusion, is a recurrent chromosomal abnormality mainly associated with specific subtypes of acute myeloid leukaemia (AML) and myelodysplastic syndrome (MDS). Patients with this type of chromosomal change are usually young and their prognosis is poor. The role of fusion protein generated from dek-can chimaeric transcript on the leukaemogenesis oft(6;9) AML or MDS is as yet unknown. We have established the first permanent cell line (FKH-1) with t(6;9). derived from the peripheral blood of a patient with t(6:9) AML transformed from Philadelphia chromosome (Ph1)-negative chronic myelocytic leukaemia (CML). The FKH-1 expressed myelomonocytic markers and dek-can chimaeric transcript. In the presence of 10 ng/ml recombinant human granulocyte colony-stimulating factor (G-CSF), the cells doubled every 54 h and showed multilineage myeloid differentiation, resulting in heterogenous morphologies such as macrophages, basophils, eosinophils and neutrophils. Thus, this cell line may be derived from a pluripotent myeloid stem cell and should be a useful tool for biomolecular studies on the pathogenesis of t(6;9) myeloid malignancies which have rarely been investigated because of the lack of continuously proliferating cells.
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PMID:Establishment of a novel human myeloid leukaemia cell line (FKH-1) with t(6;9)(p23;q34) and the expression of dek-can chimaeric transcript. 975 53

Benign nodular lymphoid lesions are not rare in the bone marrow of patients with myelodysplastic syndrome (MDS). Herein, we report a case of MDS with clonal lymphoid aggregates in the bone marrow but without evidence of systemic lymphoma. The case of a 71-year-old man was evaluated for cytopenia. His bone marrow was initially hypocellular, with 10% blasts and a few small lymphoid aggregates. The diagnosis of refractory anemia with excess blasts was made. The disease progressed gradually, and he received erythropoietin and granulocyte colony-stimulating factor for a short time. Forty-two months later, acute leukemia (M1) developed, with 60% to 70% blasts in the bone marrow. The bone marrow also showed large aggregates of lymphocytes. Immunohistochemical study of these cells in the nodular lesions showed 50% CD3+ and 50% CD20+. Cytogenetic and molecular genetic studies revealed monosomy 7 and T- and B-cell clonal gene rearrangement. Fluorescent in situ hybridization study with centromere-specific probes of a bone marrow specimen showed monosomy 7 in both nodular lymphoid lesions and surrounding bone marrow cells, indicating that both processes originated from the same abnormal pluripotential progenitor.
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PMID:Multiple lymphoid nodules in bone marrow have the same clonality as underlying myelodysplastic syndrome recognized with fluorescent in situ hybridization technique. 979 67


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