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)

62 evaluable patients with myelodysplastic syndromes (MDS) or acute leukemia were treated with different combinations of low dose ara-C, alpha-interferon (IFN), 1 alpha-hydroxyvitamin D3 (vit D3) and retinoic acid. The aim was to study the efficacy and toxicity of each combination. The overall rate was 44%. Of these, 50% responded favorably to the combination of IFN, vit D3 and retinoic acid (IDR), which was comparable to the response rate of 43% for low-dose ara-C. The results of the IDR treatment may be explained by additive or synergistic effects between the separate drugs in the combination. Ara-C and IDR treatment was generally well-tolerated but interferon gave more side effects than any other drug used in the study. Evaluation of the full combination of ara-C, IFN, vit D3 and retinoic acid was not possible because of toxicity. Marrow hypoplasia was infrequent (5/27 patients) in cases responding favorably to treatment. Complete remissions were not longer than partial remissions or significant responses.
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PMID:Therapeutic effects of low-dose cytosine arabinoside, alpha-interferon, 1 alpha-hydroxyvitamin D3 and retinoic acid in acute leukemia and myelodysplastic syndromes. 337 98

The producibility of interferon (IFN)-alpha, which indicates one of the functions of large granular lymphocytes (LGL), was impaired at a high frequency in myelodysplastic syndrome (MDS) patients. However, IFN-alpha production in refractory anaemia, which is a subtype of MDS, was almost normal. In contrast, abnormality has not been observed in either proliferative response or the production of IFN-gamma of T-cells by stimulation with PHA. NK activity of peripheral blood mononuclear cells (PBMC) from MDS patients was generally low and was not augmented by IFN-alpha treatment. These results indicate that, in addition to the abnormality at the level of haematopoietic tissues, LGL among PBMC may be impaired in MDS patients.
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PMID:Impaired alpha-interferon production and natural killer activity in blood mononuclear cells in myelodysplastic syndromes. 348 81

Recombinant interleukin 2 (rIL 2, Cetus) was administered in escalating doses to 30 patients with advanced malignancy, including 14 patients with the epidemic form of Kaposi's sarcoma, in 2 week treatment cycles as a 6 h i.v. infusion for 10 doses. The maximum tolerated dose was 2 X 10(6) U/m2, with dose-limiting toxicity consisting of fever, diarrhea, and thrombocytopenia. At a well-tolerated dose of 1 X 10(6) U/m2, serum levels of rIL 2 of 30 U/ml were maintained for the duration of the infusion. Such concentrations sustain IL 2-dependent T cell growth in vitro. We observed a significant lymphocytosis in patients receiving 1 X 10(6) U/m2 of rIL 2 following 2 weeks of treatment (p = 0.0035). The expanded T cell pool was polyclonal, as demonstrated by increases in both T4+ and T8+ T cell subsets, and activated, with statistically significant increases in IL 2 receptor (p = 0.043), in the absence of transferrin receptor induction. Proliferating cells were not detected in peripheral blood using flow cytometry. Except for alpha-interferon, no other lymphokines (beta- and gamma-interferon, tumor necrosis factor) were present in serum during treatment. Reversible rises in anti-rIL 2 IgG antibodies occurred, as measured using an enzyme-linked immunosorbent assay. No changes were observed in the T cell mitogenic response to OKT3 and phytohemagglutinin, and no enhancement of cytotoxicity against natural killer-sensitive and resistant targets developed as a consequence of treatment. Except for a partial response in a patient with a myelodysplastic syndrome, no antitumor activity was observed. The in vivo expansion of T cells with the capacity to respond to rIL 2 with enhanced in vitro cytotoxicity against tumor targets provides impetus to ongoing trials exploring different routes and schedules of administration of rIL 2.
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PMID:Expansion of activated T-lymphocytes in patients treated with recombinant interleukin 2. 349 11

Thirty hairy cell leukemia patients were evaluated repeatedly for their bone marrow (BM) histology. At the time of diagnosis, 18 (60%) had diffuse, 9 (30%) had interstitial, and 2 (10%) had a mixed (diffuse and interstitial) pattern of BM disease. The follow-up BM specimens were obtained at intervals of 3-24 months, and the follow-up observation period was 12-94 months. In patients who were nontreated or only splenectomized, no significant changes were observed except of a persistent megaloblastoid picture of the red cell series and an increase of BM fibrosis. In the alpha-interferon treated patients a complete disappearance of hairy cells was observed in one and a dramatic reduction in five. The hairy cell index was reduced from a mean of 0.8 before to 0.1 after alpha-interferon therapy; most patients displayed megaloblastoid erythropoiesis. In the complete responder features of myelodysplasia were present.
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PMID:Hairy cell leukemia: bone marrow changes following splenectomy and alpha-interferon therapy. 366 61

The clinical course of a 56-year-old female patient with Sweet's syndrome (SS) preceded by a myelodysplastic syndrome (MDS) is described. During the acute phase of the disease with high remittent fever, painful skin lesions and maximal leucocytosis IL-6 and G-CSF serum levels were extremely high, while TNF-alpha was only slightly elevated and gamma-interferon and IL1-beta were not increased. On clinical improvement IL-6 serum levels rapidly fell, whereas G-CSF values already slightly elevated before the manifestation of the disease slowly declined. High G-CSF levels triggered by a yet unknown factor could explain the leucocytosis, neutrophilic dermatosis and skin lesions in SS, while IL-6 probably induced the associated clinical symptoms of fever and pain.
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PMID:Sweet's syndrome associated with myelodysplasia: possible role of cytokines in the pathogenesis of the disease. 752 52

The clinical data and hematological features of 29 children, under the age of 12 years, with primary myelodysplasia are presented. The diagnosis was made using the FAB (French-American-British) Cooperative Group criteria. There were 24 males and 5 females aged 4 months to 12 years (median 2.5 years) with marked male preponderance. Childhood myelodysplasia constituted 16% of all hematological malignancies and 36.7% of acute myeloid leukemias. The median duration of symptoms prior to diagnosis was 3 months. There were 15 cases of refractory anemia, one of refractory anemia with excess blasts, 3 of refractory anemia with excess blasts in transformation and 10 cases of chronic myelomonocytic leukemia. Five patients evolved to acute myeloid and 4 to acute lymphatic leukemia. The median duration of preleukemic phase in these patients was 7 months (range 4-29 months). The overall mean survival was short (5-9 months) in all the subgroups. Besides supportive therapy in most patients, two patients were treated with etoposide, one with alfa interferon 2b and one with high dose methylprednisolone. Our results show that myelodysplasia is not infrequent in children. The disease has an aggressive clinical course and may evolve into acute leukemia.
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PMID:Childhood myelodysplasia. 789 Mar 42

A 35-year-old male presented with chronic myelomonocytic leukemia (CMMoL) after 6.5 years of alkylating agent therapy for IgG-kappa type multiple myeloma. The total dose of melphalan was 0.648 g. CMMoL was stable with weekly injection of alpha-interferon for one year. Thereafter, monocytosis and thrombocytopenia aggravated, and the patient died of disseminating intravascular coagulation. Prolonged drug therapy can induce CMMoL, as well as other myelodysplastic syndromes.
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PMID:Chronic myelomonocytic leukemia following prolonged alkylating agent therapy for multiple myeloma. 789 29

Interferon-alpha has been used as a differentiating agent in the treatment of patients with myelodysplastic syndrome with conflicting results and often significant toxicity. In order to maximize the differentiating effects of this agent and minimize the myelosuppressive effects, a prospective pilot study was initiated utilizing interferon alpha-2a (Roferon A, Roche Laboratories) in the treatment of complicated or poor prognosis myelodysplasia. The study regimen utilized 'mini-dose' interferon alpha-2a at 1 x 10(6) units subcutaneously three-times per week for 16 weeks followed by an 8 week observation period. Nine patients were enrolled between May 1990 and June 1991, of which seven are evaluable. Forty-three percent (3/7) had a partial or clinical response as defined by normalization of one or more of the hemoglobin concentration, white blood cell count, or platelet count, or a decrease in transfusion requirement by > or = 50%. Only one patient was removed from study for interferon-associated toxicity. Mini-dose interferon alpha-2a appears to be an effective regimen for some patients with myelodysplasia which can be administered with minimal toxicity. Further investigation with interferon-alpha for the treatment of myelodysplastic syndrome, at the dosage utilized in this study, is warranted.
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PMID:Mini-dose interferon alpha-2a in the treatment of myelodysplasia. 842 72

We studied the effect of myelodysplastic syndrome (MDS)-derived adherent cells on colony formation of granulocyte-macrophage progenitors (CFU-GM) in both normal and MDS bone marrow cells. MDS-adherent cells suppressed the growth of normal CFU-GM colony formation. Antibodies against ferritin almost totally neutralized the haematopoietic inhibitory activity. Antibody against gamma-interferon (gamma-IFN) did not have such effect. By cytogenetic analysis using G-staining method, MDS-derived CFU-GM colony showed abnormal clones. MDS have been recognized to be a mosaic of normal and abnormal clones. MDS-macrophages suppressed the growth of progenitor cells derived from normal clones by soluble factors, but did not suppress the growth of those from abnormal clones. It is suggested that progenitor cells derived from abnormal clones are freed from the negative myelopoietic regulator that may be related to the progress of leukaemia.
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PMID:MDS-macrophage derived inhibitory activity on myelopoiesis of MDS abnormal clones. 848 44

The AMEX method of fixation permitted the serial study of c-myc expression in bone-marrow (BM) biopsies obtained from 6 patients with acute myelogenous leukaemia (AML) and one with myelodysplastic syndrome (MDS) during therapy with various cytotoxic and bioactive agents. BM cytotoxic therapy and therapy with bioactive agents was capable of altering c-myc expression in vivo. While cytotoxic therapy was generally associated with a fall in myc expression, it did not produce a dramatic effect on myc expression. Recombinant human granulocyte-macrophage colony-stimulating factor (RhGM-CSF) can increase and retinoic acid/alpha-interferon can decrease c-myc expression in myeloid cells in vivo.
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PMID:The serial study of c-myc expression in bone marrow biopsy specimens during treatment for acute myelogenous leukaemia. 851 28


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