[The role of erythropoietin in the regulation of hematopoiesis and its therapeutic use].
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Biomedical subjects
Publications and source records attributed to T Robak.
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In 40 patients receiving induction therapy for acute myeloid leukaemia the influence of lithium carbonate on the regeneration of haematopoiesis was investigated. It was observed that lithium treatment decreases chemotherapy-induced suppression of granulo- and megacariopoiesis. The frequency of remissions and the survival time were significantly higher for the patients receiving lithium if compared with the control group. The number of CFU-GM colonies in vitro after 14-th days of incubation was also statistically higher in the lithium treated patients.
We investigated the influence of rh-TNF administered as a single agent or in combination with CY or MTX on the survival time of mice inoculated with lymphoid leukemia L1210 and the effects of similar treatment on normal hematopoiesis in mice. The MST of rh-TNF--treated mice was longer than that of control animals. The longest survivals were observed in mice treated with 250 and 275 micrograms/kg of rh-TNF. Groups of mice receiving a combination of rh-TNF at doses of 225 or 250 micrograms/kg and MTX lived longer than animals treated with these agents separately. We observed the longest survival time of mice treated with combined administration of rh-TNF at a dose of 250 micrograms/kg and CY, but survival time was not significantly prolonged compared with mice receiving only CY. Additional studies were performed to examine the influence of rh-TNF administered as a single agent or in combination with toxic doses of CY or MTX on the number of granulocytes, lymphocytes, erythrocytes with hematocrit values and hemoglobin concentration, and platelets in peripheral blood, and the number of mononuclear cells as well as multipotential stem cells (CFU-GEMM) in bone marrow. Rh-TNF caused dose-dependent suppression of mononuclear cells and multipotential stem cells in bone marrow. The addition of MTX to rh-TNF caused no enhanced suppression of any of the above mentioned hematological parameters. In contrast, the addition of CY to rh-TNF suppressed erythrocytes and hematocrit values, as compared with rh-TNF alone.(ABSTRACT TRUNCATED AT 250 WORDS)
In the paper the possible physiological significance and pathological role of cachectin as a mediator of endotoxic shock and wasting in chronic diseases are reviewed. The influence of this monokine on normal haematopoietic cells and their leukaemic counterparts is presented. The effect of TNF on neoplastic cells in vitro and in vivo and its possible application in the treatment of cancer is also discussed.
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The antigenic characteristics of "early" (type 1) and "late" (type 2) granulocyte-macrophage progenitor cells (CFU-GM) from patients with polycythaemia vera (PV) and idiopathic myelofibrosis (MF) were studied using antimyeloid murine monoclonal antibodies (McAbs) and anti-HLA-DR McAb (L243) in a complement dependent cytotoxic assay followed by culture in methyl cellulose. The results were compared with the previously published data on the antigen phenotype of CFU-GM from normal bone marrow and peripheral blood. McAbs L243, MY9, S3-13 and S17-25 reacted with lower percentage of CFU-GM from patients with PV and MF than with their normal counterparts MCAbs R1.B19 and WGHS 29.1, which recognized the antigens on "late" CFU-GM (type 2), reacted with a high proportion of day 7 CFU-GM from MF peripheral blood and normal marrow but did not react with CFU-GM from PV and normal peripheral blood. The antigens recognized by two other McAbs (53/10 and PM81) were present on some of normal CFU-GM and were not found on CFU-GM from MF and PV peripheral blood. Our data suggest that CFU-GM in the circulation in MF differ from those in normal blood, perhaps because they are released from the spleen which in this disease has haemopoietic function.
The paper presented a case of a patient with type III by FAB myelodysplastic syndrome, in whom during a low dose cytarabine therapy ventricular fibrillation occurred. Authors discussed roles of anemia, ischemic heart disease and hypokalemia as factors which could increase circulatory system sensitivity on cytarabine action.
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In the paper recent advances in the etiology and pathogenesis of acute lymphoblastic leukaemia are reviewed. Role of enzymes and cytogenetic abnormalities, oncogenes and gene rearrangements in the biology of this leukaemia is presented. Progress in chemotherapy, immunotherapy and bone marrow transplantation is also discussed.
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