Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: UMLS:C0002871 (anemia)
52,094 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cytokines are a class of signal peptides which represent a major communication network in living organism. Over the last decade, the discovery, cloning and purification of hematopoietic cytokines (interleukins, hematopoietic growth factors) has increased our understanding of the regulation, proliferation, differentiation and function of hematopoietic cells. More recently, the large scale production of the recombinant forms of these molecules has enabled to treat the patients with pharmacologic doses of cytokines. The therapeutic activity of interferon-alpha (IFN-alpha) has been demonstrated in patients with chronic myeloid leukaemia and other chronic myeloproliferative syndromes. IFN-gamma is useful in the prevention of infections in patients with chronic granulomatous disease. Erythropoietin (EPO) was the first hematopoietic growth factor available for clinical use, initially to treat anaemia in renal failure patients. The next cytokines introduced into the clinic were granulocyte colony-stimulating factor (G-CSF) and granulocyte-macrophage CSF (GM-CSF). They are used successfully in haematological malignant disorders to stimulate granulopoiesis after chemotherapy or bone marrow transplantation and to help mobilise marrow stem cells for peripheral blood stem cell transplantation. Interleukin (IL)-1, -2, -3, -4, -6 and -11 have been tested in clinical trials. However, the value of these agents remains to be established.
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PMID:[Cytokines in the treatment of blood diseases]. 754 26

The human recombinant hematopoietic growth factors have attracted widespread interest because of their potential efficacy in a number of clinical settings. Recombinant human erythropoietin is now an established therapy to treat and prevent the anemia associated with chronic renal failure in children and adults. This agent also shows extraordinary promise to stimulate erythrocyte production and reduce transfusion requirements in premature infants. Granulocyte and granulocyte-macrophage colony-stimulating factors stimulate the production and function of myeloid cells and have provided major clinical benefit to children with congenital disorders of neutrophil production. The myeloid growth factors also show great promise in reducing the duration and severity of neutropenias associated with cytotoxic cancer treatment and in improving granulocyte production in patients with human immunodeficiency virus infections.
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PMID:Hematopoietic growth factors in pediatrics. 769 Jun 36

The drug zidovudine (AZT), a synthetic thymidine analog, has been used in the treatment of acquired immunodeficiency syndrome (AIDS). Clinical use of zidovudine has been associated with the development of hematopoietic toxicity manifested by anemia, neutropenia, and on occasion thrombocytopenia. This toxicity has resulted in the development of alternative dideoxynucleoside drugs capable of exerting anti-viral potency while minimizing the risk for inducing organ toxicities. One such dideoxynucleoside drug is 2',3'-dideoxyinosine (ddI). Clinical trials are currently evaluating the effect of combination anti-viral drug treatment such as zidovudine plus ddI. We report here the results of studies designed to evaluate the effect of interleukin-3 (IL-3) on its ability to influence the hematopoietic toxicity associated with zidovudine and ddI following combination with retroviral-infected murine bone marrow cells. Toxicity was evaluated by quantitating several classes of hematopoietic progenitor stem cells such as granulocyte-macrophage (CFU-GM), erythroid (CFU-E and BFU-E) and megakaryocyte (CFU-Meg). Dose-escalation IL-3 provided protection of anti-viral drug induced suppression of progenitor cells when combined in the presence of the ID50 concentration of either zidovudine or ddI; however, when zidovudine and ddI were combined, IL-3 was less effective in providing protection against drug-induced toxicity at any concentration examined. These results indicate that IL-3 is effective in reducing anti-viral drug-induced hematopoietic toxicity associated with single-agent use; however, IL-3 is less effective when such drugs are used in combination.
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PMID:Influence of interleukin-3 (IL-3) on the hematopoietic toxicity associated with combination anti-viral drugs (zidovudine and DDI) in vitro using retrovirus-infected bone marrow cells. 804 75

Anemia is a frequent manifestation of rheumatoid arthritis, with a probably multifactorial etiology. We investigated the effect of peripheral blood mononuclear cell supernatants (PBMCS) from rheumatoid arthritis (RA) patients on hematopoietic colony formation in vitro, by using a methylcellulose assay. PBMCS from patients suppress in vitro erythroid (BFU-E), mixed-lineage (CFU-GEMM) and to a lesser degree granulocyte-macrophage (CFU-GM) progenitors. PBMCS from anemic RA patients were more suppressive for BFU-E than those from non-anemic patients. Addition of antibodies to tumor-necrosis factor alpha (TNF alpha) almost completely reversed the inhibition of BFU-E and CFU-GEMM, but had little effect on the CFU-GM colony formation. Antibodies to interferon-gamma (IFN gamma) and interleukin-1 (IL-1) were not effective. The above data suggest that PBMCS from RA patients suppress in vitro erythropoiesis via the production of TNF alpha; a pathogenetic role for TNF alpha in the anemia of RA can be implied.
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PMID:Peripheral blood mononuclear cells from patients with rheumatoid arthritis suppress erythropoiesis in vitro via the production of tumor necrosis factor alpha. 806 94

3'-azido-3'-deoxythymidine (AZT), the main antiviral drug used in AIDS treatment, is known to induce anemia and neutropenia. These effects have been attributed to its toxicity to hematopoietic progenitors. In this report, we present a new approach to reduce AZT hematotoxicity by using an inhibitory factor of the hematopoietic stem cells, the tetrapeptide AcSerAspLysPro (AcSDKP, Seraspenide), which has been shown to increase the survival of mice subjected to high doses of chemotherapy and to block reversibly the cycling of human granulocyte-macrophage colony forming unit (CFU-GM) and burst forming unit erythroid (BFU-E) progenitors. Normal bone marrow mononuclear cells (BMMNC) from 14 subjects were incubated with or without AcSDKP (10(-10) M) for 20 h and with or without AZT (100 microM) for another 2 h. After washing, cells were plated in methylcellulose in the presence of interleukin 3 (IL-3), granulocyte-macrophage colony stimulating factor (GM-CSF) and erythropoietin (EPO). Under these conditions, the preincubation of cells with AcSDKP reduced significantly the toxicity of AZT to both BFU-E and CFU-GM at least in 3 out of 8 and 4 out of 10 cases, respectively. A careful statistical analysis of these observations indicates that AcSDKP may be an efficient factor in preserving progenitors against AZT-induced hematopoietic toxicity.
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PMID:The tetrapeptide AcSerAspLysPro (Seraspenide), a hematopoietic inhibitor, may reduce the in vitro toxicity of 3'-azido-3'-deoxythymidine to human hematopoietic progenitors. 824 56

Because GM-CSF possesses burst-promoting activity (BPA) and megakaryocyte colony-stimulating activity (Meg-CSF) as well as stimulating activity on granulocyte-macrophage progenitors, and erythropoietin (Epo) has thrombopoietin-like activity, the combination therapy of GM-CSF and Epo seems to be more effective for stimulating erythropoiesis and thrombocytopoiesis in patients with pancytopenia. For this reason, the combination therapy of recombinant human GM-CSF (rhGM-CSF) and rhEpo was performed in two patients with refractory anemia (RA) and aplastic anemia (AA). Epo-unresponsive anemia was remarkably improved by adding rhGM-CSF to Epo and the effect lasted for 1 1/2 months in a patient with RA, but severe anemia occurred again immediately after the discontinuation of Epo. The neutralizing antibodies against GM-CSF were not demonstrated at the phase when anemia re-progressed in this patient. In a patient with AA, anemia and thrombocytopenia, which were refractory to previous administration of rhGM-CSF, responded to the combined administration of GM-CSF and Epo. Although the effects were maintained for 3 1/2 months, the anemia and thrombocytopenia became worse again after the administration of rhGM-CSF was changed from daily to every other day. These findings suggest the usefulness of combination therapy of GM-CSF and Epo for patients with pancytopenia.
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PMID:Combination therapy with rhGM-CSF and rhEpo for two patients with refractory anemia and aplastic anemia. 824 8

The effect of recombinant human erythropoietin (rhEPO) and interleukin 3 (IL3) on circulating haematopoietic progenitors consisting mainly of immature burst-forming-units-erythrocytes (BFU-E), was investigated in ten paediatric patients treated by regular haemodialysis. During a 30-week study rhEPO treatment resulted in a rise of median haemoglobin levels from 6.7 g/dl to > 10 g/dl in all patients. Before initiating rhEPO treatment the number of circulating BFU-E in chronic renal failure patients responded to grading doses of rhEPO in vitro similar to that in control children; however, the dose-response curves were not predictive for the in vivo response to rhEPO. After an initial rise in five patients BFU-E numbers declined by week 30 of rhEPO treatment. BFU-E numbers decreased to 35% of pretreatment values. The number of granulocyte-macrophage colony forming cells (GM-CFC) also decreased during rhEPO treatment. Addition of IL3 to the culture medium containing saturating concentrations of granulocyte-macrophage colony stimulating factor did not stimulate BFU-E numbers of patients before rhEPO treatment or those of controls. However, 2 weeks after start of rhEPO treatment IL3 increased the growth of patient's BFU-E in vitro to 220% of pretreatment levels, followed by a gradual decrease of stimulation until the end of observation. These findings indicate that: (1) long-term recruitment of circulating haematopoietic progenitors during rhEPO treatment is low in children with renal anaemia; (2) rhEPO sensitivity of circulating BFU-E is not predictive for the in vivo response; (3) rhEPO treatment results in enhanced sensitivity of BFU-E to IL3.
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PMID:Circulating haematopoietic progenitors during treatment of renal anaemia with recombinant human erythropoietin. 831 24

Injection of 10(6) immortalized, but non-leukemic, granulocyte-macrophage colony-stimulating factor (GM-CSF)-dependent FDC-P1 cells into GM-CSF transgenic hybrid mice with elevated GM-CSF levels led to death within three months with elevated blast cell numbers in the blood, massive organ infiltration by blast cells, and associated anemia and thrombocytopenia. No disease developed within this period in littermate mice injected with 10(6) FDC-P1 cells. All moribund transgenic recipients contained transformed FDC-P1 cells able to produce rapidly-growing transplanted leukemias in syngeneic normal DBA/2 recipients. The leukemias appeared to arise in the primary recipients by independent transformation events. The transformed cells from different mice differed in their in vitro growth characteristics, their ability to produce GM-CSF or multipotential CSF, and in the nature of the transplanted tumors derived from the primary cells. While all primary recipients at death contained fully transformed leukemic cells, the bulk of the large population of FDC-P1 cells appeared either to be untransformed or to have altered characteristics not yet representing full transformation. If the FDC-P1 engrafted model has some validity for myelodysplasia, the results suggest that sustained CSF administration to myelodysplastic patients possessing abnormal, potentially preleukemic, granulocyte-macrophage populations may increase the risk of death either from accumulated pretransformed or from fully transformed leukemic cells.
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PMID:Leukemic transformation of immortalized FDC-P1 cells engrafted in GM-CSF transgenic mice. 850 82

IL-13, a recently identified Th2 cytokine, shares some, but not all, IL-4 functions, including inhibition of monocyte and macrophage activation, stimulation of human B cells, and induction of growth and differentiation of mouse bone marrow cells in vitro. We have now tested the in vivo effects of recombinant mouse IL-13 (rIL-13) from stably transfected, high expressing BW5147 thymoma cells. After purification by anion exchange chromatography, rIL-13 was administered in the peritoneal cavity of BALB/c mice via osmotic pump for 7 days. Spleens from the rIL-13-treated mice were significantly enlarged compared with control spleens due to increased cellularity. In particular, increased numbers of immature erythroblasts and megakaryocytes were observed in splenic sections after rIL-13 treatment. Spleen cells from rIL-13-treated mice showed greatly increased responsiveness in vitro to recombinant forms of mouse IL-3, mouse granulocyte-macrophage CSF, or human CSF-1 and, to a lesser extent, to mouse IL-4 or IL-13. Moreover, the rIL-13-treated mice also showed significant increases in CFU-E, CFU-C, and erythroid burst colonies in the spleen, further indicating the presence of increased numbers of hemopoietic precursors. Hematologic analyses indicated that rIL-13 treatment induced slight anemia and striking monocytosis. Finally, spleen cells from rIL-13-treated mice produced significantly more IL-6 upon LPS stimulation. Interestingly, the strong Th2 response induced by Nippostrongylus brasiliensis infection was also accompanied by an increase in hemopoietic precursor frequencies in the spleen. Collectively, these data indicate that exogenous rIL-13 induces extramedullary hemopoiesis in mice and suggest that endogenous IL-13 may contribute to replenishment of effector cells during strong Th2 responses.
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PMID:Continuous administration of Il-13 to mice induces extramedullary hemopoiesis and monocytosis. 861 37

Circulating hematopoietic progenitors were analyzed in patients with chronic renal failure (CRF) under hemodialysis (HD) by methylcellulose culture containing interleukin-3 (IL-3) to clarify the differences in hematopoiesis between patients with and without CRF-associated anemia and between good responder whose hematocrit (Ht) was preserved in more than 25% under erythropoietin (Epo) treatment and poor responders whose Ht remained less than 25% even under Epo treatment. The numbers of peripheral blood (PB) erythroid burst-forming units (BFU-E) and granulocyte-macrophage colony-forming units (CFU-GM) in HD patients without Epo treatment, whose Ht levels were greater than 30%, were similar to those in normal subjects. However, these numbers in HD patients who required Epo treatment were significantly lower than those in normal subjects. The number of PB BFU-E in HD patients who showed a poor response to Epo was significantly lower than that in HD patients who showed a good response to Epo. The number of PB BFU-E was well correlated with the number of PB CFU-GM in all groups of HD patients. There also existed a definite correlation between these numbers and the Ht levels in HD patients without Epo treatment, but not those in HD patients with Epo treatment. The sensitivity of PB BFU-E to IL-3 was lower in HD patients who showed a poor response to Epo than in the other HD patients and normal subjects. These findings indicate that hematopoiesis in HD patients with CRF associated anemia is suppressed in both the erythroid and myeloid lineage at primitive stages, and that the lower sensitivity of PB BFU-E to IL-3 in HD patients with a poor response to Epo may be associated with this poor response. In addition, the level of the serum transferrin receptor (sTfR) in HD patients without severe anemia was higher than that in normal subjects and HD patients who required Epo treatment, indicating that erythropoiesis in HD patients who do not require Epo treatment is more active than that in normal subjects and other HD patients.
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PMID:Analysis of circulating hematopoietic progenitors in patients with chronic renal failure under hemodialysis. 871 75


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