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Query: UNIPROT:P02794 (ferritin)
 17,525 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Purified recombinant human heavy-chain (acidic) ferritin (rHF) was assessed in vivo in mice for effects on the proliferation (percentage of cells in S-phase) and absolute numbers of granulocyte-macrophage (CFU-GM), erythroid (BFU-E), and multipotential (CFU-GEMM) progenitor cells in the femur and spleen and on the nucleated cells in the marrow, spleen, and blood. rHF significantly decreased cycling rates and absolute numbers of marrow and splenic hematopoietic progenitors and marrow and blood nucleated cellularity. These effects were apparent in BDF1, C3H/Hej and DBA/2 mice and were dose dependent, time related, and reversible. Suppressive effects were noted within three hours for progenitor cell cycling, within 24 hours for progenitor cell numbers, and within 48 hours for circulating neutrophils. Additionally, hematopoietic progenitor cells in DBA/2 mice infected with the polycythemia-inducing strain of the Friend virus complex (FVC-P) were insensitive to the in vivo administration of rHF. These studies demonstrate activity of rHF in vivo on myelopoiesis of normal but not FVC-P-infected mice. Since rHF suppresses hematopoietic progenitor cell proliferation from normal donors in vitro and from normal mice in vitro and in vivo but does not suppress progenitor cells from patients with leukemia in vitro or from mice with FVC-P-infection in vitro or in vivo, rHF may be useful as a candidate adjunct molecule for the protection of normal hematopoietic progenitor cells during chemotherapy.
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PMID:Suppressive effects in vivo of purified recombinant human H-subunit (acidic) ferritin on murine myelopoiesis. 291 Mar 70

The phenotype and in vitro growth properties of blood and marrow blast cells detected in two neonates with Down's syndrome and a transient leukaemic picture are presented. In both patients, blast cells at diagnosis were heterogeneous and expressed predominantly megakaryocyte and erythroid markers identified by membrane fluorescence using monoclonal antibodies or ultrastructural detection of platelet peroxidase and ferritin. An additional trisomy involving chromosome 22 was detected in blast cells from one patient. Blood and marrow cells colony-assays performed at diagnosis revealed precursors with an abnormal differentiation capacity similar to those found in acute myelogenous leukaemia colony assays. However, an unusual feature was the persistence of high numbers of precursor cells (namely erythroid) following a normal differentiation pathway. Phenotypically and cytogenetically abnormal cells spontaneously disappeared by week 4-6, but overt relapse occurred in one patient 20 months later. These results bring strong arguments in favour of the neoplastic nature of the transient leukaemic picture observed in some neonates with Down's syndrome. Furthermore, we suggest that this disorder can be individualized as a separate entity with specific phenotypic and biological properties.
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PMID:Characterization of the blast cell population in two neonates with Down's syndrome and transient myeloproliferative disorder. 295 79

In previous studies, antitransferrin receptor antibody 42/6 inhibited growth of normal granulocyte/macrophage progenitors and some malignant myeloid cells. In these studies, leukemia cell lines cultured without serum and fresh leukemia cells were used to investigate the roles of Fe, transferrin receptors, and transferrin in leukemia cell growth, and mechanisms of 42/6 inhibition and resistance. HL60 and KG-1 leukemia cells grown in serum-free medium were inhibited by 42/6. In contrast to results in fetal calf serum (FCS), soluble Fe (ferric nitriloacetate) reversed 42/6 growth inhibition of serum-free HL60 cells. When HL60 cells were adapted for growth in serum-free, transferrin-free medium, they became refractory to 42/6 growth inhibition. By using radiolabeled transferrin and 42/6, HL60 cells cultured in FCS and transferrin displayed similar quantities of transferrin receptors (29,000-30,000/cell) and similar Kd's (3.8-4.9 X 10(-9) M). Cells grown in transferrin-free medium showed a similar Kd (3.1 X 10(-9) M), but fewer transferrin binding sites (5,000/cell). Transferrin-independent cells contained a log higher concentration of intracellular ferritin. For both FCS and serum-free HL60 cells, calculated affinities for 42/6 were lower (5.7-10.0 X 10(-9) M), but the number of binding sites was three- to fourfold higher. To investigate further the relationship between receptor display and antibody inhibition in proliferating normal and malignant myeloid cells, simultaneous immunofluorescence was used to determine the cell cycle status of transferrin receptor-positive cells. Malignant cells in S + G2/M displayed approximately 50% of the amount of transferrin receptors detected in normal dividing colony-stimulating factor-stimulated marrow cells. Receptor display by dividing cells from two patients with acute nonlymphocytic leukemia was variable. When HL60 cells were exposed to dimethyl sulfoxide, transferrin receptor display decreased, and 42/6 growth inhibition was abrogated or greatly diminished. The presence of 42/6 did not prevent dimethyl sulfoxide-induced HL60 differentiation in serum-containing or serum-free cultures. We conclude that human leukemia cells require Fe for growth and that 42/6 inhibits transferrin-dependent cells by Fe deprivation. Some dividing normal and differentiating malignant cells display reduced transferrin receptors, and can also escape antibody inhibition. The increased ferritin levels and decreased transferrin receptors in transferrin-independent HL60 cells confirm the inverse relationship between cell ferritin content and transferrin receptor display. These studies indicate a critical role for Fe in leukemia cell growth and possible roles in cellular differentiation.
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PMID:Role of transferrin, Fe, and transferrin receptors in myeloid leukemia cell growth. Studies with an antitransferrin receptor monoclonal antibody. 298 53

The cross-reactivity of antibodies to adult T-cell leukemia (ATL)-associated antigens (ATLA) in human and monkey sera was investigated by indirect immunoperoxidase and immunoferritin methods using a human cell line (MT-2) carrying a type C virus (HTLV), two monkey cell lines (Si-1 and Si-3) carrying HTLV, and a monkey cell line (Si-2) carrying a type C virus isolated from an anti-ATLA-positive monkey. Anti-ATLA-positive but not-negative human and monkey sera gave positive immunoperoxidase reaction with all four virus-positive cell lines when studied by light microscopy. Electron microscopic findings revealed ferritin or peroxidase labeling of virus particles and plasma membranes of these four cell lines with antibody-positive but not-negative human and monkey sera. These results clearly indicate the cross-reactivity of anti-ATLA antibodies in human and monkey sera at light and electron microscopic levels, and the presence of antigenic determinants common to the surface of type C virus particles of human and monkey origin.
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PMID:Immunoelectron microscopic study on the cross-reactivity of antibodies to adult T-cell leukemia-associated antigens in human and monkey sera. 300 Jan 31

The rhino mouse, an experimental model for systemic lupus erythematosus, was found to have murine leukemia virus particles present in the skin. Immunoperoxidase studies with anti-type C virus antibody indicated viral antigen presence in the sebaceous cells and surrounding follicular cysts of the dermis. Electron microscope studies show virus particles, both type C extracellularly and type A intracellularly, around follicular cysts. Virus particle was labeled with specific ferritin-conjugated antitype C virus antibody.
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PMID:Electron microscopic detection of virus particles in the rhino mouse. 301 Jul 20

The number of gene assignments to human chromosome 20 has increased slowly until recently. Only seven genes and one fragile site were confirmed assignments to chromosome 20 at the Ninth Human Gene Mapping Workshop in September 1987 (HGM9). One fragile site, 13 additional genes, and 10 DNA sequences that identify restriction fragment length polymorphisms (RFLPs), however, were provisionally added to the map at HGM9. Five mutated genes on chromosome 20 have a relation to disease: a mutation in the adenosine deaminase gene results in a deficiency of the enzyme and severe combined immune deficiency; mutations in the gene for the growth hormone releasing factor result in some forms of dwarfism; mutations in the closely linked genes for the hormones arginine vasopressin and oxytocin and their neurophysins are probably responsible for some diabetes insipidus; and mutations in the gene that regulates both alpha-neuraminidase and beta-galactosidase activities determine galactosialidosis. The gene for the prion protein is on chromosome 20; it is related to the infectious agent of kuru, Creutzfeld-Jacob disease, and Gertsmann-Straussler syndrome, although the nature of the relationship is not completely understood. Two genes that code for tyrosine kinases are on the chromosome, SRC1 the proto-oncogene and a gene (HCK) coding for haemopoietic kinase (an src-like kinase), but no direct relation to cancer has been shown for either of these kinases. The significance of non-random loss of chromosome 20 in the malignant diseases non-lymphocytic leukaemia and polycythaemia vera is not understood. Twenty-four additional loci are assigned to the chromosome: five genes that code for binding proteins, one for a light chain of ferritin, genes for three enzymes (inosine triphosphatase, s-adenosylhomocysteine hydrolase, and sterol delta 24-reductase), one for each of a secretory protein and an opiate neuropeptide, a cell surface antigen, two fragile sites, and 10 DNA sequences (one satellite and nine unique) that detect RFLPs.
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PMID:The map of chromosome 20. 307 44

Refractory macrocytic anemia with hypolobulated megakaryocytic nuclei and partial deletion of the long arm of chromosome 5 has been termed the 5q- syndrome. Although long survival has been reported in a few cases of 5q- refractory anemia, accumulating evidence suggests that this syndrome is a preleukemic state with risk of transformation to acute nonlymphocytic leukemia as well as complications of bone marrow failure. This report describes the first apparently successful therapy for this disorder in a young man who originally presented with a clinical picture consistent with pure red cell aplasia and normal marrow chromosomes but with hypolobulated megakaryocytic nuclei. He was treated with vitamins, androgens, and sequential trials of immunosuppressive therapy, all without response. Two years after diagnosis, repeated marrow cytogenetic studies showed a 5q- abnormality in 70 percent and later in 100 percent of marrow metaphases. Because of transfusion-induced hemosiderosis and the availability of a cytogenetically normal monozygotic twin, bone marrow transplantation was undertaken. In light of the clonal (and suspected preleukemic) nature of the 5q- syndrome, the patient's marrow was ablated with a busulfan plus cyclophosphamide regimen used for patients with nonlymphocytic leukemia. Sustained engraftment of cytogenetically normal marrow ensued. Two years after transplantation, and following six months of regular phlebotomy, the patient was hematologically normal with a normal serum ferritin level.
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PMID:Hematologic and cytogenetic remission of 5q-refractory anemia after syngeneic bone marrow transplantation. 308

Among nine cases of early erythroblastic leukemia previously diagnosed using a panel of antibodies, two patients have erythroid blasts expressing glycophorin A, seven patients have blasts with a more immature phenotype. These immature blasts were labeled by the FA6-152 monoclonal antibody when studied with the immunogold technique. The blasts exhibited large nucleoli, and their cytoplasm contained numerous ribosomes and large mitochondria. In the Golgi apparatus several granules resembled the theta granules as previously described and contained ferritin molecules in the absence of rhopheocytosis. A large proportion of these blasts exhibited a platelet peroxidase (PPO)-like activity. As the blasts from the two other patients with a more mature phenotype and glycophorin A reactivity lacked this PPO, this enzyme seems to be restricted to the more immature cells. Since in these leukemic samples immature erythroid blasts were admixed to promegakaryoblasts, immunogold labeling was also performed with antiplatelet antibodies. This latter population which was labeled with C17, a monoclonal antibody to platelet glycoprotein IIIa, showed strong PPO activity but lacked theta granules and ferritin. In the normal bone marrow enriched by panning for CFU-E (8%) and depleted in progenitors of other lineages, blast cells showing characteristics similar to leukemic erythroid blasts were seen. They exhibited theta granules and ferritin and a proportion of them also had a PPO-like activity. Thus, a PPO reaction is not restricted to the platelet-megakaryocyte line. In conclusion, a PPO-like activity and ferritin molecules were present in immature leukemic erythroid blasts. Similar cells could be identified from normal bone marrow.
Leukemia 1987 Mar
PMID:Ultrastructural and cytochemical characterization of blasts from early erythroblastic leukemias. 311 5

In 60 patients with Ph1-positive chronic granulocytic leukaemia (CGL) the serum ferritin concentration was measured as a part of the initial evaluation of the disease. The mean value (+SD) was 285 +/- 368.6 ng/ml, normal or slightly increased values being obtained in most cases. In 38 patients serum ferritin was again determined in clinical remission following busulphan treatment. Although the levels generally remained within the normal range, a significant decrease was observed with respect to the initial values (p = 0.0000004), suggesting that serum ferritin at presentation of CGL may be partially influenced by the disease activity. Finally, a further determination of serum ferritin concentration was made in a subgroup of 21 patients when they were diagnosed as being in the accelerated or blastic phases of CGL. Although no substantial increase was found with respect to the values obtained at presentation, a significant increase (p = 0.0008) was observed when accelerated-blastic phase ferritin levels were compared with those obtained in clinical remission. Although in patients in blast crisis no correlation was found between blast cell mass and serum ferritin, the differences observed between the different phases could indicate that in CGL serum ferritin concentrations roughly parallel the disease activity.
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PMID:Longitudinal study of serum ferritin concentrations in chronic granulocytic leukaemia. 313 87

Bone marrow cells from patients with leukemia, myelodysplastic syndromes, cancer, and other disorders on a phase I clinical trial with recombinant human granulocyte-macrophage colony-stimulating factor (rhGM-CSF) were assessed in vitro for numbers of granulocyte-macrophage (CFU-GM), erythroid (BFU-E), and multipotential (CFU-GEMM) progenitor cells, and for growth patterns (colony-to-cluster ratio) of CFU-GM, cycling rates of CFU-GM, and responsiveness in vitro to colony-stimulating and colony-inhibiting factors. The colony-to-cluster ratio of CFU-GM and the dose-response curves of CFU-GM to stimulation by rhGM-CSF in vitro did not change during the clinical trial. However, the percentage of CFU-GM in DNA synthesis, which is a measure of the proliferative rates of these cells, determined by the high specific activity tritiated thymidine kill technique in vitro, was markedly enhanced in a reversible fashion after administration in vivo of rhGM-CSF. The increased cycling rates of CFU-GM were consistent with the induced increase in neutrophil counts in these patients that has been reported elsewhere. Additionally, marrow CFU-GM from patients given rhGM-CSF in vivo were increased in sensitivity to inhibition in vitro by recombinant human H-subunit (acidic) ferritin in two of eight cases, and were increased in sensitivity to inhibition by lower dosages of recombinant human tumor necrosis factor alpha in all patients evaluated. The sensitivity of CFU-GM to inhibition in vitro by recombinant human interferon gamma and prostaglandin E1 did not change during the clinical trial. These studies demonstrate that the rhGM-CSF is having an effect on CFU-GM in the patients on the phase I clinical trial. This information may be of significance in planning future clinical studies combining rhGM-CSF with chemotherapy and/or other biotherapy.
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PMID:Growth characteristics of marrow hematopoietic progenitor/precursor cells from patients on a phase I clinical trial with purified recombinant human granulocyte-macrophage colony-stimulating factor. 326 May 58


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