Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023418 (leukemia)
 93,477 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Serum ferritin (SF) is elevated in adults with malignancies, chronic inflammatory disease, liver disease and iron overload. The purpose of this study was to determine whether the concentration of SF in children with a variety of malignancies correlated with the activity of their disease. Patients with acute lymphoblastic leukaemia (ALL) at initial diagnosis (n = 11) and relapse (n = 15) had a mean SF of 238 and 338 ng/ml, respectively, compared to the normal mean of 31 ng/ml and range of 7 to 140 ng/ml in children. In 30 patients with ALL in remission the mean SF was 109 ng/ml, less than the values in patients with active disease and greater than the normal mean (P less than 0.001). The concentration of SF was also increased in a group of 77 patients with a variety of solid tumors. The 28 cases with active disease had a mean SF of 242 ng/ml, significantly higher (P less than 0.001) that the value of 84 ng/ml in 49 patients with no evidence of residual tumor. The differences in SF concentration did reflect the activity of disease in the groups as a whole but it remains uncertain whether the assay will prove useful in following the response to treatment of patients with certain types of tumor.
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PMID:Elevated serum ferritin in children with malignancies. 19 90

Human tissues contain ferritin molecules with a range of isoelectric points but immunoassays for detecting serum ferritin have generally employed antibodies to the more basic liver or spleen proteins. To study the distribution of more acidic ferritins in tissues and serum acidic ferritin has been isolated from normal human heart and a two-site immunoradiometric assay for this protein developed. This assay gives little cross-reaction with spleen ferritin. Tissue ferritins have been fractionated by anion exchange chromatography and assayed with both spleen and heart antibodies. The spleen ferritin assay detects the more basic ferritin and the heart ferritin assay the more acidic ferritin. Acidic ferritins were found in heart, kidney, reticulocytes and HeLa cells. In sera from normal subjects and patients with iron overload, myocardial infarction, leukaemia and carcinoma only low concentrations of heart ferritin were found, although in the pathological sera spleen ferritin concentrations were generally raised. Circulating ferritin contains only a small proportion of molecules with the immunological characteristics of acidic heart ferritin.
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PMID:An immunoradiometric assay for the acidic ferritin of human heart: application to human tissues, cells and serum. 64 67

The bone marrow erythrocytic precursors of 12 patients with refractory anemia (preleukemia) or myelomonocytic leukemia were studied by transmission electron microscopy. The results were tabulated in a semiquantitative manner and a comparison was established between the two main diagnostic groups. The following results are reported. 1. Similar nuclear and cytoplasmic abnormalities of the normoblasts were observed in preleukemia and leukemia. 2. A nuclear lesion consisting of nuclear clefts and blebs was demonstrated in at least some of the normoblasts in all of the patients. Although not specific, this finding appears to be a new contribution in the field of preleukemia and myelomonocytic leukemia. 3. Iron overload, including the presence of pathologic sideroblasts, is common to both preleukemia and leukemia.
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PMID:Comparative electron-microscopic study of the erythrocytic line in refractory anemia (preleukemia) and myelomonocytic leukemia. 106 72

1. The properties of ferritin in serum have been compared with those of ferritin from a number of tissues including blood cells. On anion-exchange chromatography with DEAE-Sephadex, the behaviour of human heart ferritin is different from that of liver, kidney or spleen ferritin. Reticulocyte ferritin appears to have similar characteristics to heart ferritin. 2. Serum ferritin from normal subjects and patients with various degrees of iron load, leukaemia or liver disease all have a much lower affinity for the anion-exchange column that any tissue ferritin, suggesting a difference in isoelectric point. The elution point of serum ferritin from patients with acute myeloblastic leukaemia is significantly different from normal. 3. Density gradient centrifugation in sucrose showed that ferritin in leucocyte extracts and partially purified ferritin from the serum of two patients with iron overload behaved as apoferritin rather than the iron-rich protein. 4. The results suggest that ferritin is modified during its entry into the plasma and that even in cases of iron overload the iron content of serum ferritin may be low. The findings are of importance in considering the origin of plasma ferritin, the clearance of ferritin from plasma and its role in iron metabolism.
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PMID:The characteristics of ferritin from human tissues, serum and blood cells. 116 59

MDS is primarily a disease of the elderly. Cases who give a history of exposure to X-rays, cytotoxic drugs or leukaemogenic chemicals may be younger. Many cases of MDS present because of an incidental blood count. The most prominent clinical features are those of anaemia, neutropenia, thrombocytopenia. Because haemopoietic tissue is also dysfunctional the pathological effect is often greater than the figures would suggest, even leading to infection of bleeding with normal neutrophil or platelet counts. Occult abscesses are a particular feature. Despite documented abnormalities of the lymphoid system, neither infections characteristic of T-cell immunodeficiency nor autoimmunity is a problem. The proliferation of monocytes in CMML leads to organomegaly, leukaemia cutis, serous effusions and vasculitic lesions caused by the mishandling of circulating immune complexes. Cancer is no commoner than in age-matched controls, but coincident lymphoid tumours do occur. Many patients require long-term blood transfusion and will run into problems of iron overload unless precautions are taken.
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PMID:Clinical features of MDS. 173 80

As an iron-chelating agent, deferoxamine (DFO) is widely used in treating iron poisoning and disorders of iron overload. This study demonstrates that DFO is a potent S-phase inhibitor of DNA synthesis in human lymphocytes in vitro, and this inhibitory effect of DFO is reversible by adding appropriate amounts of ferric ion. As a nontoxic and selective-S-phase inhibitor, it may play a role in immunosuppression in experimental and therapeutic situations. It may even become an auxiliary therapy for leukemia or other malignant tumors.
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PMID:The inhibitory effect of deferoxamine on DNA synthesis in human lymphocytes. 251 33

The iron chelator desferrioxamine (DFO) has been previously shown to be an S-phase inhibitor of cell proliferation. To investigate its potential as an antileukemic drug, we first studied the effects of DFO on the in vitro growth of normal human hematopoietic progenitors (CFU-GM and BFU-E) and clonogenic cells from human leukemic cell lines. Then we evaluated the effects of DFO on progression of leukemia refractory to conventional therapy in two individuals. Micromolar concentrations of DFO determined a dose-dependent inhibition of normal progenitor growth, with inhibitory dose 50% (ID50) for CFU-GM and BFU-E being 6.7 and 5.5 microM/liter, respectively. Marked inhibitory effects were observed on clonogenic cells from HL-60 (ID50 = 1.4 microM/liter) and U-937 (ID50 = 3.6 microM/liter) human leukemic cell lines grown in semisolid medium. When DFO was given intravenously to a patient with lymphoid blast crisis of chronic myelogenous leukemia, a marked reduction in circulating blast count was observed. On the contrary, no in vivo effect was observed in a patient with acute nonlymphocytic leukemia having transfusional iron overload. We conclude that: (a) DFO is an inhibitor of both normal and leukemic myeloid cell proliferation in vitro; (b) our limited in vivo observations and a previous case study suggest that intravenous administration of DFO to patients with normal to low plasma iron may result in leukemic cytoreduction in vivo.
Leukemia 1989 Feb
PMID:Effects of desferrioxamine on normal and leukemic human hematopoietic cell growth: in vitro and in vivo studies. 291 Dec 2

Late onset transfusion-dependent anaemia is very rare in the presence of sustained engraftment after HLA-identical sibling bone marrow transplantation. The only previously described consistent cause is pyridoxine-responsive sideroblastic anaemia. We describe here a second cause, marrow hypoplasia and fibrosis, occurring in association with extensive chronic graft-versus-host disease (GVHD). A 20-year-old Caucasian male who received cyclophosphamide and fractionated total body irradiation followed by an unmanipulated HLA-identical sibling marrow transplant from his sister for acute nonlymphoblastic leukaemia in first remission developed chronic GVHD of the skin and mouth at day 101 post-transplant. At day 689 post-transplant, he developed leuco-erythroblastic anaemia with thrombocytopenia, due to patchy marrow hypoplasia and fibrosis. Between days 689 and 1987 post-transplant he received 71 units of packed red cells, requiring transfusion approximately monthly. He remains well although still on prednisone for chronic GVHD of skin and is receiving desferrioxamine 4 g five nights/week i.v. as prophylaxis for iron overload.
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PMID:Late onset transfusion-dependent anaemia with thrombocytopenia secondary to marrow fibrosis and hypoplasia associated with chronic graft-versus-host disease. 333 93

Deferoxamine is a hydroxylamine which binds ferric ions to form a highly stable complex. Since iron is thought to be required at a critical stage for cell proliferation, we investigated the effect of deferoxamine on the proliferative activity of human leukaemic cell populations in vitro by means of 3 permanent cell lines, HL60, U937 and 8402. We found deferoxamine to be a potent inhibitor of DNA synthesis and proliferation of leukaemic cells, acting by accumulating treated cells at the early S phase of the cell cycle. Suppression of leukaemic proliferation was obtained at deferoxamine concentrations in the range usually achieved in the treatment of patients for iron overload. Deferoxamine might therefore warrant further investigation as a potentially useful agent for leukaemia chemotherapy.
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PMID:Inhibition of proliferation of human leukaemic cell populations by deferoxamine. 348 3

Patients with diffusely increased uptake in both kidneys (often referred to as "host kidneys") on Tc-99m-MDP bone imaging were evaluated. Among 2056 patients reviewed, this finding was seen in 13 patients (0.63%): four with liver cirrhosis, two with lung cancer, one each with primary hepatoma, Hodgkin's disease, malignant lymphoma, thyroid cancer, leukemia, sideroblastic anemia and diabetes mellitus. Renal vascular disease and iron overload are considered to be the major causes of this finding.
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PMID:Diffusely increased Tc-99m-MDP uptake in both kidneys. 645 33


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