Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P02794 (ferritin)
 17,525 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Ferritin has been reported to inhibit the growth of some leukemia cells in serum-supplemented culture. Recently we have found that ferritin stimulates the proliferation of human acute myeloblastic leukemia cells HL-60 and erythroleukemia cells K-562-T1 in serum-free medium. In this study, we examined the effect of ferritin against 14 human leukemia cell lines using human heart ferritin in serum-depleted culture medium. Among 14 cell lines tested, 10 were stimulated to proliferate by ferritin (maximum response at 30-300 ng/ml) with 0-1% fetal calf serum (FCS). The growth of all the cell lines was significantly inhibited by ferritin in the presence of 10% FCS. These results suggest that ferritin has dual functions; it promotes the growth of leukemia cells with low concentrations of FCS, but suppresses their growth with high concentrations of FCS.
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PMID:Growth stimulation of ferritin of human leukemia cells in vitro. 788 78

Serum ferritin (SF) was estimated using double antibody sandwich ELISA in 83 patients of acute and chronic leukemia at various stages of the disease. In 35 patients of acute lymphoblastic leukemia (ALL) in remission, the SF levels fell significantly from 550.63 ng/ml at presentation to 319.56 ng/ml but remained significantly higher than the control values of 46.14 ng/ml. In 28 patients of acute myeloid leukemia (AML), the SF values at 775.0 ng/ml were much higher than those in ALL patients and showed no decline with remission. This pattern was also seen in patients of chronic myeloid leukemia in blast crisis (CML-BC) with SF levels of 804.03 ng/ml at presentation and 717.43 ng/ml at partial remission. The values of SF were lowest in patients of CML in chronic phase ranging from 271.5 ng/ml to 332.12 ng/ml and showed no relationship with variation in total leucocyte count. No correlation was found between SF values and various clinical and laboratory parameters such as age, sex, fever, organomegaly, haemoglobin and total leucocyte count. Thus, while there appeared to be a correlation between remission and SF values in ALL, no such correlation existed between the activity of the disease and SF in other types of leukemia.
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PMID:Role of serum ferritin in assessment of disease activity in acute & chronic leukemia. 792 58

Serum ferritin H and L subunit levels and H/L ratios were evaluated in normal subjects and patients with various diseases by means of enzyme-linked immunosorbent assay using monoclonal antibody against ferritin H or L subunits. In normal subjects, serum levels of H subunit were significantly lower than those of L subunit, as previously reported by Cazzola and coworkers. Although the serum levels of L subunit were elevated and the values of H/L ratios were decreased in inflammatory diseases, serum levels of H subunit were remarkably high in patients with infectious mononucleosis. In liver disease, elevation of mean values of L subunit was observed. However, in liver cirrhosis and severe acute hepatitis, the serum levels of H subunit were often elevated as well as those of L subunit, and so it was suggested that the elevation of H subunit was related to the degree of hepatocellular injury. In hepatocellular carcinoma and pancreatic cancer, since the levels of H/L ratio were higher than controls and no correlation was observed between H and L subunits, it was suggested that the production of H subunit was increased in these cancers. However, the result of H/L ratio determination in serum ferritin did not appear enough to be important for tumor marker, because of a few instances demonstrated over the cut off limit of H/L ratio in neoplastic diseases. The rate of the patients whose H or L subunit levels were over the cut off point was higher in leukemia than in solid cancer, and so it was likely that the measurement of H and L subunit at the same time was clinically useful in leukemic patients. In acute myeloblastic leukemia, relatively high levels of serum L subunits and low H/L ratio were shown. It was suggested that the measurement of H and L subunits in patients with neoplastic diseases would also be useful for monitoring the effect of the therapy.
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PMID:[Clinical significance of serum ferritin H and L subunit determination in various diseases--evaluation by enzyme-linked immunosorbent assay]. 795 82

In iron deficiency, zinc protoporphyrin (ZPP) is produced instead of heme, and the ZPP concentration in erythrocytes increased (normal value < 2.3 micrograms ZPP/g Hb). The ZPP level and comparison with the other normally used tests in iron deficiency in the group of the patients with iron deficiency, ACD, MDS, AML, plasmocytoma was investigated. The ZPP level was determined by hematofluorometry in samples from 96 patients. Thirty five patients with iron depletion showed decreased both serum ferritin (median 5.9 ng/ml), and hemoglobin level (median 9.8 g/dl) with significantly increased ZPP level (median 8.5 micrograms/gHb). An increased level of ZPP (median 3.95 micrograms/gHb) with normal level of ferritin (median 24 ng/ml) and iron (median 50 (g/dl) in the serum of patients with ACD was determined. Measurement of ZPP level in the combination with ferritin and peripheral blood morphology allows to classify the degree of iron deficiency. The ZPP levels higher than 4.55 micrograms/gHb confirms iron deficiency in the group of anaemic patients.
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PMID:[Zinc protoporphyrin (ZPP) in diagnosis of anemia]. 964 80

AML-M0 is an infrequent form of acute myeloblastic leukemia characterized by negative reaction with myeloperoxidase (MPO), Sudan Black and lymphoid antigens and positivity for CD13 or CD33. In the present study we describe the immunophenotypical and ultrastructural characteristics of a group of AML-M0 in adult patients. Nine out 218 AML leukemias (4.1%) fulfilled the AML-M0 criteria. CD13 or CD33 were positive in eight out nine cases, with two or more positive myeloid antigens being present in 82% of the cases. Immunological MPO was positive in 57% of the cases and CD68 in 33%. In no case megakaryocytic and erythroid markers present. Four cases (44%) expressed CD7 and TdT but only two coexpressed both antigens. In none of the cases was CD3 or CD22 cytoplasmic expression found. Ultrastructurally, a low number of granules was seen in all cases whereas ferritin particles or rhopheocytosis were not observed. Ultrastructural MPO was positive in one out of five cases and platelet peroxidase (PPO) was negative in the four cases studied. Two out of six cases showed karyotypic abnormalities (hypotetraploidy and a complex karyotype, respectively). In two out three cases a rearranged pattern for JH gene was observed. TCR (Cbeta and Jgamma) rearrangements were not detected in any case. AML-M0 is an infrequent form of acute myeloblastic leukemia. A large panel of myeloid monoclonal antibodies (MoAb) and the study of the cytoplasmic expression of myeloid antigens is necessary to diagnose this form of leukemia. AML-M0 usually coexpress lymphoid markers. Ultrastructural studies may be of help to discard an immature erythroid proliferation.
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PMID:Acute myeloblastic leukemia with minimal myeloid differentiation: phenotypical and ultrastructural characteristics. 1004 53

Three pediatric patients with refractory anemia with ringed sideroblasts (RARS) are presented. Bone marrow aspirates were examined using Romanowsky and Prussian blue iron stains in all three patients, and electron microscopic analysis was performed in one patient. All three patients had cytogenetic analysis of the bone marrow. Other studies included analysis of serum iron, total iron-binding capacity, ferritin, copper, vitamins B6 and B12, and folate levels. Antibody titers to Parvovirus, HIV, and other viruses were measured. The patients had contrasting clinical courses. Patients 1 and 2 had dysplastic hematopoietic features and cytogenetic findings (with either partial or one allele loss of chromosome 7), suggestive of myelodysplastic syndrome. Patient 1 experienced acute myeloid leukemia (AML) and had a good response to AML-directed therapy. Patient 2 had prolonged cytopenias and underwent bone marrow transplantation (BMT). Patient 3 had features suggestive of refractory anemia associated with mitochondrial cytopathy, including normal cytogenetics with pronounced vacuolization of marrow precursors. His anemia regressed spontaneously a few months after diagnosis. These patients represent two subgroups of pediatric RARS. Patients with the myelodysplastic syndrome (MDS) type may progress to cytopenias or leukemia and may require aggressive therapy; the type is characterized by clonal cytogenetic findings. The non-MDS type, which may relate to mitochondrial cytopathy, often shows spontaneous regression and requires only supportive treatment; it has normal cytogenetic findings.
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PMID:Refractory anemia with ringed sideroblasts in children: two diseases with a similar phenotype? 1052 57

We report a 40-year-old man who presented with acute onset of hemophagocytic syndrome (HPS) after allogeneic bone marrow transplantation (alloBMT) for acute myelogenous leukemia. On day 8 after alloBMT, the patient suddenly manifested high-grade fever, transfusion-resistant severe anemia, and thrombocytopenia. Neither veno-occlusive disease nor thrombotic microangiopathy was documented. The level of ferritin in serum was elevated to 1192 ng/mL. A bone marrow aspiration test on day 16 showed a markedly increased number of activated macrophages showing massive hemophagocytosis. Serum levels of interferon-gamma, soluble interleukin-2 receptor, interleukin-6, tumor necrosis factor-alpha, and macrophage colony-stimulating factor (M-CSF) were elevated. From these findings, we determined his transfusion-resistant cytopenias to be attributable to HPS. No viruses (including cytomegalovirus, Epstein-Barr virus, human herpes-virus-6, parvovirus B19, and adenovirus B11) were detected in serum or urine by polymerase chain reaction amplification. We speculate that in addition to the administration of M-CSF, hypercytokinemia during the early phase post-alloBMT might have contributed to the onset of HPS in this patient. Methylprednisolone pulse therapy was very effective for the treatment of the HPS. This case reveals that HPS could develop after alloBMT, even when engraftment of hematopoietic cells is not confirmed.
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PMID:Early onset of hemophagocytic syndrome following allogeneic bone marrow transplantation. 1103 76

We studied the iron status of 32 evaluable adult acute myeloid leukaemia (AML) survivors who were entered into the UK Medical Research Council acute myeloid leukaemia (AML) 10 and 12 trials at our institution between 1988 and 1998. Patients were required to have been independent of all blood products for at least 3 years. As a group, the median first serum ferritin level was 1323 mug/l (NR 19-300 mug/l) at a median of 1321 days from the last transfusion confirming the presence of significant iron overload persisting for some years after completion of all therapy and blood products. There was a general trend for the serum ferritin level to fall with time, but the fall was less pronounced in men and carriers of the C282Y mutation. Recipients of autologous stem cell transplantation (SCT) had a higher median first serum ferritin level (3245 mug/l) than patients who received chemotherapy alone (1148 mug/l) or allogeneic SCT (1334 mug/l) because of increased use of transfused blood. Nine of the 10 recipients of autologous SCT underwent venesection. No evidence of end organ damage was seen in any patient. Serial monitoring of serum ferritin and assessment of the C282Y status may be useful in all long-term AML survivors, especially autograft recipients.
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PMID:Autografting as a risk factor for persisting iron overload in long-term survivors of acute myeloid leukaemia. 1456 92

Transferrin receptor 1 (TfR1) is a type II membrane protein that mediates cellular iron uptake. Transferrin receptor 2(TfR2), another receptor for transferrin (Tf), has recently been cloned. We examined expression levels of TfR1, TfR2-alpha (membrane form) and TfR2-beta (non-membrane form) transcripts in cells from 67 patients with de novo acute myeloid leukaemia (AML) using reverse transcription-polymerase chain reaction (RT-PCR), and correlated the results with a variety of clinical features and disease outcomes of these patients. Significant correlations were noted between the levels of both TfR1 and TfR2-alpha (r = 0.771, P < 0.001) and TfR1 and TfR2-beta (r = 0.534, P < 0.001). Unexpectedly, initial white blood cell (WBC) counts were inversely correlated with levels of expression of either TfR1(r = -0.357, P = 0.003), TfR2-alpha (r = -0.486, P < 0.0001), or TfR2-beta (r = -0.435, P = 0.0003). Only TfR2 expression was significantly associated with either serum iron (r = -0.270, P = 0.045) or serum ferritin (r = -0.364, P = 0.008). Multivariate analyses using Cox's proportional hazard model showed that elevated TfR2-alpha, but not TfR1 or TfR2-beta mRNA levels significantly contributed to a better prognosis for AML patients. Furthermore, a group with high expression levels of both TfR2-alpha and TfR2-beta survived significantly longer than a group without high expression of both of them (P < 0.01 by log-rank). The present study suggests that (i) TfRs-independent iron uptake might have an important role in in vivo proliferation of AML cells; (ii) expression of TfR2 (especially the alpha form) is a novel prognostic factor for patients with AML.
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PMID:Elevated levels of transferrin receptor 2 mRNA, not transferrin receptor 1 mRNA, are associated with increased survival in acute myeloid leukaemia. 1501 67

There are increasing evidences regarding the association between iron overload and extra-hepatic malignancies. We studied the prevalence of 12 hereditary hemochromatosis (HH) gene mutations (C282Y, V53M, V59M, H63D, H63H, S56C, Q127H, E168Q, E168X, W169X and Q283P in the HFE gene and Y250X in the TFR2 gene) and its correlation with the iron status in 82 adult patients with acute leukemia (AL); 48 patients (58.5%) were affected by acute myeloid leukemia (AML) and 34 patients (41.5%) by acute lymphoblastic leukemia (ALL); 27 patients (32.9%) had at least one HH gene mutation (6 heterozygous for C282Y, 6 homozygous for H63D, 13 heterozygous for H63D and 2 heterozygous for S56C). Mean serum ferritin levels at diagnosis were increased (822.5+/-811.4 microg/L). However, there was no difference between patients positive or negative for the HH gene mutations. Similarly, we did not observe any statistically significant difference as far as iron status between AML and ALL patients. Our study does not support the evidence of an association between hemochromatosis gene mutations and iron overload in AL patients.
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PMID:Analysis of HFE and TFR2 gene mutations in patients with acute leukemia. 1586 6


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