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Query: UMLS:C0023418 (leukemia)
93,477 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A new antigan has been revealed by means of antisera against Rauscher virus in mice with Rauscher virus-induced leukemia. This antigen appears to be different from both Rauscher type-specific antigen and MULV-gs-1 (p-30), as shown by studies of electrophoretic mobility and immunochemical specificity. Except in leukemic mice it was also found in low levels in both serum and spleen extracts of healthy mice of a number of strains. Furthermore, this antigen was regularly demonstrated by immunofluorescence on the surface of erythroblasts, but not on the surface of erythrocytes, lymphocytes, polymorphonuclear cells and thymocytes, and was shown to be different from fetal hemoglobin. Therefore, it is referred to as antigen of erythroblasts (Ag-Eb), which seems to represent a surface marker for a certain differentiation stage of erythroid cells.
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PMID:Specific antigen of murine erythroblasts. 5 10

The Friend erythroleukemia cell line T3-C12, which produces Friend murine leukemia virus (F-MuLV) and can be induced to synthesize hemoglobin by dimethyl sulfoxide (DMSO), was monitored for viral RNA-dependent DNA polymerase reverse transcriptase (RT) activity. The amount of viral 60-70S RNA released from DMSO-treated cells was unaffected or increased compared to that from control cells, while RT activity from treated cells was decreased. Accordingly, the specific activity in F-MuLV from DMSO-treated cells expressed as RT/70S RNA was decreased to 8% of the control activity. The 5-bromo-2'-deoxyuridine added to cultures containing DMSO reversed the differentiation process, and the F-MuLV thus treated did not exhibit the reduced RT activity normally observed in DMSO-treated virus. Cell-free F-MuLV incubated with and without DMSO showed the same RT activity, indicating that DMSO itself did not inhibit RT activity. However, when F-MuLV-containing pellets from control and DMSO-treated culture fluids were mixed, there was marked inhibition of the control RT activity, suggesting that RNase hybrid activity was stimulated or that an inhibitor was produced. Assays of F-MuLV-RNase hybrid released from control and DMSO-treated cells showed no difference in activity, indicating that a specific inhibitor of RT was produced or activated. Additions of certain nucleotide triphosphates to RT incubation mixtures did not result in any stimulation of RT activity in DMSO-treated F-MuLV, suggesting that phosphatase was not responsible for the observed inhibition. The results suggested that DMSO treatment of T3-C12 cells caused a reduction in viral RT activity by stimulating the production of an inhibitor, the nature of which is unknown.
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PMID:Viral reverse transcriptase suppression associated with erythroid differentiation of Friend leukemia cells. 6 77

Fetal hemoglobin (HbF) concentrations were measured by a radial immunodiffusion assay in 233 patients with various malignancies. In 96 of these, alpha-fetoprotein (AFP) was also measured by radioimmunoassay. The concentration of HbF exceeded 2 SDs above the normal mean in 39 of 233 patients, most notably in patients with leukemia, lymphomas, multiple myeloma and testicular tumors. The proportion of HbF was not correlated with the total hemoglobin concentration or with serum AFP concentration.
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PMID:Fetal hemoglobin and alpha-fetoprotein in various malignancies. 7 80

Radial immunodiffusion assay was used to measure fetal hemoglobin (HbF) concentrations in 312 patients with various malignancies. In 305 of these, alpha-fetoprotein (AFP) was measured by radioimmunoassay. The concentration of HbF exceeded 3 SDs above the normal mean in 68 of 312 patients, most notably in patients with leukemia, multiple myeloma, lymphoma, bladder carcinoma and testicular tumors. HbF was correlated with total hemoglobin concentration and with serum AFP concentration in hepatoma and bladder carcinoma.
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PMID:Fetal proteins in various tumors. 8 98

A congenital erythrocyte pyruvate kinase (PK) deficiency was found in a 72-year old female patient with chronic myelomonocytic leukemia (CMML). Erythrocyte PK deficiency was associated with an increase in the activity of hexokinase, 6-phosphogluconate dehydrogenase and glutathione peroxidase in erythrocytes as well as a decrease in acetylcholinesterase, glutathione reductase and glucosephosphate isomerase activities. The enzymatic abnormalities were accompanied by alterations in hemoglobin and in i antigen content of erythrocyte membrane. In addition, bone marrow ultrastructural studies showed dyshemopoietic changes in all blood cell lines and especially in erythroblasts. The present findings confirm the close relationship between CMML and acquired dyserythropoietic syndromes and constitute a new observation of the infrequent association of hereditary erythrocyte enzymopathies and leukemia. A survey of the literature is presented.
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PMID:Chronic myelomonocytic leukemia associated with hereditary pyruvate kinase deficiency and multiple acquired erythrocyte abnormalities. 10 94

Nicotinamide, a specific inhibitor of poly(ADP-ribose) synthetase, was found to be a moderate inducer of hemoglobin synthesis in Friend erythroid leukemia cells (FLC). Therefore, the effect of other inducers, s-ch as dimethyl sulfoxide (DMSO), hexamethylene-bisacetamide (HMBA), and butyrate, on poly(ADP-ribose) synthesis was examined. The extent of poly(ADP-ribose) synthesis in nuclei of FLC treated with DMSO or HMBA began to decrease before many phenotypic changes including hemoglobin production and reached 30--50% of the level of nontreated control when the cells enter the stationary phase. FLC variants unresponsive to HMBA or DMSO did not exhibit as low an activity of poly(ADP-ribose) synthesis as their parent cells did by treatment with these inducers. In contrast, butyrate stimulated poly(ADP-ribose) synthesis transiently but distinctly (about 50%) at an early stage of culture (6--24 hr), but suppressed it at a later stage. Neither the cell growth nor degradation of poly(ADP-ribose) is correlated with the effect of inducers. These results suggest that the level of poly(ADP-ribose) synthesis is correlated with the differentiation of FLC.
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PMID:Erythroid differentiation and poly(ADP-ribose) synthesis in Friend leukemia cells. 15 37

The RNA genome of the Moloney isolate of murine sarcoma virus (M-MSV) consists of two parts--a sarcoma-specific region with no homology to known leukemia viral RNAs, and a shared region present also in Moloney murine leukemia virus RNA. Complementary DNA was isolated which was specific for each part of the M-MSV genome. The DNA of a number of mammalian species was examined for the presence of nucleotide sequences homologous with the two M-MSV regions. Both sets of viral sequences had homologous nucleotide sequences present in normal mouse cellular DNA. MSV-specific sequences found in mouse cellular DNA closely matched those nucleotide sequences found in M-MSV as seen by comparisons of thermal denaturation profiles. In all normal mouse cells tested, the cellular set of M-MSV-specific nucleotide sequences was present in DNA as one to a few copies per cell. The rate of base substitution of M-MSV nucleotide sequences was compared with the rate of evolution of both unique sequences and the hemoglobin gene of various species. Conservation of MSV-specific nucleotide sequences among species was similar to that of mouse globin gene(s) and greater than that of average unique cellular sequences. In contrast, cellular nucleotide sequences that are homologous to the M-MSV-murine leukemia virus "common" nucleotide region were present in multiple copies in mouse cells and were less well matched, as seen by reduced melting profiles of the hybrids. The cellular common nucleotide sequences diverged very rapidly during evolution, with a base substitution rate similar to that reported for some primate and avian endogenous virogenes. The observation that two sets of covalently linked viral sequences evolved at very different rates suggests that the origin of M-MSV may be different from endogenous helper viruses and that cellular sequences homologous to MSV-specific nucleotide sequences may be important to survival.
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PMID:Rate of divergence of cellular sequences homologous to segments of Moloney sarcoma virus. 18 62

Using a method involving elution of hemoglobin bands from cellulose acetate strips following electrophoresis of hemolysates, hemoglobin A2 (Ab A2) was quantitated in bloods from 300 healthy individuals and 904 patients. The percentage of Hb A2 was elevated in beta-thalassemia heterozygotes and some patients who had megaloblastic anemia. In the latter, the highest Hb A2 levels were observed in patients with the most severe anemia. Low Hb A2 percentages were found in iron-deficiency anemia, hereditary persistance of fetal hemoglobin, and Hb H disease. In iron-deficiency anemia, the lowest levels of Hb A2 were observed in association with the most severe anemia. Iron and folate deficiency each suppressed Hb A2 levels in beta-thalassemia heterozygotes; however, vitamin B12 deficiency did not alter the percentage of Hb A2 in thalassemia. Malignant tumors, renal and hepatic insufficiency, chronic infections and inflammation, hemolytic disease, lead poisoning, aplastic anemia, leukemia, myelofibrosis, and hypothyroidism did not change Hb A2 levels. The pathogenesis of altered Hb A2 levels and their clinical significance in various diseases are discussed.
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PMID:Hemoglobin A2 levels in health and various hematologic disorders. 26 35

Bone marrow lymphoblasts from 109 children admitted with untreated acute lymphoblastic leukemia (ALL) were tested for spontaneous rosette formation with sheep erythrocytes. Twenty-six children (24%) had lymphoblasts that formed rosettes (E+). Of 13 initial clinical characteristics, 8 were significantly associated with E+ lymphoblasts: mediastinal enlargement (86% of patients E+), leukocyte counts over 100 X 10(9)/liter (65% E+), nodes greater than 2 cm in any diameter (65% E+), age over 5 yr (46% E+), hemoglobin over 8 g/dl (44% E+), hepatomegaly greater than 5 cm (38% E+), boys (35% E+), and lymph node enlargement outside of the cervical area (28% E+). Spleen size, initial platelet counts, and periodic acid-Schiff scores did not distinguish E+ from E- patients. Since few patients were black and few presented with central nervous system leukemia, the association of these two characteristics with E+ blasts could not be determined. A hierarchical classification scheme and a linear logistic regression model were used to define the patterns of characteristics associated with E+ lymphoblasts. The initial clinical characteristics and the poorer course of E+ patients suggest that ALL comprises at least two biologically and clinically distinct types. The E+ ALL may result from a leukemic transformation of a non-Hodgkin lymphoma.
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PMID:Initial prognostic factors and lymphoblast-erythrocyte rosette formation in 109 children with acute lymphoblastic leukemia. 26 81

Two patients with idiopathic refractory sideroblastic anemia (IRSA) were found to have acquired hemoglobin H. Both developed leukemic syndromes. Six other patients with IRSA had normal hemoglobin electrpohoretic patterns, and none has developed acute leukemia in up to five years. We suggest that hemoglobin electrphoresis be performed routinely in IRSA. The finding of hemoglobin H in this population may be a relatively frequent occurrence and may serve to distinguish the preleukemic patients from those not destined to develop leukemia.
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PMID:Acquired hemoglobin H in refractor sideroblastic anemia. A preleukemic marker. 27 89


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