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)

An antiserum was produced by immunization of rabbits with the membrane fraction of a lymphoblastoid cell line, RPMI 4265. This antiserum reacted against leukemia-associated antigens on immature blast cells of 24 patients with acute leukemia (13 myeloblastic, 11 lymphoblastic). No reactivity was observed against morphologically normal blood mononuclear cells from patients in remission, cells from normal control subjects and patients with unrelated disorders, phytohemagglutinin-induced lymphoblasts, or normal bone marrow cells. Reactivity against leukemia cells was not reduced by absorption with fetal tissues. These findings were consistent with the presence of tumor-associated antigens on leukemia cells. The antigens were detectable neither during hematologic remission nor on cells from patients with unrelated diseases.
J Natl Cancer Inst 1976 Jun
PMID:Leukemia-associated antigens detected by heterologous antisera. 6 42

Hyperferritinemia in various diseases, mainly hematological, was confirmed by immunological methods. For ferritin detection, anti-human placental ferritin antiserum, anti-human hepatic ferritin antiserum, and anti-human leukemia cell ferritin antiserum were used and the result was compared with each other. Leukemia, malignant lymphoma, multiple myeloma, and aplastic anemia are hematological diseases which showed a positive reaction in this test, among which leukemia showed the highest positivity. Cases of hepatic diseases and non-hematological malignant neoplasms also showed a positive reaction. The positivity was quite low and almost negligible in other diseases and healthy individuals. Anti-human placental ferritin antiserum seemed to be suitable for cancer diagnosis and, antihuman hepatic ferritin antiserum for hepatic diseases. The results of analysis of purified human hepatic and placental ferritins highly suggested the presence of immunological heterogeneities between them. Also, a possibility was pointed out that one of the components of the so-called leukemia-specific antigens might sometimes be the isoferritin of leukemia cells.
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PMID:Immunological heterogeneity in human ferritinemia. 6 5

Ethidium bromide (2,3-diamino-5-ethyl-6-phenylphenanthridinium bromide) significantly inhibited the RNA-dependent DNA polymerase of types A and C particles isolated from transplanted adenovirus 12-induced tumors of CBA mice. It was also cytotoxic for an established in vitro line of adenovirus 12-induced tumor cells of CBA mice and caused cell death, inhibition of [3H]thymidine uptake, and a significant reduction of cells in metaphase. Ethidium bromide significantly inhibited the in vivo growth of transplanted adenovirus 12-induced tumor cells of CBA mice, simian virus 40-induced tumor cells of hamsters, and murine leukemia virus-induced lymphoma cells of BALB/c mice. The compound may have exerted the antitumor activity by selectively affecting oncornavirus in the tumor cells.
J Natl Cancer Inst 1976 Oct
PMID:Effect of ethidium bromide on transplanted virus-induced tumor cells. 6 62

The major internal polypeptide of the bovine leukemia virus (BLV) was purified to homogeneity with the use of gel filtration and affinity chromatography. Like previous results, the protein had a molecular weight of 25,000 daltons as determined by electrophoresis in polyacrylamide gels with sodium dodecyl sulfate. More than 90% of the 125I-labeled protein was precipitated by bovine sera that reacted in immunofluorescence tests with acetone-fixed BLV-infected cells. In contrast, minimal precipitation (less than 5%) was observed with sera from 36 cattle in leukemia-free herds; these sera, negative by immunofluorescence, included six samples that had high titers of antibodies to the foamy-like bovine syncytia virus (BSV). Antisera prepared against several other oncornaviruses or the Mason-Pfizer monkey virus (M-PMV) did not bind the BLV p25 protein. Conversely, the labeled p30 polypeptides of several oncornaviruses tested did not react with bovine sera that had high titers of antibodies to BLV p25. Competitive radioimmunoassay(s) (RIA) also failed to detect cross-reactions between BLV p25 protein and the internal polypeptides of other mammalian and avian oncornaviruses, M-PMV, or foamy-like BSV. The RIA for BLV p25 antigen was also highly sensitive and specific for the detection and quantitation of the antigen in virus preparations and cell homogenates.
J Natl Cancer Inst 1976 Oct
PMID:Detection, quantitation, and characterization of the major internal virion antigen of the bovine leukemia virus by radioimmunoassay. 6 63

The degree of inhibition of mammalian DNA-dependent RNA polymerases I and II and Moloney leukemia virus RNA-dependent DNA polymerase by pyran copolymer was dependent on the concentration of the divalent cation cofactor in the reaction mixture. Inhibition was completely blocked by an excess of divalent cations. It was concluded that pyran inhibited these enzymes by complexing with the essential divalent cation cofactor.
J Natl Cancer Inst 1976 Dec
PMID:Role of divalent ion complex formation in pyran--inhibition of nucleic acid biosynthesis. 6 66

A prolonged cytotoxic effect of 5-azacytidine (aza-CR) on leukemic colony-forming units (LCFU) was observed in mice with transplanted L1210 leukemia. LCFU showed rapid reaccumulation in the marrow 12 hr after injection of 0.1 mg of aza-CR per mouse. However, after 0.5 mg of aza-CR, repopulation was delayed for at least 6 days. Experiments were performed to determine the mechanism of this prolonged antileukemic effect. Suspensions of leukemic marrow prepared from mice treated 4 days previously with 0.5 mg of aza-CR were exposed to [3H]thymidine in vitro in order to kill cells in S phase. Suspensions exhibited a 40% reduction in LCFU, indicating the prolonged effect was not due to cell cycle progression delay. Mice given whole-body irradiation prior to receiving L1210 demonstrated the same delayed repopulation following the high dose of aza-CR as nonirradiated mice, suggesting that the effect was likely not due to an immune reaction. aza-CR, when given to normal mice as long as 2 days prior to leukemic transplantation, was able to prolong the survival of leukemic mice, but not when given at longer intervals. Administration of aza-CR to mice 1 day or 1 hr prior to leukemic transplantation resulted in decreased LCFU survival as well as delayed repopulation of LCFU; the rate of repopulation was not changed. This indicated a prolonged residual activity of the drug, but not sufficient to explain the total in vivo suppression. In contrast, administration of aza-CR to leukemic mice suppressed repopulation of a subsequent leukemic transplant for 4 days, even when the cells were given 2 days after the aza-CR. Cytidine was partially able to reverse the delayed repopulation of LCFU when given 1 day after aza-CR, but it was unable to reverse the phenomenon 2 days after aza-CR. Therefore, a high dose of aza-CR produces a prolonged antileukemic effect which is probably mediated by continued availability of an aza-CR metabolite. Since this effect is more pronounced in leukemic mice than in nonleukemic mice, the pharmacokinetics of high doses of aza-CR probably differ in normal and leukemic mice.
Cancer Res 1977 Feb
PMID:Biological characterization of a prolonged antileukemic effect of 5-azacytidine. 6 94

The still increasing amount of carriers and anemics by thalassemia (Th) and other Hb-pathies (approximately 4,000 among approximately 48,000 investigated people) have shown that Campania is the most affected world area by all Hb Lepre conditions. Among 161 people with heterozygous Hb Lepore we have noticed 10 cases associated with (hemo-) blastomata as follows: 2 Chr. Lymphatic Leukemia, 2 Ac. Lymphoblastic Leukemia, 1 Lymphosarcom, 1 Colon Cancer, 1 Uterin Cancer, 1 Plasmocytom, 1 Hodkgin Disease, 1 Ac. Promyelocyte Leukemia (or fatal ac. agranulocytemia?). In the literature we recently found 2 other similar cases. The incidence of such malignancies in our Hb Lepore people reaches 6%. On the contrary in the heterozygous Th. group, among 3,150 carriers, we diagnosed only 20 people with (hemo-) blastomata as follows: 12 Ac. Leukemia (9Lymphoblastic) and 8 Chr. Myeloid Leukemia, with an incidence rate of 0.6% namely a little higher than in normal people. This highly significant discrepancy rate shows an elective predisposition to (haemo-) blastomata from Leporian people.
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PMID:Hb Lepore and (haemo-) blastomata. 6 34

The majority of human lymphocytic and myelocytic leukemia cells express a polymorphic antigen that is found on peripheral blood B-lymphocytes and cultured lymphoblastoid B-cell lines. These B-lymphocyte antigens were detected by 34 human alloantisera that were repeatedly absorbed with pooled platelets to remove all activity against HLA antigens and T-lymphocytes. Absorption studies indicated that a common antigen was present on both B-lymphocytes and positive leukemia cells. Leukemia cells could be subdivided into two groups based on the presence of the B-lymphocyte antigen. Fourteen of 18 acute myelocytic leukemia cells, 10 of 13 acute lymphoblastic leukemia cells, 4 of 6 chronic myelocytic leukemia cells, and 2 of 2 chronic lymphocytic leukemia cells were positive. This group of leukemia cells also reacted with rabbit anti-B-cell sera raised to papain digests of spleen cell membranes. F(ab')2 fragments of the rabbit antsera were shown to specifically block the reactions of the human antisera against B-cells and leukemia cells. These results suggested that the rabbit and human anti-B-cell sera were reacting with identical molecules. This conclusion was supported by immunoprecipitation data.
J Natl Cancer Inst 1977 Feb
PMID:Human B-lymphocyte antigens expressed by lymphocytic and myelocytic leukemia cells. II. Detection by human anti-B-cell alloantisera. 6 14

The activities of streptovaricin complexes, streptovaricins, streptovals, and streptovarinic degradation products were elevated against RNA-directed DNA polymerases of Rauscher leukemia virus, DNA-dependent DNA polymerase of bacterial and mammalian cells, and DNA-dependent RNA polymerases of mammalian origin. The activities of streptovaricins were also listed for comparison purposes. The effects of streptovaricin complexes on viral DNA polymerases varied significantly from lot to lot, and streptovaricin complex lot 7 was the most active. All the streptovals and streptovaricin degradation products except varicinal A showed a marked improvement (twofold to tenfold) in activity against the viral enzyme over the parent streptovaricins. None of these compounds, however, displayed any significant effect on either the DNA polymerase of L1210 leukemia cells and Escherichia coli or the RNA polymerase of isolated nuclei of mouse liver. As a result of tests in these systems, some specific inhibitors of RNA-directed DNA polymerases of Rauscher leukemia virus were selected.
J Natl Cancer Inst 1977 Feb
PMID:Effects of streptovaricins and their degradation products on RNA-directed DNA polymerase of Rauscher leukemia virus. 6 15

The virucidal effects of streptovaricin (Sv) A, SvC, SvD, streptoval (Sval) C, Sval Fc, and streptovarone were evaluated by incubation of the drug with Rauscher leukemia virus (RLV) at 37 degrees C for 60 minutes prior to dillution and addition to cells (in vitro assay) or before ip injection into animals (in vivo assay). The in vitro and in vivo assays were plaque formation and splenomegaly, respectively. A dose-related effect was observed with all six compounds with the in vitro assay. On an equimolar basis, the Sv degradation products, i.e., Sval C, Sval Fc, and streptovarone were most inhibitory, followed by SvD; SvA and SvC were least active. At 0.0625 mumoles, the three Sv degradation products inactivated over 90% of the RLV. Similar results were obtained through the in vivo assay. At 0.06 mumoles, streptovarone, Sval C, and SvD showed 78,62, and 29% inhibition of splenomegaly, respectively; SvA and SvC were essentially inactive. A direct relationship was observed between inhibition on RNA-directed DNA polymrase of RLV by these compounds and their virucidal effects. No drug given at the time of injection, however, showed any significant effect on virus infective processes in vitro or in vivo. The reason for the lack of therapeutic effects of these compounds is discussed.
J Natl Cancer Inst 1977 Feb
PMID:Effects of streptovaricins and their degradation products on infectivity of Rauscher leukemia virus. 6 16


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