Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023467 (acute myeloid leukemia)
 35,200 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Aggressive treatment with cytarabine, vincristine sulfate, and prednisone for acute myelogenous leukemia, administered from the 31 st week of pregnancy, resulted in both sustained complete remission of the leukemia and delivery of a normal infant with a normal birthweight and a normal male karyotype. It is concluded that chemotherapy with cytarabine combinations can be administered in the third, and probably the second, trimester of pregnancy without risk of serious damage to the developing fetus.
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PMID:Successful treatment of acute leukemia during pregnancy. Combination therapy in the third trimester. 26 69

Seven of 17 children (41%) under 5 years of age with acute granulocytic leukemia (AGL) treated with either cytosine arabinoside-cytoxan (CA-CYT) or Mini-COAP (CA-CYT with vincristine sulfate [VCR] and prednisone) have been in continuous complete remission 4 years or more. CA and CYT were each given in the dosage of 120 mg/m2 intravenously, daily in 3 divided doses, for 4 days. Induction consisted of two courses given at intervals of 2 weeks; during maintenance the courses were repeated at intervals of 4 weeks. In the Mini-COAP regimen, standard 28-day VCR-prednisone therapy was superimposed on CA-CYT induction and 4-day VCR-prednisone pulses were superimposed on CA-CYT maintenance. Transient moderate to severe myelosuppression was frequent; other manifestations of toxicity were mild. Administration of drugs at home was feasible in many instances. Mini-COAP was proved to be an effective therapeutic regimen for young children with AGL and should be considered as initial therapy.
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PMID:Improved survival in young children with acute granulocytic leukemia treated with combination therapy using cyclophosphamide, oncovin, cytosine arabinoside, and prednisone. 28 34

Antisera have been raised in rabbits to the lymphoblastoid cell line NALM 1 precoated with anti-lymphocyte serum (ALS). Following absorption with chronic lymphocytic leukemia cells (CLL) the antisera reacted mainly with acute lymphocytic leukemia (ALL) cells, and were very similar in specificity to antisera raised to ALL cells precoated with ALS. Leukemia cells from the following numbers of patients were positive for the anti-NALM 1 sera in a complement-dependent cytotoxicity test; 11/14 ALL, 3/15 acute myelocytic leukemia (AML), 1/5 chronic myelocytic leukemia (CML) and 0/8 CLL. Normal B and T peripheral blood lymphocytes were negative. The titer of the anti-NALM 1 sera against positive cells was 1:64 to 1:256 whereas the undiluted sera did not react with negative cells. Ten out of 11 of the positive ALL cells were of the non-B non-T type. However, cells from 1/4 T ALL patients and a cultured T ALL line 8402 were also positive. Six of 12 cultured lymphoblastoid cell lines were positive, all of which were of malignant origin. The molecular weight of the ALL antigen detected by anti-NALM-1 serum was determined by immunoprecipitation and sodium dodecyl sulfate (SDS) polyacrylamide gel electrophoresis (PAGE) to be approximately 98,000 daltons.
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PMID:Heteroantiserum against acute lymphocytic leukemia raised to the lymphoblastoid cell line NALM-1. 30 68

The authors have purified glucose phosphate isomerase (GPI) from human leukocytes ; they used as starting material leukemic leukocytes obtained from a patient with hyper-leukocytic acute myeloid leukemia ; it was possible to obtain several milligrams of pure enzyme from a single patient. The purification procedure includes a two step precipitation by ammonium sulfate and one column chromatography on a cation exchanger with specific elution by 6 phosphogluconate, a ligand of GPI ; of the two cation exchangers tested, phosphocellulose was found to lead to a better yield than CM-Sephadex. The end product of purification had a specific activity of 855 UI/mg and gave only one band in sodium dodecyl sulphate polyacrylamide gel electrophoresis. Anti GPI monospecific rabbit serum was obtained with purified enzyme. GPI from the various blood cells of ten normal controls was studied immunologically and the ratio of the enzymatic activity to the immunological reactivity was measured ; this ratio (i.e. the molecular specific activity) was lower in granulocytes than in lymphocytes and still more depressed in platelets and hemolysate. The significance of such differences is discussed.
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PMID:Human leukocyte glucose-phosphate-isomerase purification by affinity elution and immunological study. 81 39

Two forms of deoxythymidine kinase from blast cells of acute myelocytic leukemia were identified by electrophoresis. One was associated mainly with the cytoplasm and the other with mitochondria. Both isozymes were separated and purified by differential affinity column chromatography which resulted in 2416- and 1634-fold purification of the cytoplasmic and mitochondrial enzymes, respectively. Affinity gel was prepared by linkage through position 3' of deoxythymidine. Each enzyme had the same electrophoretic mobility in the purified state as it did in the enzyme derived from the corresponding subcellular fraction of the homogenate. Thymidine phosphorylase was not retarded by the affinity column. The purified cytoplasmic and mitochondrial deoxythymidine kinase had different molecular weights, sensitivities to inhibition by ammonium sulfate, activation energies for the reaction and divalent cation requirements. Adenosine, guanosine, and cytosine 3':5'-monophosphates, putrescine, spermine, and spermidine were neither activators nor inhibitors of either deoxythymidine kinase.
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PMID:Human deoxythymidine kinase. I. Purification and general properties of the cytoplasmic and mitochondrial isozymes derived from blast cells of acute myelocytic leukemia. 106 25

We previously studied fibrinolysis and fibrinogenolysis by analyzing fragments of fibrin/fibrinogen degradation products (FDP) employing sodium dodecyl sulfate-polyacrylamide gel electrophoresis and immunoblotting. In this report, we characterized the fragments of FDP in four patients with disseminated intravascular coagulation (DIC), that were caused by various diseases. In the patients suffering from acute lymphoblastic leukemia (case 1) and acute suppurative cholangitis (case 3), DD and DY/X fragments resulting from fibrinolysis accounted for the most part of the FDP fragments. In case 3, D fragments resulting from fibrinogenolysis were also observed to much less extent. In a DIC associated with acute myeloblastic leukemia (case 2), both fibrinolysis and fibrinogenolysis were increased and resulted in high levels of D, Y and DY/X fragments, concomitant with moderate levels of DD and high molecular weight (HMW) fragments in the patient's sera. The increased fibrinogenolysis in this case was attributed to accelerated activation of plasmin. In a DIC patient of case 4, who underwent an operation due to hepatocellular carcinoma, marked increase in DY/X and HMW fragments and slight increase in DD fragment were observed on the day of operation. Hyperfibrinolysis documented in case 4 was explained by both increased production of thrombin and moderately accelerated activation of plasmin. Both qualitative and quantitative changes in the fragments of FDP during the courses of treatment in two cases of DIC were also noted. In summary, each underlying disease expresses characteristic pattern of FDP fragments in DIC.
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PMID:[Studies on the fragments of FDP in 4 patients with DIC]. 130 14

An animal model for malignant mastocytosis is described in mice reconstituted with bone marrow cells expressing the v-erbB oncogene. The lethal mast cell disease is characterized by massive infiltration of bone marrow, spleen, and several other visceral organs by connective tissue mast cells, which normally reside in the skin and the peritoneal cavity. As is frequently found in malignant mastocytosis, the v-erbB-induced mast cell disease was accompanied in some primary recipients by an acute myelogenous leukemia (AML) that killed all secondary recipients regardless of whether the AML was already evident in the primary host. The infiltrating mast cells stained strongly positive with berberine sulfate, suggesting that they were terminally differentiated and in vitro they showed only a weak proliferative capacity. The leukemias were clonal but apparently of different origin than the malignant mast cells, implying the transformation of two independent cell populations. Leukemic cells expressed various myeloid-specific markers as well as the B220 antigen, normally associated with the B-cell lineage. However, the Ig heavy chain genes were still in germ line configuration. In culture, these cells proliferated in the absence of exogenous growth factors and had the capacity to differentiate into mature myeloid cells. Preliminary experiments suggest that v-erbB may use parts of a signal transduction pathway normally coupled to the c-kit receptor. The v-erbB-induced malignant mast cell disease should provide a useful animal model for elucidating the cause for malignant mastocytosis in humans and to explore possible therapeutic strategies.
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PMID:Development of a lethal mast cell disease in mice reconstituted with bone marrow cells expressing the v-erbB oncogene. 135 Jul 40

A common polymorphism at codon 72 of the p53 gene in patients with acute myelogenous leukemia (AML) was analyzed by single-strand conformation polymorphism assay and sodium dodecyl sulfate polyacrylamide-gel electrophoresis of immunoprecipitated 35S-labeled P53 protein. No association between this polymorphism and a marked predisposition to AML was found. The half-lives of these two polymorphic forms of P53 were equivalent in normal phytohemagglutinin-stimulated lymphocytes, while the P53 Pro72 isoform was found to be twice as stable as the Arg72 isoform in Daudi cells.
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PMID:Polymorphism at codon 72 of the p53 gene in human acute myelogenous leukemia. 163 75

Normal and leukemic hematopoietic cell lysates were labeled with [3H]-diisopropylfluorosorophosphate ([3H]-DFP), an active site inhibitor of serine hydrolases. The labeled proteins in the lysates were examined by sodium dodecyl sulfate-polyacrylamide gel electrophoresis followed by counting of gel segments for radioactivity. The results indicate the presence of distinct [3H]-DFP binding patterns for different normal and leukemic hematopoietic cells; significantly lower labeling in normal or leukemic lymphoid cells compared to myeloid or monocytoid cells; lower labeling in acute myeloblastic leukemia (FAB-M1) as compared to acute myelomonocytic leukemia (FAB-M4), chronic myelomonocytic leukemia or monocytes and an increase in [3H]-DFP binding with cell maturation along granulocytic series. Thus, these patterns could be useful in discriminating acute lymphoblastic leukemia from myeloid/monocytoid types of leukemia and for following maturation of myeloid cells, and perhaps for studying functional or maturation defects in hematopoietic cells in other pathological conditions.
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PMID:Diisopropylfluorophosphate binding proteins (serine hydrolases) from normal and leukemic hematopoietic cells. 211 31

Previous studies reported that 5'-nucleotidase activity was undetectable or at much lower levels in the homogenate of human chronic lymphocytic leukemic (CCL) cells than in normal lymphocytes. In the present study, 5'-nucleotidase specific activity in acute myelocytic leukemia (AML), which varied in a range from undetectable to 1.4 (nmoles/min.mg protein), was enhanced by cell fractionation, from undetectable in the homogenate, up to 18.8 +/- 1.2, 6.4 +/- 0.7 and 0.68 +/- 0.12 in plasma membranes, microsomes, and cytosol fraction, respectively. In a further fractionation of the cytosol of various leukemic cells with ammonium sulfate, 5'-nucleotidase specific activity increased up to 14-fold in the 60% (NH4)2SO4 fraction, with a recovery of 1266 +/- 115%. These data suggest that 5'-nucleotidase activity in fractionated leukemic cells is higher than reported previously and that the sum of 5'-nucleotidase activity in subcellular compartments is higher than that detected in the homogenate. Furthermore, even when 5'-nucleotidase was undetectable in a homogenate, it became detectable in the plasma membranes, suggesting that its ecto-enzyme function is still active in leukemic cells. The undetectable or low 5'-nucleotidase in the homogenate is indicative of (1) the enzyme itself being in an inactive form but becoming active after the fractionations, or (2) the presence of a factor(s) that prevents the enzyme from being detected but that is separated from the enzyme by the fractionations. In both cases, the rate of nucleotide catabolism by inactive 5'-nucleotidase in rapidly proliferating leukemic cells should be slower than when the enzyme is active. The present finding is consistent with our previous findings that during normal cell aging the high 5'-nucleotidase activity is associated with senescent non-proliferating cells but low or undetectable activity with rapidly proliferating immortal cells. The implications of 5'-nucleotidase for DNA synthesis in aging and cancer are discussed.
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PMID:Enhancement of 5'-nucleotidase activity of human leukemic cells after fractionation: implications for cancer and aging. 255 27


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