Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023473 (chronic myeloid leukemia)
 18,916 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Granulocytes from the peripheral blood of patients with chronic myeloid leukemia (CML) are known to exhibit a defect in internalization of aggregated IgG relative to normal cells. As this aberration may arise due to defective transmembrane signalling, this study was undertaken to analyze alterations, if any, in protein phosphorylation between the two cell types. Normal and CML granulocytes were labeled with 32P-sodium orthophosphate and then stimulated with aggregated IgG. The phosphoproteins in the unstimulated and stimulated cells were analyzed by 2D-SDS-PAGE followed by autoradiography. The results show that there are five distinctly identifiable, reproducibly phosphorylated proteins referred to as Pp1-Pp5. In the unstimulated normal cells, Pp1 is less phosphorylated than Pp3, while in CML cells, Pp1 is more intense than Pp3. On stimulation of normal cells, with aggregated IgG, intensity of Pp1 increases while that of Pp3 decreases. In CML cells this response is reversed. We conclude that one of the causes for the defective internalization of IgG by CML granulocytes may probably be the observed differences in the phosphorylation of the proteins under study.
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PMID:Differential phosphorylation--cause for defective internalization of aggregated IgG by chronic myeloid leukemic granulocytes? 156 Jun 73

Hyperammonemia is a rare and serious complication of intensive cytotoxic chemotherapy. We report the case of a patient who developed profound idiopathic hyperammonemia following bone marrow transplantation for chronic myelogenous leukemia. Despite rapid institution of hemodialysis, sodium benzoate, and the experimental agent sodium phenylacetate, the patient ultimately succumbed to complications of this metabolic derangement. The literature is reviewed, and recommendations for an approach to this complication of marrow transplantation are proposed.
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PMID:Hyperammonemia following allogeneic bone marrow transplantation. 195 5

Cytoplasmic protein from peripheral blood myeloid cells of chronic myelogenous leukemia (CML) patients altered the electrophoretic mobility of complexes formed between nuclear proteins and interferon-inducible transcriptional enhancers. Immature myeloid marrow cells (blasts and promyelocytes) have a higher level of this activity than do mature myeloid marrow cells (bands and polys). This activity, which is not detectable in the peripheral blood cells of normal individuals, is at least 50-fold higher in CML marrow blasts and promyelocytes than that found in marrow blasts and promyelocytes of normal individuals. This activity was inhibited by in vivo incubation of immature myeloid cells with the phosphatase inhibitor, sodium orthovanadate (0.2 mM), and by adding orthovanadate (20 mM) directly to cytoplasmic proteins of myeloid cells. Interferon-alpha (1,000 U/ml) reduced the effects of the CML myeloid cell cytoplasmic protein on the electrophoretic mobility of nuclear protein-DNA complexes. These data suggest that a unique phosphatase may be involved in the abnormalities in CML which are modulated by interferon-alpha.
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PMID:A phosphatase activity present in peripheral blood myeloid cells of chronic myelogenous leukemia patients but not normal individuals alters nuclear protein binding to transcriptional enhancers of interferon-inducible genes. 224 38

A murine monoclonal IgM erythrocyte antibody appeared to have anti-P (anti-globoside) specificity. The antibody was a relatively weak cold agglutinin, but a strong haemolysin and its reactivity with red cells was markedly enhanced by enzyme treatment. This antibody was used to study the cell and tissue distribution of globoside. Globoside was not only detectable on red cells and erythroblasts, but also on endothelial cells and on subsets of platelets, megakaryocytes and fibroblasts. It was not detectable on granulocytes, monocytes and most peripheral blood lymphocytes. Neither was it present on erythroblast precursors (CFU-E, BFU-E), pro-erythroblasts or on the cells of the pro-erythroblastic cell lines K562 and HEL. However, K562 cells expressed globoside when induced to mature into erythroblasts by sodium butyrate. Cells of patients with various leukaemias were also tested. A significant number of positively reacting cells was frequently (six out of 18) seen in cases with a CML blast crisis (CML-BC) and rarely in AML (four out of 37 cases). In CML-BC the P-positive cells were probably erythroblasts and/or megakaryoblasts. Thus, globoside appeared to be an interesting marker in CML-BC of the erythroblastic or mixed erythroblastic-megakaryoblastic type.
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PMID:A murine monoclonal IgM antibody specific for blood group P antigen (globoside) 242 10

The resolution of bivariate flow karyotypes of human chromosomes stained with Hoechst 33258 and chromomycin A3 can be increased by adding sodium citrate and sodium sulfite to the chromosomes shortly before measurement. A flow karyotype of a patient with chronic myelocytic leukemia is shown to illustrate that the addition of these compounds allows high-resolution measurements to be made and evaluated reliably from clinical samples.
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PMID:Improved resolution of flow cytometric measurements of Hoechst- and chromomycin-A3-stained human chromosomes after addition of citrate and sulfite. 245 78

Ultraviolet light (UV)-induced DNA repair during myeloid leukemic cell differentiation was examined. Human myeloid leukemic cells could be induced to differentiate in vitro into mature cells by various chemical inducers that lost their proliferating potencies. In spite of decrease of proliferation capacity, almost all these terminally differentiated myeloid leukemic cells invariably showed UV-induced unscheduled DNA synthesis (UDS) at low energy of UV irradiation (3-5J/m2). This indicated that the terminally differentiated myeloid leukemic cells are functionally quite different from mature granulocytes in chronic myeloid leukemia (CML) or in normal peripheral blood. In HL-60 cells, UV-survival was enhanced in the process of differentiation induced by 1.25% DMSO or 0.6 mM sodium n-butyrate. The degree of enhancement of UV-survival was correlated with the increased amount of UDS. The process of myeloid leukemic cell differentiation which is completed without loss of capacity performing repair DNA synthesis was one of the characteristics of the terminally differentiated myeloid leukemic cells induced by chemical inducers in vitro and this function may support the hypothesis that DNA breaking and rejoining are involved in a mechanism of cytodifferentiation.
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PMID:UV-induced DNA repair in leukemic cell differentiation. 258 62

We analyzed hemolytic reaction following vinca alkaloid administration in patients with acute lymphoblastic leukemia, blast crisis of chronic myelogenous leukemia and malignant lymphoma in the leukemic phase. During the course of chemotherapy in which vinca alkaloids were included, indirect-form dominant hyperbilirubinemia was observed in 21 of the 31 evaluable patients. In 8 patients with hyperbilirubinemia, reticulocytosis coincided with vinca alkaloid administration. Peripheral blood films showed prominent anisocytosis in 4 patients and increased stomatocytes in 10 patients. Red cell membrane studies in patients with hemolysis revealed increased sodium transport and increased activity of Na+, K+-ATPase. These findings were considered to represent the abnormal membrane "leakiness". Thus, vinca alkaloids might induce erythrocytotoxicity, which leads to acquired stomatocytosis with hemolysis in some patients.
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PMID:A transient hemolytic reaction and stomatocytosis following vinca alkaloid administration. 274 52

Adenosine deaminase (ADA) deficiency is associated with a fatal severe combined immunodeficiency. Because most patients do not have a suitable marrow donor, the introduction of a normal ADA gene into the patient's marrow cells is a potentially useful alternative therapy. To identify vectors that provide optimal gene expression in human hematopoietic cells, we investigated retroviral vectors containing the ADA gene under the transcriptional control of the promoter/enhancers of Moloney murine leukemia virus, the simian virus 40 early region, the cytomegalovirus immediate-early gene, the lymphotropic papovavirus, and the human beta-globin gene. ADA expression from these vectors was monitored in the ADA- human histiocytic lymphoma cell line DHL-9, and in the multipotential chronic myeloid leukemia cell line K562. ADA expression in infected K562 cells was also measured after induction of megakaryoblastic differentiation by phorbol ester, and after induction of erythroid differentiation by sodium n-butyrate or hemin. In these hematopoietic cell lines, the vectors that contained ADA controlled by either the Moloney murine leukemia virus promoter (LASN) or the cytomegalovirus promoter (LNCA) expressed ADA at much higher levels than the other vectors tested. Furthermore, in K562 cells infected with LASN and LNCA vectors, induction of terminal differentiation resulted in the same or higher level expression of ADA. These cell lines have permitted the evaluation of transduced gene expression in proliferating and differentiating hematopoietic cells that provide a model for bone marrow-targeted gene therapy.
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PMID:Expression of human adenosine deaminase from various strong promoters after gene transfer into human hematopoietic cell lines. 275 48

The processing and intracellular transport of lactoferrin of the neutrophil specific granules was investigated by biosynthetic labeling with (14C)leucine of bone marrow cells from healthy individuals and patients with chronic myeloid leukemia. Lactoferrin was precipitated with antilactoferrin serum and the immunoprecipitates were analyzed by sodium dodecyl sulfate (SDS), polyacrylamide gel electrophoresis (PAGE) followed by fluorography. In contrast to myeloperoxidase of azurophil granules, lactoferrin was not synthesized as a larger precursor, and it was not found to be phosphorylated. The transfer to granules of newly synthesized lactoferrin was demonstrated in pulse-chase labeling experiments followed by centrifugation of cell homogenate in a Percoll gradient. Monensin, which exchanges protons for Na+ and NH4+ cation, blocked the transfer completely, indicating a need for acidification mechanisms. Unlike myeloperoxidase, newly synthesized lactoferrin rapidly became resistant to endoglycosidase H, indicating a transport through the medial and transcisternae of the Golgi apparatus with conversion of "high mannose" to "complex" oligosaccharide side chains. Intracellular transfer of some major neutrophil azurophil and specific granule constituents is obviously regulated differently. Lactoferrin seems to be processed like proteins destined for secretion, while myeloperoxidase is processed more or less like lysosomal enzymes.
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PMID:Biosynthesis and processing of lactoferrin in bone marrow cells, a comparison with processing of myeloperoxidase. 282 14

Chronic myeloid leukemia (CML) is a disorder arising from a defect in the hemopoietic stem cell. Consequently, the malignant clone can involve all cells within the stem cell's capacity for differentiation, including erythrocytes, granulocytes, monocytes, megakaryocytes, and lymphocytes. Similarly, the K562 cell line, which was derived from a patient with CML, has been shown to be capable of differentiation towards erythrocytes, granulocytes, monocytes, and megakaryocytes, and in this respect may represent a model of the hemopoietic stem cell. However, although K562 shows properties of a myeloid stem cell, no lymphocyte-specific features or differentiation have yet been described. In the present study, K562 cells have been induced to differentiate by culture in the presence of sodium butyrate. The direction and extent of induced differentiation over 12 days were determined with a panel of monoclonal antibodies and with cytochemical stains. This treatment consistently induced expression of pre-B-cell markers, including B-lymphocyte-specific B4 and B1, and of the common acute lymphoblastic leukemia antigen (CALLA), recognized by J5. In addition to the increased expression of B-lymphocyte markers, butyrate induction of K562 resulted in a decrease in granulocyte markers, increases in certain monocyte and platelet markers, and an increase in beta 2 microglobulin expression. Butyrate-induced expression of B-lymphocyte markers was not observed with the myelomonocytic cell line U937. The expression of B-lymphocyte-specific antigens on butyrate-induced K562 may result from the relaxed control of gene expression, but alternatively these observations may indicate the lymphoid-myeloid stem cell nature of K562.
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PMID:Induction of B-lymphocyte antigens on the chronic myeloid leukemic cell line K562 using sodium butyrate. 295 19


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