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Journal articles on the topic 'Cellules HL60'

Author: Grafiati

Published: 4 June 2021

Last updated: 1 February 2022

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1

Ul-Haq, R., and C. R. Chitambar. "Modulation of transferrin receptor mRNA by transferrin-gallium in human myeloid HL60 and lymphoid CCRF-CEM leukaemic cells." Biochemical Journal 294, no. 3 (1993): 873–77. http://dx.doi.org/10.1042/bj2940873.

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Gallium binds to the iron transport protein transferrin (Tf), is incorporated into cells through transferrin receptors (TfR) and inhibits iron-dependent DNA synthesis. Since cellular TfR expression is tightly regulated by the availability of iron, we investigated the effects of transferrin-gallium (Tf-Ga) on TfR mRNA levels in myeloid HL60 and lymphoid CCRF-CEM cells. In HL60 cells, Tf-Ga increased TfR mRNA levels in a dose-dependent fashion. This increase in TfR mRNA was blocked by Tf-Fe and by cycloheximide. Analysis of the rate of mRNA decay in the presence of actinomycin D revealed that th

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2

Rudin, Deborah, Maurice Schmutz, Noëmi Johanna Roos, Jamal Bouitbir, and Stephan Krähenbühl. "Reactive Metamizole Metabolites Enhance the Toxicity of Hemin on the ATP Pool in HL60 Cells by Inhibition of Glycolysis." Biomedicines 8, no. 7 (2020): 212. http://dx.doi.org/10.3390/biomedicines8070212.

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Metamizole is an analgesic, whose pharmacological and toxicological properties are attributed to N-methyl-aminoantipyrine (MAA), its major metabolite. In the presence of heme iron, MAA forms reactive metabolites, which are toxic for granulocyte precursors. Since decreased cellular ATP is characteristic for MAA-associated toxicity, we studied the effect of MAA with and without hemin on energy metabolism of HL60 cells, a granulocyte precursor cell line. The combination MAA/hemin depleted the cellular ATP stronger than hemin alone, whereas MAA alone was not toxic. This decrease in cellular ATP wa

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3

Hu, Yumin, Gang Chen, Yu Jia, et al. "The Combination of PEITC (Phenehyl Isothiocyanate) with a Histone Deacetylase Inhibitor (HDACi) Has Synergistic Antileukemia Activity by Overcoming a Redox-Mediated Resistance Pathway." Blood 114, no. 22 (2009): 1739. http://dx.doi.org/10.1182/blood.v114.22.1739.1739.

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Abstract Abstract 1739 Poster Board I-765 Introduction Histone deacetylase inhibitors (HDACI) have limited but well established clinical activity in human leukemia. Results of a phase 1 trial of vorinostat in AML indicate that a gene signature composed mainly of antioxidants was associated with clinical resistance to vorinostat (Blood 2008;111:1060-60). This study suggested that generation of reactive oxygen species (ROS) appears to be a mechanism of action of vorinostat whereas increase of antioxidants may correlate with vorinostat resistance. The aims of this study were to further investigat

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4

Halada, Petr, Petr Man, Dana Grebeňová, Zbyněk Hrkal, and Vladimír Havlíček. "Identification of HL60 Proteins Affected by 5-Aminolevulinic Acid-Based Photodynamic Therapy Using Mass Spectrometric Approach." Collection of Czechoslovak Chemical Communications 66, no. 11 (2001): 1720–28. http://dx.doi.org/10.1135/cccc20011720.

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A combination of mass spectrometric techniques was used for identification of HL60 leukemia cell proteins affected by 5-aminolevulinic acid-based photodynamic therapy (ALA-PDT). We compared two-dimensional electrophoresis (2-DE) protein maps of ALA-treated non-irradiated and irradiated cells and found extensive changes in the proteome of HL60 cells. The silver-stained 2-DE pattern of HL60 proteins contained more than 1 350 spots. Matrix-assisted laser desorption/ionisation mass spectrometry and microcapillary liquid chromatography/tandem mass spectrometry have identified twelve proteins differ

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5

Liu, Liqiong, Ping Wang, Xingbin Wang, Junxia Gu, Xiaoqing Li, and Shiang Huang. "Trans-Cinnamaldehyde Induces Granulocytic Differentiation and Impairs Survival and Migration of Acute Myeloid Leukemic Cells." Blood 112, no. 11 (2008): 5035. http://dx.doi.org/10.1182/blood.v112.11.5035.5035.

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Abstract Trans-cinnamaldehyde (TCA), the major active component of oil isolated from the stem bark of Cinnamomum cassia traditionally used to treat dyspepsia, gastritis and inflammatory disease world widely, has been shown to inhibit proliferation and promote apoptosis in a number of cancer cells. However, the functional roles TCA plays in hematopoietic system have not been fully investigated. In this study, we show the effects of TCA on acute promyelocytic leukemia (APL) cell line HL60 and primary bone marrow mononuclear cells (BMMNC) as well as bone marrow stromal cells (BMSC) from acute mye

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6

Amirkhosravi, Ali, Sonja Loges, Todd Meyer, et al. "An in vitro study on the mechanisms of coagulation activation in acute myelogenous leukemia (AML): role of tissue factor regulation by cytotoxic drugs and GM-CSF." Thrombosis and Haemostasis 92, no. 11 (2004): 1136–46. http://dx.doi.org/10.1160/th04-04-0215.

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SummaryAML patients may suffer from a disseminated coagulopathy, which can aggravate a pre-existing bleeding tendency due to thrombocytopenia and platelet dysfunction. The cellular and molecular mechanisms underlying this coagulopathy, however, are not completely understood. Indeed, the broad and increasing therapeutic use of cytotoxic drugs and growth factors is likely to contribute to the complexity of hemostatic abnormalities encountered in this hematologic malignancy. The nature of coagulation activation in AML was therefore investigated in vitro using the human leukemic cell line, HL60. T

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7

Bouvy, Céline, Adeline Wannez, Christian J. Chatelain, and Jean-Michel Dogné. "Transfer of Multidrug Resistance Among Acute Myeloid Leukemia Cells Via Extracellular Vesicles and Their Micrornas Cargo." Blood 128, no. 22 (2016): 2864. http://dx.doi.org/10.1182/blood.v128.22.2864.2864.

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Abstract Resistance of cancer cells to chemotherapy is a major issue in acute myeloid leukemia (AML) and is usually due to a clonal selection of resistant leukemic cells. Recently, a horizontal transfer of chemoresistance among tumor cells has been reported via extracellular vesicles (EVs). EVs are vesicles ranging from 0.03 to 1µm generated by almost all cell types. They carry cellular components such as nucleic acids, membrane and cytosolic proteins. By interacting with cells and by transferring their content, these vesicles could modify target cells' phenotype. Because of their presence in

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8

Campos, Lydia, Pascale Flandrin, Daniela Olaru, and Denis Guyotat. "Hsp90 Inhibitors Induce Apoptosis in Human Leukemia Cells." Blood 104, no. 11 (2004): 93. http://dx.doi.org/10.1182/blood.v104.11.93.93.

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Abstract The 90-Kda heat shock protein (Hsp90), together with a number of other chaperones are involved in normal cellular differentiation and cancerogenesis. Hsp90 is implicated in the conformational maturation of a large variety of protein kinases. We have shown its overexpression in a series of 116 acute myeloid leukemias (AML). Geldanamycin and its analogue 17-AAG selectively block the activities of Hsp90, but do not interact with other members of the Hsp family. The objective of the study was to test the effect of 17-AAG on cell lines (Jurkat, U-937, HL60, HL60R : resistant to daunorubici

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9

Noble, S. L., L. E. Wendel, M. M. Donahue, G. T. Buzzard, and A. E. Rundell. "Sparse-Grid-Based Adaptive Model Predictive Control of HL60 Cellular Differentiation." IEEE Transactions on Biomedical Engineering 59, no. 2 (2012): 456–63. http://dx.doi.org/10.1109/tbme.2011.2174361.

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10

Sinclair, J., D. McClain, and R. Taetle. "Effects of insulin and insulin-like growth factor I on growth of human leukemia cells in serum-free and protein-free medium." Blood 72, no. 1 (1988): 66–72. http://dx.doi.org/10.1182/blood.v72.1.66.66.

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Abstract Human myeloid leukemia cells (HL60) and malignant lymphocytes (Namalwa) were grown in protein-free, Fe-supplemented media and used to study growth responses to insulin and insulin-like growth factor 1 (IGF-I). HL60 cells previously grown in serum-free medium containing microgram quantities of insulin showed an 18-fold reduction in cumulative cell production when grown without insulin. However, the same cells showed reduced or absent growth stimulation with 1 to 100 ng/mL insulin or IGF- I for at least four days following insulin deprivation, indicating that culture conditions modified

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11

Sinclair, J., D. McClain, and R. Taetle. "Effects of insulin and insulin-like growth factor I on growth of human leukemia cells in serum-free and protein-free medium." Blood 72, no. 1 (1988): 66–72. http://dx.doi.org/10.1182/blood.v72.1.66.bloodjournal72166.

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Human myeloid leukemia cells (HL60) and malignant lymphocytes (Namalwa) were grown in protein-free, Fe-supplemented media and used to study growth responses to insulin and insulin-like growth factor 1 (IGF-I). HL60 cells previously grown in serum-free medium containing microgram quantities of insulin showed an 18-fold reduction in cumulative cell production when grown without insulin. However, the same cells showed reduced or absent growth stimulation with 1 to 100 ng/mL insulin or IGF- I for at least four days following insulin deprivation, indicating that culture conditions modified insulin

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12

Meng, Fanyi, Xiaodong Li, Bingjie Ding, et al. "Molecular Mechanism and Optimal Treatment Strategy in Acute Myeloid Leukemia with Resistance to Drugs and Radiation By NVP-LED225." Blood 126, no. 23 (2015): 3691. http://dx.doi.org/10.1182/blood.v126.23.3691.3691.

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Abstract PURPOSE: Total body irradiation (TBI) combined with chemotherapy is currently the most effective procedure of traditional preparative myeloablative regimen. However, resistance to chemotherapy in refractory acute myeloid leukemia (AML) is associated with short-time recurrence after Allo-HSCT. To investigate the mechanism of Hedgehog signaling pathway resulting in resistance, we used primary AML cells originated in refractory patients and 3 cell lines including HL60, HL60/ADR (a adriamycin-resistant cells), and HL60/RX (a radiation-resistant cell line established from HL60) as cellular

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13

Pigazzi, M., E. Manara, E. Baron, A. Beghin, and G. Basso. "The inducible cyclic adenosine 3’,5’-monophosphate early repressor (ICER) enhances drug sensitivity in acute myeloid leukemia." Journal of Clinical Oncology 27, no. 15_suppl (2009): e22045-e22045. http://dx.doi.org/10.1200/jco.2009.27.15_suppl.e22045.

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e22045 Background: The Inducible Cyclic Adenosine 3’,5’-monophosphate early repressor (ICER) is a transcription factor that principally counteracts the cAMP response element binding protein (CREB) activity. CREB was previously demonstrated to be overexpressed in acute leukemia, whereas ICER was found rapidly degradated being unable to control gene transcription. ICER exogenous expression was demonstrated to repress CREB targets preventing leukemia progression. We hypothesized that ICER restoration deserves a special consideration for playing a role in CREB oncogenic feature and in modeling leu

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14

Chitambar, CR, and D. Sax. "Regulatory effects of gallium on transferrin-independent iron uptake by human leukemic HL60 cells." Blood 80, no. 2 (1992): 505–11. http://dx.doi.org/10.1182/blood.v80.2.505.505.

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Abstract Gallium, a pharmacologically important metal, resembles iron with respect to transferrin (Tf) binding and Tf receptor-mediated cellular uptake. In the present study, we examined the effect of gallium on Tf- independent iron uptake by HL60 cells. In contrast to the inhibitory effect of Tf-gallium on Tf-iron uptake, gallium nitrate, in a time-, temperature-, and concentration-dependent manner, stimulated Tf- independent uptake of iron-nitrilotriacetic acid (Fe-NTA). Preexposure of cells to gallium followed by removal of gallium also resulted in sustained stimulation of iron uptake. The

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15

Chitambar, CR, and D. Sax. "Regulatory effects of gallium on transferrin-independent iron uptake by human leukemic HL60 cells." Blood 80, no. 2 (1992): 505–11. http://dx.doi.org/10.1182/blood.v80.2.505.bloodjournal802505.

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Gallium, a pharmacologically important metal, resembles iron with respect to transferrin (Tf) binding and Tf receptor-mediated cellular uptake. In the present study, we examined the effect of gallium on Tf- independent iron uptake by HL60 cells. In contrast to the inhibitory effect of Tf-gallium on Tf-iron uptake, gallium nitrate, in a time-, temperature-, and concentration-dependent manner, stimulated Tf- independent uptake of iron-nitrilotriacetic acid (Fe-NTA). Preexposure of cells to gallium followed by removal of gallium also resulted in sustained stimulation of iron uptake. The anti-Tf r

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16

Ferreira, Carmen Veríssima, Carina L. Bos, Henri H. Versteeg, Giselle Z. Justo, Nelson Durán, and Maikel P. Peppelenbosch. "Molecular mechanism of violacein-mediated human leukemia cell death." Blood 104, no. 5 (2004): 1459–64. http://dx.doi.org/10.1182/blood-2004-02-0594.

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Abstract Violacein, a pigment isolated from Chromobacterium violaceum in the Amazon River, presents diverse biologic properties and attracts interest as a consequence of its antileukemic activity. Elucidation of the molecular mechanism mediating this activity will provide further relevant information for understanding its effects on the cellular physiology of untransformed cells and for considering its possible clinical application. Here, we show that violacein causes apoptosis in HL60 leukemic cells but is ineffective in this respect in other types of leukemia cells or in normal human lymphoc

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17

Nagy, L. I., L. Z. Fehér, G. J. Szebeni, et al. "Curcumin and Its Analogue Induce Apoptosis in Leukemia Cells and Have Additive Effects with Bortezomib in Cellular and Xenograft Models." BioMed Research International 2015 (2015): 1–11. http://dx.doi.org/10.1155/2015/968981.

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Combination therapy of bortezomib with other chemotherapeutics is an emerging treatment strategy. Since both curcumin and bortezomib inhibit NF-κB, we tested the effects of their combination on leukemia cells. To improve potency, a novel Mannich-type curcumin derivative, C-150, was synthesized. Curcumin and its analogue showed potent antiproliferative and apoptotic effects on the human leukemia cell line, HL60, with different potency but similar additive properties with bortezomib. Additive antiproliferative effects were correlated well with LPS-induced NF-κB inhibition results. Gene expressio

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18

Makaryan, Vahagn, Breanna Fletcher, Merideth L. Kelley, et al. "CRISPR/Cas9 Knock-in HL60 Cells Closely Simulate Cellular and Functional Abnormalities of ELANE associated Neutropenia; Phenotype Rescue with MK-0339 Neutrophil Elastase Inhibitor." Blood 132, Supplement 1 (2018): 3683. http://dx.doi.org/10.1182/blood-2018-99-113054.

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Abstract Background: Mutations in ELANE are the most common cause of both cyclic and severe congenital neutropenia. Congenital neutropenia is characterized by low neutrophil counts in peripheral blood and impaired survival and maturation of myeloid precursors in bone marrow. G-CSF and HSCT are currently the only effective treatment options. To date, more than 100 different ELANE mutations have been reported. We previously described that some mutations (e.g. G214R and C151Y) are associated with more severe outcomes, while others (e.g. P139L and R220Q) result in relatively mild clinical phenotyp

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Saran, Amit D., and Jayesh R. Bellare. "CdSe Quantum Dots Induce Cellular Differentiation in HL-60 Cells." Nanoscience & Nanotechnology-Asia 10, no. 2 (2020): 175–83. http://dx.doi.org/10.2174/2210681209666190211160721.

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Background: CdSe QDs, synthesized using a green micro-emulsion method, have been evaluated for their potential in inducing HL-60 differentiation by employing various biochemical assays and as cellular imaging agents. Methods: CdSe QDs have been found to effectively induce differentiation with lower rate of cell apoptosis as compared with the positive control (DMSO). Results: Our results exhibit effective induction of HL-60 differentiation by CdSe QDs implicating their therapeutic role in cancerous cells in addition to their usual application as cell-imaging agents. Conclusion: Our studies repo

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Zivny, Jan, Pavel Klener, Ondrej Toman, et al. "Proteomic and mRNA Expression Chip Analysis of Acquired TRAIL-Resistance in Human HL60 Myeloid Leukemia Cells." Blood 110, no. 11 (2007): 4155. http://dx.doi.org/10.1182/blood.v110.11.4155.4155.

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Abstract Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL or Apo2L) is a proapoptotic cytokine implicated in cancer cell surveillance. TRAIL induces apoptosis of target cells by the extrinsic, receptor-mediated, apoptotic pathway. A potential of TRAIL as cancer-specific therapeutic agent has been proposed, either as a single agent or in combination with chemotherapy agents. Development of TRAIL-resistant clones in the originally TRAIL-sensitive tumor cell population may be a critical complication of TRAIL based cancer therapy. Prolonged exposure of TRAIL-sensitive leukemia cell l

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Wildenhain, Sarah, Christian Ruckert, Svenja Daschkey, Martin Dugas, Julia Hauer, and Arndt Borkhardt. "ChIP-on-Chip Analysis Identified HLXB9 as a Transcription Factor In Hematopoietic Cells and Alters the Expression of Genes Involved In Cell-Adhesion." Blood 116, no. 21 (2010): 2486. http://dx.doi.org/10.1182/blood.v116.21.2486.2486.

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Abstract Abstract 2486 Infants with t (7;12)/HLXB9-TEL positive Acute Myeloid Leukemia (AML) have an Event-Free Survival (EFS) of 0 % and are characterized by concomitant HLXB9 (MNX1) expression. However, the role of the homeobox protein HLXB9 on hematopoietic cell development remains unknown. Expression profiling of t (7;12) and t (11;X) positive leukemias revealed up-regulation of cell-cell interacting genes in t (7;12) positive leukemia (Wildenhain et al., 2010). Furthermore, no increased expression of HOX-Genes, like HOXA9 and MEIS1, could be observed in t (7;12) positive leukemia compared

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Chitambar, CR, and Z. Zivkovic. "Release of soluble transferrin receptor from the surface of human leukemic HL60 cells." Blood 74, no. 2 (1989): 602–8. http://dx.doi.org/10.1182/blood.v74.2.602.602.

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Abstract Information regarding transferrin (Tf) receptor degradation is largely incomplete. HL60 cells were shown to release to their growth medium a Tf-binding protein which could be immunoprecipitated by anti-Tf receptor monoclonal antibodies (MoAbs) B3/25 and OKT9. Soluble Tf receptor was detected in the medium within one hour of replating of cells, and its release was inhibited at 4 degrees C. The affinity of Tf for the soluble receptor released by cells (kd = 2.3 x 10(-10) mol/L) was slightly lower than its affinity for the detergent-solubilized cellular receptor (kd = 1.2 x 10(-10) mol/L

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Chitambar, CR, and Z. Zivkovic. "Release of soluble transferrin receptor from the surface of human leukemic HL60 cells." Blood 74, no. 2 (1989): 602–8. http://dx.doi.org/10.1182/blood.v74.2.602.bloodjournal742602.

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Information regarding transferrin (Tf) receptor degradation is largely incomplete. HL60 cells were shown to release to their growth medium a Tf-binding protein which could be immunoprecipitated by anti-Tf receptor monoclonal antibodies (MoAbs) B3/25 and OKT9. Soluble Tf receptor was detected in the medium within one hour of replating of cells, and its release was inhibited at 4 degrees C. The affinity of Tf for the soluble receptor released by cells (kd = 2.3 x 10(-10) mol/L) was slightly lower than its affinity for the detergent-solubilized cellular receptor (kd = 1.2 x 10(-10) mol/L). 125I-T

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Sanchez-Gonzalez, Blanca, Hui Yang, Carlos Bueso-Ramos, et al. "Antileukemia activity of the combination of an anthracycline with a histone deacetylase inhibitor." Blood 108, no. 4 (2006): 1174–82. http://dx.doi.org/10.1182/blood-2005-09-008086.

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Abstract We studied the cellular and molecular effects of the combination of an anthracycline with 2 different histone deacetylase inhibitors (HDACIs): vorinostat (suberoylanilide hydroxamic acid) and valproic acid (VPA). The 10% inhibitory concentration (IC10) of idarubicin was 0.5 nM in MOLT4 and 1.5 nM in HL60 cells. Concentrations above 0.675 μM of vorinostat resulted in at least 80% loss of cell viability in both cell lines. Concentrations of 1.5 to 3 mM of VPA induced 50% to 60% loss in viability in HL60 and 80% in MOLT4 cells. The combination of idarubicin with vorinostat at 0.075 μM or

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Fischer, Cornelia, Brigitte Spath, Ali Amirkhosravi, Walter Fiedler, Carsten Bokemeyer, and Florian Langer. "Differential Effects of Protein Disulfide Isomerase (PDI) Inhibitors On the Expression of Tissue Factor Procoagulant Activity (TF PCA) by AML Blasts." Blood 120, no. 21 (2012): 1112. http://dx.doi.org/10.1182/blood.v120.21.1112.1112.

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Abstract Abstract 1112 Acute myelogenous leukemia (AML) may be complicated by DIC. TF plays a critical role in AML-associated coagulopathy, and induction of apoptosis significantly increases TF PCA on leukemic blasts, mainly via phosphatidylserine (PS) membrane exposure. However, PDI, a thiol isomerase with oxidoreductase and chaperone activity, has also been implicated in cellular TF regulation. Particularly, PDI inhibitors have been shown to exert antithrombotic activity in animal models. Besides its predominant localization in the endoplasmic reticulum, PDI is present on cell surfaces, wher

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Makaryan, Vahagn, Isabella N. Archibald, Merideth L. Kelley, Breanna Fletcher, and David C. Dale. "CRISPR/Cas9 Mediated ELANE Knock-out Restores Survival and Granulocytic Differentiation of HL60 Cells Expressing Mutant Neutrophil Elastase: Is Neutrophil Elastase a Dispensible Granulocyte Protease?" Blood 134, Supplement_1 (2019): 435. http://dx.doi.org/10.1182/blood-2019-124988.

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Background : Mutations in ELANE are the most common cause of both cyclic and severe congenital neutropenia. ELANE encodes neutrophil elastase (NE), a tissue specific serine protease expressed primarily in neutrophils. Expression of the mutant protein impairs survival and maturation of myeloid precursors in bone marrow. More than 130 different ELANE mutations have been found in patients with cyclic and congenital neutropenia, and genotype-phenotype studies suggest that specific mutations cause more severe disease. (Curr Op Hematol. 2015;22:3-11) Mutant NE is also implicated as the primary cause

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Kim, Ju Young, Hyun Ki Park, Jin Sun Yoon, et al. "Advanced Glycation End Products (AGEs)-Mediated Cell Growth of Human Acute Myelogenous Leukemia Via Mitogen-Activated Protein (MAP) Kinase Pathways." Blood 106, no. 11 (2005): 2762. http://dx.doi.org/10.1182/blood.v106.11.2762.2762.

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Abstract Advanced glycation end products (AGEs) are products of non-enzymatic glycation/oxidation of proteins/lipids that accumulate slowly during natural aging and at a much accelerated rate in a variety of disorders such as diabetes, renal failure, and Alzheimer’s disease. AGE modifications do not only change the physicochemical properties of the afflicted molecules, but also induce cellular signaling, activation of transcription factors and subsequent gene expression in vitro and in vivo. Most of the biologic activities associated with AGEs have been transduced by receptor for AGE (RAGE). R

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Youlyouz-Marfak, Ibtissam, Christophe Le Clorennec, Imen Najjar, et al. "Antitumor Genotoxic Agents, Such as Fludarabine*, Doxorubincin or Cis-Platine, Induce Activation of STAT1 in a p53 Protein Dependent Manner." Blood 106, no. 11 (2005): 4384. http://dx.doi.org/10.1182/blood.v106.11.4384.4384.

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Abstract Introduction: Chemotherapeutic drug such as Fludarabine*; doxorubicin or cis-platine induce cell cycle arrest and apoptosis via activation of p53. Convergent studies suggest that p53 and STAT1 cooperate in the induction of apoptosis, and that STAT1 favors p53 activation. However, to our knowledge, the role of p53 in the activation of STAT1 is not documented. We present our results suggesting that (i) genotoxic agents are STAT1 inducers, (ii) STAT1 activation depends on the presence of p53 protein, and (iii) this phenomenon is modulated by the tyrosine kinase inhibitor STI571. Material

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Robertson, K. A., E. S. Colvin, M. R. Kelley, and M. L. Fishel. "APX3330 inhibition of the redox function of ape-1/ref-1 (Ref-1) in promyelocytic leukemia cells enhances retinoic acid (ATRA) induced myeloid differentiation and limits cell proliferation as an approach to the prevention of the retinoic acid syndrome (RAS)." Journal of Clinical Oncology 27, no. 15_suppl (2009): e14613-e14613. http://dx.doi.org/10.1200/jco.2009.27.15_suppl.e14613.

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e14613 Background: ATRA + chemotherapy has improved the treatment of promyelocytic leukemia(APL). However, 25% of ATRA treated APL patients experience toxicities that comprise the RAS (life-threatening respiratory distress, edema, renal failure, hypotension, coagulopathy and rising blast count). One approach to prevent RAS is to limit blast proliferation and enhance myeloid differentiation. Ref-1 is a DNA repair protein that functions in redox regulation of cellular proteins, such as Fos, Jun, p53, and NFkB. HL60 myeloid leukemia cells are promyeloblasts that respond to ATRA with granulocytic

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Holt, S. E., W. E. Wright, and J. W. Shay. "Regulation of telomerase activity in immortal cell lines." Molecular and Cellular Biology 16, no. 6 (1996): 2932–39. http://dx.doi.org/10.1128/mcb.16.6.2932.

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Telomerase is a ribonucleoprotein whose activity has been detected in germ line cells, immortal cells, and most cancer cells. Except in stem cells, which have a low level of telomerase activity, its activity is absent from normal somatic tissues. Understanding the regulation of telomerase activity is critical for the development of potential tools for the diagnosis and treatment of cancer. Using the telomeric repeat amplification protocol, we found that immortal, telomerase-positive, pseudodiploid human cells (HT1080 and HL60 cells) sorted by flow repressed in quiescent cells. This was true wh

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Stuart, J. A., K. L. Anderson, P. J. French, C. J. Kirk, and R. H. Michell. "The intracellular distribution of inositol polyphosphates in HL60 promyeloid cells." Biochemical Journal 303, no. 2 (1994): 517–25. http://dx.doi.org/10.1042/bj3030517.

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1. HL60 promyeloid cells contain high intracellular concentrations of inositol polyphosphates, notably inositol 1,3,4,5,6-pentakisphosphate (InsP5) and inositol hexakisphosphate (InsP6). To determine their intracellular location(s), we studied the release of inositol (poly)phosphates, of ATP, and of cytosolic and granule-enclosed enzymes from cells permeabilized by four different methods. 2. When cells were treated with digitonin, all of the inositol phosphates were released in parallel with the cytosolic constituents. Most of the InsP5 and InsP6 was released before significant permeabilizatio

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Natarajan, Karthika, Mehmet Burcu, and Maria R. Baer. "Inhibition of the Serine/Threonine Kinase Pim-1 Has Anti-Proliferative Effects In Acute Myeloid Leukemia (AML) and Sensitizes Multidrug Resistant Cells to Chemotherapy." Blood 116, no. 21 (2010): 1832. http://dx.doi.org/10.1182/blood.v116.21.1832.1832.

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Abstract Abstract 1832 Poster Board I-812 The serine/threonine kinase Pim-1, encoded by a proto-oncogene originally identified as the proviral integration site in Moloney murine leukemia virus lymphomagenesis, phosphorylates and thereby increases expression of multiple cellular proteins, including the pro-apoptotic protein BAD, the cell cycle regulatory proteins p21, p27, Cdc25A and Cdc25C, the transcription factors SOCS-1, RUNX3 and c-myc and, as we recently demonstrated, the drug resistance-associated ATP-binding cassette (ABC) proteins P-glycoprotein (Pgp, ABCB1) and breast cancer resistanc

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Park, Jinny, Young-Rae Lee, Hyun-Jaung Shim, et al. "All Trans-Retinoic Acid (ATRA) in Combination with PPAR-g Ligand Synergistically Enhances Inhibition of Cell Growth and Induction of Tumor Suppressor PTEN in Leukemic Cells." Blood 104, no. 11 (2004): 4328. http://dx.doi.org/10.1182/blood.v104.11.4328.4328.

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Abstract Peroxisome proliferator-activated receptor-γ (PPAR-γ), a transcriptional factor that plays an essential role in mediating the pharmacologic actions of PPAR-γ ligands, is highly expressed in normal monocytes, various leukemias, and epithelial malignancies. PPAR-γ ligands have been developed to induce differentiation, growth arrest, and apoptosis. PPAR-γ must form a heterodimer with the retinoic acid receptor (RAR) to bind DNA, and its transcriptional activity is thought to be maximal in the presence of both PPAR-γ ligand and RAR ligand. Recently, it has been shown that activated PPAR-γ

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34

Jalal El-Din, Heba M., and Jasmeen S. Merzaban. "Towards a Targeted Therapy:Phosphoproteomics Reveals Signaling Pathways That Are Normalized in AML Cells Following Treatment with Anti-CD44 Antibodies." Blood 126, no. 23 (2015): 1402. http://dx.doi.org/10.1182/blood.v126.23.1402.1402.

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Abstract Acute myeloid leukemia (AML) is a clonal malignant disease characterized by a blockage in the differentiation of myeloid cells resulting in the accumulation of highly proliferating immature blast cells. With the success of All Trans Retinoic acid (ATRA) in acute promyelocytic leukemia (AML3), differentiation therapy has become a very attractive treatment option. Ligation of CD44 (a cell surface antigen) with anti-CD44 monoclonal antibodies (mAbs) is reported to reverse the blockage of differentiation and suppress the proliferation of blasts derived from most AML subtypes. However, the

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Charrad, Rachida-Sihem, Zeineb Gadhoum, Junyuan Qi, et al. "Effects of anti-CD44 monoclonal antibodies on differentiation and apoptosis of human myeloid leukemia cell lines." Blood 99, no. 1 (2002): 290–99. http://dx.doi.org/10.1182/blood.v99.1.290.

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Acute myeloid leukemia (AML) is a heterogeneous leukemia characterized by the blockage of myeloid differentiation at different stages, which define distinct AML subtypes. We have recently reported that the ligation of CD44 with 2 activating monoclonal antibodies (mAbs), A3D8 and H90, triggers terminal differentiation of leukemic blasts in AML-M1/2 to AML-M5 subtypes, which are the most frequent ones. However, fresh AML blasts have short in vitro lifespans. Therefore, to find relevant in vitro cellular models for further studying the mechanisms involved in CD44-induced differentiation, we inves

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36

MELLOR, Howard R., David C. A. NEVILLE, David J. HARVEY, Frances M. PLATT, Raymond A. DWEK, and Terry D. BUTTERS. "Cellular effects of deoxynojirimycin analogues: inhibition of N-linked oligosaccharide processing and generation of free glucosylated oligosaccharides." Biochemical Journal 381, no. 3 (2004): 867–75. http://dx.doi.org/10.1042/bj20031824.

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In the accompanying paper [Mellor, Neville, Harvey, Platt, Dwek and Butters (2004) Biochem. J. 381, 861–866] we treated HL60 cells with N-alk(en)yl-deoxynojirimycin (DNJ) compounds to inhibit glucosphingolipid (GSL) biosynthesis and identified a number of non-GSL-derived, small, free oligosaccharides (FOS) most likely produced due to inhibition of the oligosaccharide-processing enzymes α-glucosidases I and II. When HL60 cells were treated with concentrations of N-alk(en)ylated DNJ analogues that inhibited GSL biosynthesis completely, N-butyl- and N-nonyl-DNJ inhibited endoplasmic reticulum (ER

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37

Clément, Marie-Véronique, Jayshreekumari L. Hirpara, Sanaul-Haq Chawdhury, and Shazib Pervaiz. "Chemopreventive Agent Resveratrol, a Natural Product Derived From Grapes, Triggers CD95 Signaling-Dependent Apoptosis in Human Tumor Cells." Blood 92, no. 3 (1998): 996–1002. http://dx.doi.org/10.1182/blood.v92.3.996.

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Abstract Resveratrol, a constituent of grapes and other food products, has been shown to prevent carcinogenesis in murine models. We report here that resveratrol induces apoptotic cell death in HL60 human leukemia cell line. Resveratrol-treated tumor cells exhibit a dose-dependent increase in externalization of inner membrane phosphatidylserine and in cellular content of subdiploid DNA, indicating loss of membrane phospholipid asymmetry and DNA fragmentation. Resveratrol-induced cell death is mediated by intracellular caspases as observed by the dose-dependent increase in proteolytic cleavage

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38

Clément, Marie-Véronique, Jayshreekumari L. Hirpara, Sanaul-Haq Chawdhury, and Shazib Pervaiz. "Chemopreventive Agent Resveratrol, a Natural Product Derived From Grapes, Triggers CD95 Signaling-Dependent Apoptosis in Human Tumor Cells." Blood 92, no. 3 (1998): 996–1002. http://dx.doi.org/10.1182/blood.v92.3.996.415k23_996_1002.

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Resveratrol, a constituent of grapes and other food products, has been shown to prevent carcinogenesis in murine models. We report here that resveratrol induces apoptotic cell death in HL60 human leukemia cell line. Resveratrol-treated tumor cells exhibit a dose-dependent increase in externalization of inner membrane phosphatidylserine and in cellular content of subdiploid DNA, indicating loss of membrane phospholipid asymmetry and DNA fragmentation. Resveratrol-induced cell death is mediated by intracellular caspases as observed by the dose-dependent increase in proteolytic cleavage of caspas

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39

Smolarz, Helena D., Ewaryst Mendyk, Anna Bogucka-Kocka, and Janusz Kockic. "Pinostrobin – An Anti-Leukemic Flavonoid from Polygonum lapathifolium L. ssp. nodosum (Pers.) Dans." Zeitschrift für Naturforschung C 61, no. 1-2 (2006): 64–68. http://dx.doi.org/10.1515/znc-2006-1-212.

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Abstract Aim of study: Search for plant compounds possessing anti-leukemic properties. Results: We have shown that 5-hydroxy-7-methoxy flavanone (pinostrobin) isolated from Polygonum lapathifolium ssp. nodosum quickly penetrates through cytoplasm to the cellular nucleus of the cultured cells, and gives intensive apoptotic response in stimulating leukemic cells in vitro. The number of apoptotic cells increased with the concentration of pinostrobin: 10 nm D 25% and 60%; 100 nm D 45% and 76%; 1 μm D 70% and 88% for Jurkat and HL60 cell lines, respectively. Conclusion: Pinostrobin may be considere

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Meng, Fanyi, Xuejie Jiang, Kaikai Huang, Hongsheng Zhou, Mo Yang та Liu Xiaoli. "Synergistic Effect of Panobinostat and Bortezomib on Chemoresistant Acute Myelogenous Leukemia Cells Via Akt/NF-κB Pathway",. Blood 118, № 21 (2011): 3621. http://dx.doi.org/10.1182/blood.v118.21.3621.3621.

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Abstract Abstract 3621 Introduction: The mechanism of MDR (multiple drug resistance) in acute myelogenous leukemia (AML) is complicated. Activation of the phosphoinositide 3-kinase (PI3K)/Akt pathway plays a crucial role in cellular proliferation, survival and apoptosis in leukemia cells. Both histone deacetylase (HDAC) inhibitor and proteasome inhibitor have emerged as new kinds of therapeutic drugs against multiple myeloma (MM), their anti-tumor effects are later confirmed in other hematologic malignancies. Panobinostat, a novel HDAC inhibitor, can improve histone acetylation level and non-h

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Takeuchi, Toru, and Kanehisa Morimoto. "Crocidolite asbestos increased 8-hydroxydeoxyguanosine levels in cellular DNA of a human promyelocytic leukemia cell line, HL60." Carcinogenesis 15, no. 4 (1994): 635–39. http://dx.doi.org/10.1093/carcin/15.4.635.

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Hunt, Alan N., Alison J. Skippen, Grielof Koster, Anthony D. Postle та Shamshad Cockcroft. "Acyl chain-based molecular selectivity for HL60 cellular phosphatidylinositol and of phosphatidylcholine by phosphatidylinositol transfer protein α". Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biology of Lipids 1686, № 1-2 (2004): 50–60. http://dx.doi.org/10.1016/j.bbalip.2004.08.003.

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43

Wadelin, Frances R., Keith A. Spriggs, Franco H. Falcone, and David M. Heery. "Transcriptional and Translational Regulation of the Cancer-Testis Antigen PRAME Mediated by Pathogen-Associated Molecular Patterns." Blood 116, no. 21 (2010): 2475. http://dx.doi.org/10.1182/blood.v116.21.2475.2475.

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Abstract Abstract 2475 PRAME (preferentially expressed antigen in melanoma) is a germinal tissue-specific gene that is expressed at high levels in a number of haematological malignancies. In AML, PRAME is a positive prognostic indicator, being associated with a favourable response to chemotherapy and increased overall survival, even in the presence of unfavourable karyotypes. In contrast, over-expression of PRAME mRNA is associated with poor prognosis in CML, NHL, HD, CLL and myeloma, being associated with progressive disease and chemo-resistance. Despite proposals to implement PRAME as a tool

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Niewiarowski, W., E. Gendaszewska, G. Rebowski, et al. "Multidrug resistance-associated protein--reduction of expression in human leukaemia cells by antisense phosphorothioate olignucleotides." Acta Biochimica Polonica 47, no. 4 (2000): 1183–88. http://dx.doi.org/10.18388/abp.2000_3971.

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Multidrug resistance-associated protein (MRP1) causes cellular drug resistance in several cancer cell lines. In this paper we show that antisense oligonucleotides decrease MRP1 expression in human leukaemia cells. We investigated biological activity of a series of 12 linear phosphorothioate oligonucleotides, complementary to several regions of MRP1 mRNA. The oligonucleotides were administered to leukaemia HL60/ADR cells overexpressing MRP1 protein. Then, the level of MRP1 mRNA was determined by means of semiquantitative RT-PCR and the protein level by reaction with specific monoclonal antibodi

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Chakraborty, A., SM White, TS Schaefer, ED Ball, KF Dyer, and DJ Tweardy. "Granulocyte colony-stimulating factor activation of Stat3 alpha and Stat3 beta in immature normal and leukemic human myeloid cells." Blood 88, no. 7 (1996): 2442–49. http://dx.doi.org/10.1182/blood.v88.7.2442.bloodjournal8872442.

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Granulocyte colony-stimulating factor (G-CSF) is the cytokine critical for directing neutrophilic granulocyte differentiation. Acute myelogenous leukemia (AML) cells, which frequently arise from this lineage, respond aberrantly to G-CSF by proliferating without differentiating. The basis for this abnormal responses is unknown. In the present study, we investigated whether G-CSF signaling in immature normal and leukemic human myeloid cells diverges at the level of activation of signal transducers and activators of transcription (STAT) proteins. We compared the profile of STAT proteins activated

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Wang, Zhixiang, Xuejie Jiang, Kaikai Huang, et al. "Decitabine Act As Demethylation Modulators in Acute Myeloid Leukemia for Reversal of Drug Resistance." Blood 124, no. 21 (2014): 5218. http://dx.doi.org/10.1182/blood.v124.21.5218.5218.

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Abstract Background and objectives The DNA methyltransferase inhibitors decitabine represent archetypal drugs for epigenetic cancer therapy. One alternative approach for the treatment of (Acute Myelocytic Leukemia) AML is the use of hypomethylating agents, including the 5-aza-2-deoxycytidine (decitabine; DAC) and other epigenetic regulators. However, the exact mechanism of DAC for drug resistance AML remains poorly understood. We conducted this study to explore how DAC regulated the sensitivity to adriamycin and aclacinomycin of AML cell line HL60/ADR and assessed the efficacy and safety of de

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Barker, C. J., P. J. French, A. J. Moore, et al. "Inositol 1,2,3-trisphosphate and inositol 1,2- and/or 2,3-bisphosphate are normal constituents of mammalian cells." Biochemical Journal 306, no. 2 (1995): 557–64. http://dx.doi.org/10.1042/bj3060557.

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1. An inositol trisphosphate (InsP3) distinct from Ins(1,4,5)P3 and Ins(1,3,4)P3, which we previously observed in myeloid and lymphoid cells [French, Bunce, Stephens, Lord, McConnell, Brown, Creba and Michell (1991) Proc R. Soc. London B 245, 193-201; Bunce, French, Allen, Mountford, Moore, Greaves, Michell and Brown (1993) Biochem. J. 289, 667-673], is present in WRK1 rat mammary tumour cells and pancreatic endocrine beta-cells. 2. It has been identified as Ins(1,2,3)P3 by a combination of oxidation to ribitol, a structurally diagnostic polyol, and ammoniacal hydrolysis to identified inositol

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Makaryan, Vahagn, Merideth L. Kelley, Breanna Fletcher, and David C. Dale. "The Effects of the Neutrophil Elastase Inhibitors MK0339 and Sivelestat on the Survival, Proliferation and Maturation of iPSC and HL60 Cells Expressing Mutant Neutrophil Elastase." Blood 128, no. 22 (2016): 406. http://dx.doi.org/10.1182/blood.v128.22.406.406.

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Abstract Background : Mutations in ELANE, the gene for neutrophil elastase (NE), are the most frequent cause of both cyclic neutropenia (CyN) and severe congenital neutropenia (SCN). G-CSF and HSCT are currently the only effective treatment options. We have examined the possibility that inhibitors of NE might also be treatment options. Methods: Cells: HL60 human promyelocytic cells, a commercially available cell line, and induced pluripotent stem cells (iPSc) derived from patient dermal fibroblasts or bone marrow stromal cells, reprogrammed using episomal vectors. NE inhibitors: Two cell perme

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Ozpolat, Bulent, Ugur Akar, Nancy H. Colburn, and Gabriel Lopez-Berestein. "Novel Tumor Suppressor Protein Programmed Cell Death 4 (PDCD4) Suppresses Activity of PI3K/Akt Pathway and Regulates Expression of p27 (Kip1) and c-myc, DAP5 and Willm’s Tumor (WT1) in Acute Myeloid Leukemia." Blood 110, no. 11 (2007): 2656. http://dx.doi.org/10.1182/blood.v110.11.2656.2656.

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Abstract Programmed cell death 4 (PDCD4) is a recently identied novel tumor suppressor protein that inhibits cap-dependent mRNA translation. PDCD4 inhibits tumor promoter incuced carcinogenesis and transformation by suppressing the helicase activity of eIF4A, leading to translational inhibition. Recently we found that PDCD4 is required for all-trans-retinoic acid (ATRA)-induced granulocytic differentiation of acute promyelocytic leukemia (APL) cells (Ozpolat&Akar et al, Mol Cancer Res, in press), type of acute myeloid leukemia characterized by a t(15;17) and a differentiation block. Here w

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Pawarode, Attaphol, Kieran L. O’Loughlin, Nicholas W. Cuviello, et al. "The mTOR Inhibitor Rapamycin Inhibits Drug Transport in Multidrug Resistant Cell Lines and in Acute Myeloid Leukemia (AML) Cells." Blood 106, no. 11 (2005): 1512. http://dx.doi.org/10.1182/blood.v106.11.1512.1512.

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Abstract Mechanisms of drug resistance in acute myeloid leukemia (AML) include cellular drug efflux mediated by the multidrug resistance (MDR)-associated ATP-binding cassette (ABC) proteins P-glycoprotein (Pgp), multidrug resistance protein-1 (MRP-1) and breast cancer resistance protein (BCRP) and impaired cytoplasmic-nuclear drug transport mediated by the major vault protein lung resistance protein (LRP), as well as aberrant signal transduction due to activation of the mammalian target of rapamycin (mTOR) and other signaling molecules. Rapamycin has antiproliferative effects in AML by virtue

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