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Journal articles on the topic 'Apoptosis. Acute myeloid leukemia'

Author: Grafiati

Published: 4 June 2021

Last updated: 13 February 2022

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1

Dimitroulakos, Jim, Dana Nohynek, Karen L. Backway, et al. "Increased Sensitivity of Acute Myeloid Leukemias to Lovastatin-Induced Apoptosis: A Potential Therapeutic Approach." Blood 93, no. 4 (1999): 1308–18. http://dx.doi.org/10.1182/blood.v93.4.1308.

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Abstract We recently demonstrated that 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase, the rate-limiting enzyme of de novo cholesterol synthesis, was a potential mediator of the biological effects of retinoic acid on human neuroblastoma cells. The HMG-CoA reductase inhibitor, lovastatin, which is used extensively in the treatment of hypercholesterolemia, induced a potent apoptotic response in human neuroblastoma cells. This apoptotic response was triggered at lower concentrations and occurred more rapidly than had been previously reported in other tumor-derived cell lines, including

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2

Dimitroulakos, Jim, Dana Nohynek, Karen L. Backway, et al. "Increased Sensitivity of Acute Myeloid Leukemias to Lovastatin-Induced Apoptosis: A Potential Therapeutic Approach." Blood 93, no. 4 (1999): 1308–18. http://dx.doi.org/10.1182/blood.v93.4.1308.404k08_1308_1318.

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We recently demonstrated that 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase, the rate-limiting enzyme of de novo cholesterol synthesis, was a potential mediator of the biological effects of retinoic acid on human neuroblastoma cells. The HMG-CoA reductase inhibitor, lovastatin, which is used extensively in the treatment of hypercholesterolemia, induced a potent apoptotic response in human neuroblastoma cells. This apoptotic response was triggered at lower concentrations and occurred more rapidly than had been previously reported in other tumor-derived cell lines, including breast a

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3

Xiong, Jie, Xingyi Kuang, Tingting Lu, et al. "The Crucial Role of NR4A1 Dependent Apoptosis Induced By Fenretinide in Acute Myeloid Leukemia." Blood 132, Supplement 1 (2018): 5266. http://dx.doi.org/10.1182/blood-2018-99-117776.

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Abstract OBJECTIVE: NR4A1 is a member of the orphan nuclear receptor family, which is involved in biological processes such as cell proliferation, apoptosis, metabolism, and differentiation. The expression of NR4A1 is increased in a variety of solid tumors, which promotes oncogenesis and enhances the viability of tumor cells. However, in hematological malignancies, its expression is significantly lower than normal. Studies have shown that clearance of NR4A1 can lead to the progression of mice to acute myeloid leukemia, reducing the amount of NR4A gene expression can make mice progress to MDS /

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4

Testa, U., and R. Riccioni. "Deregulation of apoptosis in acute myeloid leukemia." Haematologica 92, no. 1 (2007): 81–94. http://dx.doi.org/10.3324/haematol.10279.

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5

Del Principe, Maria Ilaria, Giovanni Del Poeta, Adriano Venditti, et al. "Apoptosis and immaturity in acute myeloid leukemia." Hematology 10, no. 1 (2005): 25–34. http://dx.doi.org/10.1080/10245330400020454.

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6

Strati, Paolo, Courtney DiNardo, Naval Daver, Michael Andreeff, and Marina Konopleva. "Targeting Apoptosis Pathways in Acute Myeloid Leukemia." Clinical Lymphoma Myeloma and Leukemia 19 (September 2019): S53—S54. http://dx.doi.org/10.1016/j.clml.2019.07.417.

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7

de Melo Silva, Alex José. "Bcl-2 Family Overexpression and Chemoresistance in Acute Myeloid Leukemia." Serbian Journal of Experimental and Clinical Research 19, no. 4 (2018): 299–309. http://dx.doi.org/10.2478/sjecr-2018-0064.

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Abstract The family of Bcl-2 proteins is one of the most responsible for apoptosis pathway, that is a critical process to the maintenance of tissue homeostasis. Bcl-2 is an essential apoptotic regulator belonging to a family of functionally and structurally related proteins known as the Bcl-2 family. Some members of this family act as anti-apoptotic regulators, whereas others act in pro-apoptotic function. The relationship between the pro and anti-apoptotic proteins can regulate whether cells begin the apoptosis or remain its life cycle. Increasing of Bcl-2 expression has been found in some he

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8

Shah, Mithun Vinod, Karen S. Flatten, B. Douglas Smith, Allan D. Hess, and Scott H. Kaufmann. "MTH1 Inhibitor-Induced Cytotoxicity in Acute Myeloid Leukemia." Blood 126, no. 23 (2015): 1273. http://dx.doi.org/10.1182/blood.v126.23.1273.1273.

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Abstract BACKGROUND: Acute myeloid leukemia (AML) is an aggressive leukemia with 5-year overall survival of 20-25%. The major reason for treatment failure in AML is resistance to chemotherapy. Thus, there is an urgent need for identification of novel therapeutic agents for AML. Neoplastic cells, including AML, have dysfunctional redox regulation that results in increased reactive oxygen species (ROS). Accumulation of ROS leads to oxidation of free and incorporated nucleotides, leading to DNA damage and cell death. MTH1 is a nudix family hydrolase that sanitizes the oxidized nucleotide pool to

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9

Garzon, Ramiro, Catherine E. A. Heaphy, Violaine Havelange, et al. "MicroRNA 29b functions in acute myeloid leukemia." Blood 114, no. 26 (2009): 5331–41. http://dx.doi.org/10.1182/blood-2009-03-211938.

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Abstract MicroRNAs (miRNAs) are associated with cytogenetics and molecular subtypes of acute myelogeneous leukemia (AML), but their impact on AML pathogenesis is poorly understood. We have previously shown that miR-29b expression is deregulated in primary AML blasts. In this work, we investigated the functional role of miR-29b in leukemogenesis. Restoration of miR-29b in AML cell lines and primary samples induces apoptosis and dramatically reduces tumorigenicity in a xenograft leukemia model. Transcriptome analysis after ectopic transfection of synthetic miR-29b into leukemia cells indicates t

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10

Roma, Alessia, Sarah G. Rota, and Paul A. Spagnuolo. "Diosmetin Induces Apoptosis of Acute Myeloid Leukemia Cells." Molecular Pharmaceutics 15, no. 3 (2018): 1353–60. http://dx.doi.org/10.1021/acs.molpharmaceut.7b01151.

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11

Rosso, Valentina, Cristina Panuzzo, Jessica Petiti, et al. "Reduced Expression of Sprouty1 Contributes to the Aberrant Proliferation and Impaired Apoptosis of Acute Myeloid Leukemia Cells." Journal of Clinical Medicine 8, no. 7 (2019): 972. http://dx.doi.org/10.3390/jcm8070972.

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In most of the acute myeloid leukemia patients there is an aberrant tyrosine kinase activity. The prototype of Sprouty proteins was originally identified in Drosophila melanogaster as antagonists of Breathless, the mammalian ortholog of fibroblast growth factor receptor. Usually, SPRY family members are inhibitors of RAS signaling induced by tyrosine kinases receptors and they are implicated in negative feedback processes regulating several intracellular pathways. The present study aims to investigate the role of a member of the Sprouty family, Sprouty1, as a regulator of cell proliferation an

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12

Valentin, Rebecca, Stephanie Grabow, and Matthew S. Davids. "The rise of apoptosis: targeting apoptosis in hematologic malignancies." Blood 132, no. 12 (2018): 1248–64. http://dx.doi.org/10.1182/blood-2018-02-791350.

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Abstract Dysregulation of the B-cell leukemia/lymphoma-2 (BCL-2) family of proteins of the intrinsic apoptotic pathway is fundamental to the pathophysiology of many hematologic malignancies. The BCL-2 family consists of regulatory proteins that either induce apoptosis (proapoptotic) or inhibit it (prosurvival). BCL-2, myeloid cell leukemia-1, and B-cell lymphoma–extra large are prosurvival proteins that are prime targets for anticancer therapy, and molecules targeting each are in various stages of preclinical and clinical development. The US Food and Drug Administration (FDA)-approved BCL-2 in

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13

Yuk, Yen Ju, Young Jin Seo, Hyoung Jin Kang, et al. "Hypoxia Suppresses Arsenic Trioxide-Induced Apoptosis in Human Acute Myeloid Leukemia Cells." Blood 114, no. 22 (2009): 3109. http://dx.doi.org/10.1182/blood.v114.22.3109.3109.

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Abstract Abstract 3109 Poster Board III-46 Acute myeloid leukemia (AML) is a class of prevalent hematopoietic malignancies, which often remains incurable because of the development of drug resistance. Leukemic cells originated from hypoxic condition in bone marrow that gives a benefit to leukemic cells by protecting them from anti-cancer drugs through physical barrier and by induction of some survival signal mediators. As the development of drug resistance is a key element in the failure of chemotherapy for leukemia, it has been studied about many factors make leukemic cells resist to chemothe

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14

Mazar, Julia, Alexandra Lichtenstein, Leora Katz, Ofer Shpilberg, Itai Levi, and Ilana Nathan. "TPCK Induces Apoptosis in Human Acute Myeloid Leukemia U-937 Cells." Blood 104, no. 11 (2004): 4478. http://dx.doi.org/10.1182/blood.v104.11.4478.4478.

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Abstract Many types of antitumor therapy in general and AML in particular exert their effect by activating apoptosis. Apoptosis of AML cells can be induced by cytostatic drugs, corticosteroids, and radiation. Recently, the role of different proteases as possible targets for chemotherapy was described. N-tosyl-L-phenylalanine chloromethyl ketone (TPCK), a chymotrypsin-like protease (CLP) inhibitor was shown to exert a dual effect on leukemic cells: proapoptotic and antiapoptotic. In the present study the mechanism of its proapoptotic effect was addressed. It was found that the CLP inhibitors, T

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15

Pan, Pan, and Xiao Chen. "Nuclear Receptors as Potential Therapeutic Targets for Myeloid Leukemia." Cells 9, no. 9 (2020): 1921. http://dx.doi.org/10.3390/cells9091921.

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The nuclear receptor (NR) superfamily has been studied extensively in many solid tumors and some receptors have been targeted to develop therapies. However, their roles in leukemia are less clear and vary considerably among different types of leukemia. Some NRs participate in mediating the differentiation of myeloid cells, making them attractive therapeutic targets for myeloid leukemia. To date, the success of all-trans retinoic acid (ATRA) in treating acute promyelocytic leukemia (APL) remains a classical and unsurpassable example of cancer differentiation therapy. ATRA targets retinoic acid

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16

Konopleva, Marina, Twee Tsao, Peter Ruvolo, et al. "Novel triterpenoid CDDO-Me is a potent inducer of apoptosis and differentiation in acute myelogenous leukemia." Blood 99, no. 1 (2002): 326–35. http://dx.doi.org/10.1182/blood.v99.1.326.

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It has been shown that the novel synthetic triterpenoid CDDO inhibits proliferation and induces differentiation and apoptosis in myeloid leukemia cells. In the current study the effects of the C-28 methyl ester of CDDO, CDDO-Me, were analyzed on cell growth and apoptosis of leukemic cell lines and primary acute myelogenous leukemia (AML). CDDO-Me decreased the viability of leukemic cell lines, including multidrug resistant (MDR)-1–overexpressing, p53null HL-60-Dox and of primary AML cells, and it was 3- to 5-fold more active than CDDO. CDDO-Me induced a loss of mitochondrial membrane potential

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17

Xie, Jingjing, Zhigang Lu, and Chengcheng Zhang. "KBP-1 Supports Acute Myeloid Leukemia Development." Blood 126, no. 23 (2015): 1378. http://dx.doi.org/10.1182/blood.v126.23.1378.1378.

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Abstract Novel targets are needed to develop effective therapeutic approaches to treat acute myeloid leukemia (AML). We have developed a systematic strategy to identify factors important for leukemia development. We first use clinical databases to identify plasma membrane proteins that have correlations with the clinical outcomes of leukemia patients. We then validate the functions of candidate proteins in leukemia models and compare these functions to those in normal cells. The signaling pathways identified provide candidate targets for development of therapeutic approaches. Using this approa

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18

Lam, Wilbur A., Michael J. Rosenbluth, and Daniel A. Fletcher. "Chemotherapy Exposure Decreases Leukemia Cell Deformability as Determined by Atomic Force Microscopy: Implications for Leukostasis in Acute Leukemia." Blood 108, no. 11 (2006): 2359. http://dx.doi.org/10.1182/blood.v108.11.2359.2359.

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Abstract Leukostasis, a life-threatening complication of acute leukemia, occurs when leukemia cells obstruct the circulation of vital organs like the brain and lungs leading to intracranial hemorrhage or respiratory failure. Although the pathophysiology of leukostasis is poorly understood, an elevated concentration of circulating leukemia cells, pathologic adhesion, and decreased cell deformability are thought to play significant roles. Clinical deterioration can occur soon after chemotherapy is initiated, suggesting that chemotherapy itself may be a risk factor for leukostasis. To investigate

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19

Stone, Richard M., Margaret R. O'Donnell, and Mikkael A. Sekeres. "Acute Myeloid Leukemia." Hematology 2004, no. 1 (2004): 98–117. http://dx.doi.org/10.1182/asheducation-2004.1.98.

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Abstract Advances in our understanding of the pathophysiology of acute myeloid leukemia (AML) have not yet led to major improvements in disease-free and overall survival of adults with this disease. Only about one-third of those between ages 18–60 who are diagnosed with AML can be cured; disease-free survival is rare and current therapy devastating in older adults. In this chapter, challenges in the management of the adult with AML are discussed, including ongoing questions concerning the optimal choice of induction and postremission therapy such as the rationale for and role of allogeneic and

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20

Dai, Yun, Shuang Chen, Li Wang, et al. "Bortezomib Interacts Synergistically with Belinostat to Induce Apoptosis In Human Acute Myeloid and Lymphoid Leukemia Cells." Blood 116, no. 21 (2010): 3266. http://dx.doi.org/10.1182/blood.v116.21.3266.3266.

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Abstract Abstract 3266 Previous studies have demonstrated interactions between histone deacetylase (HDAC) and proteasome inhibitors (PIs) in multiple myeloma, NHL, and CLL. However, exploration of this strategy in acute leukemias has been more limited. In this context, we have previously demonstrated that HDACIs activate the cytoprotective NF-κB pathway in acute myeloid leukemia (AML) cells, and that interruption of this process dramatically increases lethality. Such findings raise the possibility that PIs, which block degradation of the NF-κB-inhibitory protein IκBα, may act via an analogous

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21

Hsieh, Yao-Te, Enzi Jiang, Jennifer Pham, et al. "VLA4 Blockade In Acute Myeloid Leukemia." Blood 122, no. 21 (2013): 3944. http://dx.doi.org/10.1182/blood.v122.21.3944.3944.

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Abstract Despite aggressive chemotherapy and early allogeneic transplantation, acute myeloid leukemia (AML) frequently relapses, so that over-all disease-free survival remains below 50%. Strategies to overcome the chemoresistance of relapse-initiating residual AML blasts are, therefore, warranted. Evidence has been provided that AML cells are sheltered from the insult of chemotherapeutic agents by interacting with bone marrow stroma. Integrin alpha4beta1 (VLA4) mediates adhesion of hematopoietic cells to bone marrow stroma cells and extracellular matrix and has been implicated in cell adhesion

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22

Opydo-Chanek, Małgorzata, Iwona Cichoń, Agnieszka Rak, Elżbieta Kołaczkowska, and Lidia Mazur. "The pan-Bcl-2 inhibitor obatoclax promotes differentiation and apoptosis of acute myeloid leukemia cells." Investigational New Drugs 38, no. 6 (2020): 1664–76. http://dx.doi.org/10.1007/s10637-020-00931-4.

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Summary One of the key features of acute myeloid leukemia (AML) is the arrest of differentiation at the early progenitor stage of myelopoiesis. Therefore, the identification of new agents that could overcome this differentiation block and force leukemic cells to enter the apoptotic pathway is essential for the development of new treatment strategies in AML. Regarding this, herein we report the pro-differentiation activity of the pan-Bcl-2 inhibitor, obatoclax. Obatoclax promoted differentiation of human AML HL-60 cells and triggered their apoptosis in a dose- and time-dependent manner. Importa

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23

Kogan, Scott C., Diane E. Brown, David B. Shultz та ін. "Bcl-2 Cooperates with Promyelocytic Leukemia Retinoic Acid Receptor α Chimeric Protein (Pmlrarα) to Block Neutrophil Differentiation and Initiate Acute Leukemia". Journal of Experimental Medicine 193, № 4 (2001): 531–44. http://dx.doi.org/10.1084/jem.193.4.531.

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The promyelocytic leukemia retinoic acid receptor α (PMLRARα) chimeric protein is associated with acute promyelocytic leukemia (APL). PMLRARα transgenic mice develop leukemia only after several months, suggesting that PMLRARα does not by itself confer a fully malignant phenotype. Suppression of apoptosis can have a central role in tumorigenesis; therefore, we assessed whether BCL-2 influenced the ability of PMLRARα to initiate leukemia. Evaluation of preleukemic animals showed that whereas PMLRARα alone modestly altered neutrophil maturation, the combination of PMLRARα and BCL-2 caused a marke

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24

Lück, Sonja C., Annika C. Russ, Konstanze Döhner, et al. "Deregulated Apoptotic Pathways Point to Effectiveness of IAP Inhibitor Therapy in Acute Myeloid Leukemia." Blood 114, no. 22 (2009): 1275. http://dx.doi.org/10.1182/blood.v114.22.1275.1275.

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Abstract Abstract 1275 Poster Board I-297 Core binding factor (CBF) leukemias, characterized by translocations t(8;21) or inv(16)/t(16;16) targeting the core binding factor, constitute acute myeloid leukemia (AML) subgroups with favorable prognosis. However, 40-50% of patients relapse, and the current classification system does not fully reflect the heterogeneity existing within the cytogenetic subgroups. Therefore, illuminating the biological mechanisms underlying these differences is important for an optimization of therapy. Previously, gene expression profiling (GEP) revealed two distinct C

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Pomares, Helena, Claudia M. Palmeri, Daniel Iglesias-Serret, et al. "Targeting prohibitins induces apoptosis in acute myeloid leukemia cells." Oncotarget 7, no. 40 (2016): 64987–5000. http://dx.doi.org/10.18632/oncotarget.11333.

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26

Ball, Somedeb, and Gautam Borthakur. "Apoptosis targeted therapies in acute myeloid leukemia: an update." Expert Review of Hematology 13, no. 12 (2020): 1373–86. http://dx.doi.org/10.1080/17474086.2020.1852923.

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27

Pigneux, Arnaud, Maïalen Uhalde, François X. Mahon, et al. "Triptolide Cooperates with Cytarabine To Induce Apoptosis in Acute Myeloid Leukemia." Blood 108, no. 11 (2006): 1902. http://dx.doi.org/10.1182/blood.v108.11.1902.1902.

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Abstract Triptolide, a diterpene triepoxide isolated from the Chinese herb Tripterygium wilfordii Hook.f, has shown antitumor activity in a broad range of solid tumors and on leukemic cells in vitro. Here, we examined its pro-apoptotic effects on THP1 myeloid cell line and primay AML blasts in association with cytarabine. THP1 cells were treated with increasing concentrations of Ara-C in the presence or not of Triptolide (5 ng/ml). Apoptosis was measured by flow cytometry at the mitochondrial level by using the ΔΨm sensitive probe DiOC6(3). This low dose of Triptolide did not induce any apopto

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28

Mirabilii, Simone, Maria Rosaria Ricciardi, Matteo Allegretti, et al. "Modulation Of The Glycolytic Metabolism In Acute Myeloid Leukemia Cells." Blood 122, no. 21 (2013): 5045. http://dx.doi.org/10.1182/blood.v122.21.5045.5045.

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Abstract Glycolysis is the central axis of cellular metabolism. The cancer cell bioenergetic status heavily relies on high glycolytic rates, even in aerobic conditions, thus sustaining the expensive processes of cell growth and proliferation. Growing evidences show that signaling aberrations - especially those involving PI3K/Akt/mTOR, HIF1a, Ras/Raf/MEK/ERK - are strictly connected to the establishment of a pro-glycolytic metabolism, through a multi-level crosstalk between proteins and metabolites that contribute to the acquisition of an energetic background granting a proliferative advantage.

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Hess, Corine J., Johannes Berkhof, Fedor Denkers, et al. "New Insights in Mechanims Involved in Apoptosis Resistance in Acute Myeloid Leukemia." Blood 106, no. 11 (2005): 1215. http://dx.doi.org/10.1182/blood.v106.11.1215.1215.

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Abstract Defects in apoptotic mechanisms play an important role in chemotherapy resistance in AML, resulting in either refractoriness or high levels of Minimal Residual Disease (MRD) ultimately leading to relapse. For that reason the search for prognostic markers has focused on genes involved in apoptosis. At present the general concept encompasses a balance between pro- and anti apoptotic family members, but few studies have addressed large sets of genes. We tried to identify gene-profiles with maximal predictive power for patient survival by simultaneous quantification of 35 apoptosis relate

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Kojima, Kensuke, Steven M. Kornblau, Vivian Ruvolo, et al. "Prognostic Impact and Targeting of CRM1 in Acute Myeloid Leukemia." Blood 120, no. 21 (2012): 870. http://dx.doi.org/10.1182/blood.v120.21.870.870.

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Abstract Abstract 870 p53 is a transcription factor that prevents abnormal cell growth. Cellular levels of p53 are critically regulated by MDM2, which is frequently over-expressed in AML. Nutlin-3a disrupts MDM2-p53 interaction, increases cellular levels of p53 in both nucleus and cytoplasm, and activates p53 signaling in cells. p53 status is the major determinant of response to MDM2 inhibitors. p53 is shuttled between the nucleus and the cytoplasm, and CRM1 mediates its nuclear export. Karyopharm Therapeutics has developed novel, potent and irreversible small molecule selective inhibitors of

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31

Yang, Mingzhen, Xiaoyu Zhang, Zhenqi Huang, Qingsheng Li, Lin Wang, and Qinhua Liu. "The Apoptosis of Acute Myeloid Leukemia Cell Line (SHI-1 cells) Induced by Bortezomib In Vitro." Blood 116, no. 21 (2010): 4382. http://dx.doi.org/10.1182/blood.v116.21.4382.4382.

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Abstract Abstract 4382 Background: The proteasome plays a critical role in the regulation of many cellular processes, including the cell cycle and tumor growth. The proteasome inhibitor Bortezomib has been used in multiple myeloma and other lymphoid malignancies because of its antitumor activity. Here we investigated the induction of apoptosis by proteasome inhibitor Bortezomib in human acute myeloid leukemia (AML) cell lines SHI-1 cells and try to explore the mechanism of anti-leukemia. Method: We incubated SHI-1 leukemic cells with different concentration of bortezomib. cell proliferation wa

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Radomska, Hanna S., Finith Jernigan, Sohei Nakayama, et al. "A Cell-Based High-Throughput Screening for Inducers of Myeloid Differentiation." Journal of Biomolecular Screening 20, no. 9 (2015): 1150–59. http://dx.doi.org/10.1177/1087057115592220.

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Recent progress of genetic studies has dramatically unveiled pathogenesis of acute myeloid leukemia (AML). However, overall survival of AML still remains unsatisfactory, and development of novel therapeutics is required. CCAAT/enhancer binding protein α (C/EBPα) is one of the crucial transcription factors that induce granulocytic differentiation, and its activity is perturbed in human myeloid leukemias. As its reexpression can induce differentiation and subsequent apoptosis of leukemic cells in vitro, we hypothesized that chemical compounds that restore C/EBPα expression and/or activity would

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San José-Enériz, Gimenez-Camino, Agirre, and Prosper. "HDAC Inhibitors in Acute Myeloid Leukemia." Cancers 11, no. 11 (2019): 1794. http://dx.doi.org/10.3390/cancers11111794.

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Acute myeloid leukemia (AML) is a hematological malignancy characterized by uncontrolled proliferation, differentiation arrest, and accumulation of immature myeloid progenitors. Although clinical advances in AML have been made, especially in young patients, long-term disease-free survival remains poor, making this disease an unmet therapeutic challenge. Epigenetic alterations and mutations in epigenetic regulators contribute to the pathogenesis of AML, supporting the rationale for the use of epigenetic drugs in patients with AML. While hypomethylating agents have already been approved in AML,

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Rosen, David B., M. D. Minden, Santosh Putta, et al. "Classification of Acute Myeloid Leukemia (AML) Based On Apoptosis and Myeloid Signaling Networks." Blood 114, no. 22 (2009): 325. http://dx.doi.org/10.1182/blood.v114.22.325.325.

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Abstract Abstract 325 Background: Acute Myeloid Leukemia (AML) is the most common myeloid malignancy in adults and represents an aggressive disease with significant biological and clinical heterogeneity. Currently, cytogenetics and molecular changes are used to inform treatment strategies. However a wide range of clinical responses are observed in these patient subgroups necessitating alternative methodologies to provide information that could inform clinical decisions for AML disease management. Since the net result of the cytogenetic and molecular changes is necessarily a functional alterati

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Tallman, Martin S., D. Gary Gilliland, and Jacob M. Rowe. "Drug therapy for acute myeloid leukemia." Blood 106, no. 4 (2005): 1154–63. http://dx.doi.org/10.1182/blood-2005-01-0178.

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AbstractAlthough improvement in outcomes has occurred in younger adults with acute myeloid leukemia (AML) during the past 4 decades, progress in older adults has been much less conspicuous, if at all. Approximately 50% to 75% of adults with AML achieve complete remission (CR) with cytarabine and an anthracycline such as daunorubicin or idarubicin or the anthracenedione mitoxantrone. However, only approximately 20% to 30% of the patients enjoy long-term disease survival. Various postremission strategies have been explored to eliminate minimal residual disease. The optimal dose, schedule, and nu

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Jianbiao Zhou, Jessie Yiying Quah, Yvonne Ng, et al. "ASLAN003, a potent dihydroorotate dehydrogenase inhibitor for differentiation of acute myeloid leukemia." Haematologica 105, no. 9 (2019): 2286–97. http://dx.doi.org/10.3324/haematol.2019.230482.

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Differentiation therapies achieve remarkable success in acute promyelocytic leukemia, a subtype of acute myeloid leukemia. However, excluding acute promyelocytic leukemia, clinical benefits of differentiation therapies are negligible in acute myeloid leukemia except for mutant isocitrate dehydrogenase 1/2. Dihydroorotate dehydrogenase catalyses the fourth step of the de novo pyrimidine synthesis pathway. ASLAN003 is a highly potent dihydroorotate dehydrogenase inhibitor that induces differentiation, as well as reduces cell proliferation and viability, of acute myeloid leukemia cell lines and p

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Chen, Rong, Bonnie Leung, Yuling Chen, and William Plunkett. "Activities and Mechanism Based Combinations Of Omacetaxine In Acute Myeloid Leukemia." Blood 122, no. 21 (2013): 1288. http://dx.doi.org/10.1182/blood.v122.21.1288.1288.

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Abstract Omacetaxine, an inhibitor of translation, was recently granted accelerated approval for the treatment of chronic myeloid leukemia (CML). Omacetaxine blocks translation elongation by competing with the incoming aminoacyl-tRNAs for binding to the A-site cleft in the peptidyl-transferase center. Our previous studies showed that by transiently inhibiting translation, omacetaxine reduced the expression of the key, short-lived oncoproteins Bcr/Abl and Mcl-1, leading to cell death in the CML cells. This action sensitized the cells to the Abl kinase inhibitor and killed the CML cells synergis

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Seipel, Katja, Karin Schmitter, Ulrike Bacher, and Thomas Pabst. "Rationale for a Combination Therapy Consisting of MCL1- and MEK-Inhibitors in Acute Myeloid Leukemia." Cancers 11, no. 11 (2019): 1779. http://dx.doi.org/10.3390/cancers11111779.

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Amplification and overexpression of the myeloid cell leukemia differentiation protein MCL1 and the murine double minute protein MDM2 have been reported in various human tumors as well as hematological malignancies including acute myeloid leukemia (AML). While MCL1 is an anti-apoptotic member of the BCL-2 family proteins, MDM2 is an important cellular inhibitor of the p53 tumor suppressor. The key oncogene in AML is the FLT3 growth factor receptor gene. FLT3 signaling pathways including the MAPK cascade (RAS-RAF-MEK-ERK) are highly active in AML cells, leading to induced protein translation and

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Zeng, Zhihong, Ismael Samudio, Michael Andreeff, and Marina Konopleva. "Synergistic Induction of Apoptosis by Simultaneous Disruption of the Bcl-2 and mTOR/Akt Pathways in Acute Myeloid Leukemia." Blood 110, no. 11 (2007): 1588. http://dx.doi.org/10.1182/blood.v110.11.1588.1588.

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Abstract Activation of the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt)/mammalian target of rapamycin (mTOR) signaling pathway provides survival signals for leukemic cells and blockade of this pathway may facilitate cell death. Akt/mTOR activation is a frequent event in AML that translates into significantly shorter survival of AML patients (S.M. Kornblau, ASH 2007). Bcl-2 family proteins are key regulators of apoptosis that are known to promote tumorigenesis and chemoresistance. We have recently reported that ABT-737, a small molecule BH3 mimetic, effectively kills AML progenit

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Palath, Varghese, Rohini Vekhande, Andreia Lee, et al. "A Recombinant Human Antibody to EphA3 with Pro-Apoptotic and Enhanced ADCC Activity Shows Selective Cytotoxicity against Myeloid Leukemia Cells and CD123-Positive Leukemic Stem Cells." Blood 114, no. 22 (2009): 1728. http://dx.doi.org/10.1182/blood.v114.22.1728.1728.

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Abstract Abstract 1728 Poster Board I-754 Members of the Eph family of receptor tyrosine kinases play important roles in embryonic development but have restricted tissue distribution and activity in adult tissues. The EphA3 receptor is an oncofetal antigen expressed at high levels on the surface of several solid tumor types and certain leukemias. KaloBios is in pre-clinical development with KB004, a high-affinity recombinant human antibody, derived from a monoclonal anti-EphA3 antibody by Antibody HumaneeringTM Technology. KB004 binds EphA3 and stimulates apoptosis in primary cells from myeloi

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Otevřelová, Petra, and Barbora Brodská. "Chemotherapy-Induced Survivin Regulation in Acute Myeloid Leukemia Cells." Applied Sciences 11, no. 1 (2021): 460. http://dx.doi.org/10.3390/app11010460.

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Survivin is a 16.5 kDa protein highly expressed in centrosomes, where it controls proper sister chromatid separation. In addition to its function in mitosis, survivin is also involved in apoptosis. Overexpression of survivin in many cancer types makes it a suitable target for cancer therapy. Western blotting and confocal microscopy were used to characterize the effect of chemotherapy on acute myeloid leukemia (AML) cells. We found enhanced survivin expression in a panel of AML cell lines treated with cytarabine (Ara-C), which is part of a first-line induction regimen for AML therapy. Simultane

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Xagorari, Angeliki, Sarantis Tsetsakos, Zoi Katana, et al. "CD34+ Derived Microparticles Regulate Apoptosis in Normal and Acute Myeloid Leukemia Cells." Blood 132, Supplement 1 (2018): 5090. http://dx.doi.org/10.1182/blood-2018-99-114425.

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Abstract Introduction Microparticles (MPs) are small vesicles 100nm-1μm derived from the apoptotic or stimulated cells. The mechanism of their production is distinctive from exosomes or apoptotic bodies. MPs have been detected in the blood in many pathological conditions associated mainly with endothelial injury, thrombosis and inflammation. Our previous study showed that MPs originated also from CD34+ cells of umbilical cord blood, which is an alternative source for hemopoeitic stem cell transplantation. MPs considered as markers of cell activation, as well as apoptosis. Apoptosis is a comple

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Allouche, Michèle, Rachida Sihem Charrad, Ali Bettaieb, Catherine Greenland, Cécile Grignon, and Florence Smadja-Joffe. "Ligation of the CD44 adhesion molecule inhibits drug-induced apoptosis in human myeloid leukemia cells." Blood 96, no. 3 (2000): 1187–90. http://dx.doi.org/10.1182/blood.v96.3.1187.

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Abstract Adhesion molecules can improve hematopoietic cell survival; however, their role in leukemic cell resistance to drug-induced apoptosis is poorly documented. The CD44 adhesion molecule is strongly expressed on acute myeloid leukemia (AML) blasts. Using 2 myeloid cell lines, HL60 and NB4, evidence is presented that prior incubation with the CD44-specific monoclonal antibody (mAb) A3D8, reported to induce differentiation of AML blasts, significantly decreases apoptosis induced by 3 drugs used in AML chemotherapy: daunorubicin (DNR), mitoxantrone, and etoposide. In addition, in HL60 cells,

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Allouche, Michèle, Rachida Sihem Charrad, Ali Bettaieb, Catherine Greenland, Cécile Grignon, and Florence Smadja-Joffe. "Ligation of the CD44 adhesion molecule inhibits drug-induced apoptosis in human myeloid leukemia cells." Blood 96, no. 3 (2000): 1187–90. http://dx.doi.org/10.1182/blood.v96.3.1187.015k01_1187_1190.

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Adhesion molecules can improve hematopoietic cell survival; however, their role in leukemic cell resistance to drug-induced apoptosis is poorly documented. The CD44 adhesion molecule is strongly expressed on acute myeloid leukemia (AML) blasts. Using 2 myeloid cell lines, HL60 and NB4, evidence is presented that prior incubation with the CD44-specific monoclonal antibody (mAb) A3D8, reported to induce differentiation of AML blasts, significantly decreases apoptosis induced by 3 drugs used in AML chemotherapy: daunorubicin (DNR), mitoxantrone, and etoposide. In addition, in HL60 cells, CD44 lig

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Kim, Hee Nam, Li Yu, Nan young Kim, et al. "Polymorphisms in Myeloid Cell Leukemia-1 and the Risk for Acute Myeloid Leukemia." Blood 112, no. 11 (2008): 3977. http://dx.doi.org/10.1182/blood.v112.11.3977.3977.

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Abstract The essential pathogenic mechanism in acute myeloid leukemia (AML) is a heterogeneous group of malignant diseases arising as the result of progressive genetic damage occurring in hemopoietic progenitor cells. Mcl-1 (myeloid cell leukemia-1), an antiapoptotic protein of the Bcl-2 family, is located on chromosome 1 and has three exons and two introns. Overexpression of Mcl-1 delays apoptosis induced by cytotoxic agents, c-myc overexpression, and growth factor withdrawal in hematopoietuc cells. To evaluate the association between genetic variants of Mcl-1 gene and risk of AML, we genotyp

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Pikman, Yana, Alexandre Puissant, Gabriela Alexe, et al. "Targeting MTHFD2 in Acute Myeloid Leukemia." Blood 126, no. 23 (2015): 443. http://dx.doi.org/10.1182/blood.v126.23.443.443.

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Abstract Alterations in differentiation pathways contribute to the development of acute myeloid leukemia (AML). Differentiation therapy with all-trans retinoic acid (ATRA) has dramatically altered the treatment of acute promyelocytic leukemia, transforming it from a nearly fatal disease to a curable one. We set out to identify cellular pathways that contribute to AML differentiation, with the goal of identifying new therapeutic targets. We analyzed gene expression data from AML cell lines treated with phorbol 12-myristate 13-acetate (PMA), ATRA, Vitamin D, the BET inhibitor JQ1 and the DOT1L i

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Yeh, Su-Peng, Yu-Chien Chang, Wen-Jyi Lo, et al. "Deferasirox Inhibit Doxorubicin-Induced Reactive Oxygen Species Generation in Both Acute Myeloid Leukemia and Normal Heart Cell While Maintain the Cytotoxicity of Doxorubicin Only on Acute Myeloid Leukemia." Blood 120, no. 21 (2012): 3620. http://dx.doi.org/10.1182/blood.v120.21.3620.3620.

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Abstract Abstract 3620 Background: Deferasirox (DFX) was recently found to have anti-leukemia effect both in vitro and in vivo. DFX can also potently inhibit the generation of intracellular reactive oxygen species (ROS). On the other hand, the generation of ROS by Doxorubicin (DOX) is critical for the cytotoxicity on both leukemia and normal heart cells. It is not known whether combining DFX and DOX will have synergistic or antagonizing effect on leukemic cells. Similarly, it is also unknown whether adding DFX to DOX will have protective effect on normal heart cell. Method: Cells of human acut

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Banker, Deborah E., Mark Groudine, Tom Norwood, and Frederick R. Appelbaum. "Measurement of Spontaneous and Therapeutic Agent-Induced Apoptosis With BCL-2 Protein Expression in Acute Myeloid Leukemia." Blood 89, no. 1 (1997): 243–55. http://dx.doi.org/10.1182/blood.v89.1.243.

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Abstract We have designed in vitro assays to investigate the possible association between apoptosis and chemotherapeutic sensitivity in acute myeloid leukemias (AMLs). Consistent low levels of spontaneous apoptosis were observed in myeloid cells from normal bone marrow samples, while untreated cells collected from 56 de novo AML patients showed variable apoptosis. Control myeloid cells showed increased apoptosis after in vitro treatments with daunomycin (DNR), cytosine arabinoside (ARA-C), or gamma irradiation (RAD). Most AML samples showed less treatment-associated apoptosis, suggesting that

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Banker, Deborah E., Mark Groudine, Tom Norwood, and Frederick R. Appelbaum. "Measurement of Spontaneous and Therapeutic Agent-Induced Apoptosis With BCL-2 Protein Expression in Acute Myeloid Leukemia." Blood 89, no. 1 (1997): 243–55. http://dx.doi.org/10.1182/blood.v89.1.243.243_243_255.

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We have designed in vitro assays to investigate the possible association between apoptosis and chemotherapeutic sensitivity in acute myeloid leukemias (AMLs). Consistent low levels of spontaneous apoptosis were observed in myeloid cells from normal bone marrow samples, while untreated cells collected from 56 de novo AML patients showed variable apoptosis. Control myeloid cells showed increased apoptosis after in vitro treatments with daunomycin (DNR), cytosine arabinoside (ARA-C), or gamma irradiation (RAD). Most AML samples showed less treatment-associated apoptosis, suggesting that apoptosis

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Ramaswamy, Kavitha, Lauren Forbes, Fiona C. Brown, et al. "Peptidomimetic Blockade of MYB in Acute Myeloid Leukemia." Blood 128, no. 22 (2016): 3945. http://dx.doi.org/10.1182/blood.v128.22.3945.3945.

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Abstract Aberrant gene expression is a hallmark of acute leukemias. However, therapeutic strategies for its blockade are generally lacking, in large part due to the pharmacologic challenges of drugging transcription factors. MYB-driven gene trans-activation with CREB-binding protein (CBP) is required for the initiation and maintenance of a variety of acute lymphoblastic and myeloid leukemias, including refractory MLL-rearranged leukemias. Using structure-guided molecular design, we developed a prototypical peptidomimetic inhibitor MYBMIM that interferes with the assembly of the molecular MYB:C

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