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Littérature scientifique sur le sujet « Apoptosis. Acute myeloid leukemia »

Auteur : Grafiati

Publié le 4 juin 2021

Mis à jour le 13 février 2022

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Articles de revues sur le sujet "Apoptosis. Acute myeloid leukemia"

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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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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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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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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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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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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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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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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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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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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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Thèses sur le sujet "Apoptosis. Acute myeloid leukemia"

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Lo, Carfield. "Identified of novel splicing variants of livin in acute myeloid leukemia." Click to view the E-thesis via HKUTO, 2009. http://sunzi.lib.hku.hk/hkuto/record/B41897031.

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Vo, Thanh-Trang. "Mitochondrial Priming Determines Chemotherapeutic Response in Acute Myeloid Leukemia." Thesis, Harvard University, 2012. http://dissertations.umi.com/gsas.harvard:10384.

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Gain- and loss-of-function studies of the BCL-2 family of proteins have shown that they can impact chemotherapeutic sensitivity. However, cells contain myriad anti-apoptotic and pro-apoptotic BCL-2 family members making it difficult to predict cell fate decisions based on the initial conditions of these proteins. BH3 profiling is a tool that measures mitochondrial priming, the readiness of a cell to die through the intrinsic (or mitochondrial) apoptotic pathway. Priming is due to the cumulative effect of the BCL-2 family of proteins that act as the gate keepers of the mitochondrial apoptoti

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Lo, Carfield, and 盧德心. "Identified of novel splicing variants of livin in acute myeloid leukemia." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2009. http://hub.hku.hk/bib/B41897031.

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Nakatani, Kana. "Inhibition of CDK4/6 and autophagy synergistically induces apoptosis in t(8;21) acute myeloid leukemia cells." Doctoral thesis, Kyoto University, 2021. http://hdl.handle.net/2433/263584.

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Lainey, Elodie. "Evaluation préclinique de l’azacytidine et de l’erlotinib seuls ou en association dans le traitement des syndromes myélodysplasiques." Thesis, Paris 11, 2013. http://www.theses.fr/2013PA11T066.

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Les syndromes myélodysplasiques (SMD) sont un ensemble d’hémopathies clonales de la cellule souche. Ils touchent les sujets âgés et se caractérisent par une hématopoïèse inefficace, une différenciation anormale et une transformation fréquente en leucémie aiguë myéloblastique (LAM). La prise en charge thérapeutique a considérablement évolué ces dix dernières années, principalement avec l’arrivée de la 5-azacytidine (Aza) dans les SMD de haut risque. Malheureusement, il existe fréquemment un échec ou une perte de réponse rapide au traitement responsable d’une survie médiane globale de seulement

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Tailler, Maximilien. "Les dérégulations de l’apoptose dans les syndromes myélodysplasiques et les leucémies aigues myéloïdes." Thesis, Paris 11, 2011. http://www.theses.fr/2011PA11T059.

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Les syndromes myélodysplasiques (SMD) peuvent être conçus comme des conditions pré-leucémiques dans lesquelles l’apoptose avorte les produits de différenciation de cellules souches mutées, potentiellement malignes. Néanmoins, peut-être à cause d’une inhibition progressive de l’apoptose, les SMD se transforment fréquemment en leucémies aiguës myéloïdes (LAM). Nos données indiquent que les SMD à faible risque se caractérisent par l’absence d’activation de NF-κB au sein des cellules portant des altérations cytogénétiques typiques. Par contre, dans les SMD à haut risque de transformation en LAM (a

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Shah, Viral Virendra [Verfasser]. "Enhancing PARP inhibition mediated DNA Damage and leveraging inherent anti-apoptotic dependencies in acute myeloid leukemia / Viral Virendra Shah." Mainz : Universitätsbibliothek der Johannes Gutenberg-Universität Mainz, 2020. http://d-nb.info/1223205320/34.

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Yaseen, Mumtaz. "Proteomics of Acute Myeloid Leukemia:." Diss., lmu, 2007. http://nbn-resolving.de/urn:nbn:de:bvb:19-69882.

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Palle, Josefine. "Optimizing Chemotherapy in Childhood Acute Myeloid Leukemia." Doctoral thesis, Uppsala University, Department of Women's and Children's Health, 2008. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-9189.

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<p>Despite major advances in our understanding of the biology of childhood acute myeloid leukemia (AML) and the development of new cytotoxic drugs, the prognosis of long-term survival is still only 60-65 %.</p><p>In the present research, we studied the pharmacokinetics of drugs used in the induction therapy of childhood AML and performed in vitro drug sensitivity testing of leukemic cells from children with AML.</p><p>The aims of the studies were to correlate the results of the analysis to biological and clinical parameters and to identify subgroups of AML with specific drug sensitivity profil

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Watson, Alexander Scarth. "Autophagy in hematopoiesis and acute myeloid leukemia." Thesis, University of Oxford, 2014. http://ora.ox.ac.uk/objects/uuid:2e66c5c3-4774-44d1-8345-d0dc827da16d.

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Acute myeloid leukemia (AML) develops following oncogenic alterations to hematopoietic stem (HSC) and progenitor cells (HSPCs) in the bone marrow, resulting in dysregulated proliferation of immature myeloid progenitors that interferes with normal hematopoiesis. Understanding the mechanisms of HSPC protection against damage and excessive division, and how these pathways are altered during leukemic progression, is vital for establishing effective therapies. Here, we show that autophagy, a lysosomal degradation pathway, is increased in HSPCs using a novel imaging flow cytometry autophagy assay. L

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Livres sur le sujet "Apoptosis. Acute myeloid leukemia"

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Fortina, Paolo, Eric Londin, Jason Y. Park, and Larry J. Kricka, eds. Acute Myeloid Leukemia. Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4939-7142-8.

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Röllig, Christoph, and Gert J. Ossenkoppele, eds. Acute Myeloid Leukemia. Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-72676-8.

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Andreeff, Michael, ed. Targeted Therapy of Acute Myeloid Leukemia. Springer New York, 2015. http://dx.doi.org/10.1007/978-1-4939-1393-0.

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Mertzlufft, Nancy. Gift of life. Sheed & Ward, 1985.

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Barge, A. Acute myeloid leukaemia: The role of haematopoietic growth factors. Gardner-Caldwell Communications, 1998.

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National Institute for Clinical Excellence. Guidance on the use of imatinib for chronic myeloid leukaemia. National Institute for Clinical Excellence, 2003.

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National Institute for Clinical Excellence. Guidance on the use of imatinib for chronic myeloid leukaemia. National Institute for Clinical Excellence, 2002.

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Hiddemann, W., and R. Mertelsmann, eds. New Findings on Aclarubicin in the Treatment of Acute Myeloid Leukemia. Springer Berlin Heidelberg, 1990. http://dx.doi.org/10.1007/978-3-642-75720-4.

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Handler, Evan. It's only temporary: The good news and the bad news of being alive. Riverhead Books, 2008.

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Handler, Evan. It's only temporary: The good news and the bad news of being alive. Riverhead Books, 2008.

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Chapitres de livres sur le sujet "Apoptosis. Acute myeloid leukemia"

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Reed, John C. "Roles of Apoptosis-Regulating Bcl-2 Family Genes in AML." In Targeted Therapy of Acute Myeloid Leukemia. Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4939-1393-0_3.

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Bremer, Edwin, and Wijnand Helfrich. "AML-Selective Apoptosis Induction by Rationally Designed Death Ligand Fusion Proteins." In Targeted Therapy of Acute Myeloid Leukemia. Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4939-1393-0_8.

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Karawajew, L., C. Wuchter, V. Ruppert, F. Herrmann, B. Dörken, and W. D. Ludwig. "CD95-Mediated Apoptosis in Acute Myeloid Leukemia (AML): Dependence on Maturational Stage and Growth Characteristics in Vitro." In Haematology and Blood Transfusion / Hämatologie und Bluttransfusion. Springer Berlin Heidelberg, 1998. http://dx.doi.org/10.1007/978-3-642-71960-8_17.

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Kansal, Rina. "Acute Myeloid Leukemia." In Tumors and Cancers. CRC Press, 2017. http://dx.doi.org/10.1201/9781315120546-20.

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Arber, Daniel A. "Acute Myeloid Leukemia." In Atlas of Bone Marrow Pathology. Springer New York, 2018. http://dx.doi.org/10.1007/978-1-4939-7469-6_11.

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Grimwade, David, Steven Knapper, and Krzysztof Mrózek. "Acute Myeloid Leukemia." In Molecular Pathology in Clinical Practice. Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-19674-9_40.

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Adachi, Souichi, Akitoshi Kinoshita, Daisuke Tomizawa, Takashi Taga, and Hiroyuki Takahashi. "Acute Myeloid Leukemia." In Hematological Disorders in Children. Springer Singapore, 2017. http://dx.doi.org/10.1007/978-981-10-3886-0_3.

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Lazarus, Hillard M., and Masumi Ueda. "Acute myeloid leukemia." In Clinical Manual of Blood and Bone Marrow Transplantation. John Wiley & Sons, Ltd, 2017. http://dx.doi.org/10.1002/9781119095491.ch11.

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Wolach, Ofir, and Richard M. Stone. "Acute Myeloid Leukemia." In Targeted Therapy in Translational Cancer Research. John Wiley & Sons, Inc., 2015. http://dx.doi.org/10.1002/9781118468678.ch9.

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Johansson, Bertil, and Christine J. Harrison. "Acute Myeloid Leukemia." In Cancer Cytogenetics. John Wiley & Sons, Inc., 2010. http://dx.doi.org/10.1002/9781118010136.ch5.

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Actes de conférences sur le sujet "Apoptosis. Acute myeloid leukemia"

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Rosen, David B., Mark D. Minden, Santosh Putta, et al. "Abstract 3842: Identification of distinct apoptosis and myeloid signaling profiles within acute myeloid leukemia (AML) blast subpopulations." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-3842.

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Ruvolo, Peter P., Zhihong Zeng, Vivian R. Ruvolo, et al. "Abstract 3659: The AKT inhibitor MK-2206 promotes apoptosis in acute myeloid leukemia cells." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-3659.

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Chen, Lisa S., Sanjeev Redkar, Pietro Taverna, Jorge E. Cortes, and Varsha Gandhi. "Abstract 1649: Pim kinase inhibitor, SGI-1776, induces apoptosis in acute myeloid leukemia primary cells." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-1649.

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Kojima, Kensuke, Yuki Nishida, Aya Maeda, et al. "Abstract 2938: BMI-1 inhibition by PTC-209 induces mitochondrial apoptosis in acute myeloid leukemia cells." In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-2938.

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Finlay, Darren, Nicole Bata, Allison Limpert, et al. "Abstract 2405: Inhibitor of apoptosis protein antagonists as novel targeted chemotherapeutic agents for acute myeloid leukemia." In Proceedings: AACR Annual Meeting 2020; April 27-28, 2020 and June 22-24, 2020; Philadelphia, PA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.am2020-2405.

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Rocha, Kelvyn M. L., Érica C. M. Nascimento, and João B. L. Martins. "Estudo de Docking da Bcr-Abl (PDB, 1OPJ) com Inibidores de Segunda Geração: Dasatinibe e Afatinibe." In VIII Simpósio de Estrutura Eletrônica e Dinâmica Molecular. Universidade de Brasília, 2020. http://dx.doi.org/10.21826/viiiseedmol2020151.

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Chronic myeloid leukemia is a type of cancer which affects hematopoetic cells, causing excessive proliferation of white blood cells which eventually leads to loss of function and resistance to apoptosis (stage known as acute leukemia). Researchers have shown that many CML cases are associated with mutant transcripts of the Philadelphia chromosome (i.e. BCR-ABL), whose effects are pharmacologically treated. The first successful drug in that matter is imatinib, a competitive inhibitor which caused groundbreaking advances in the treatment of CML. However, many patients develop resistance to the t

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Holbert, Cassandra, Jeffrey Forrester, and Michael Roberts. "Abstract 3561: Role of bcl-2 family proteins in phorbol ester-induced apoptosis of acute myeloid leukemia cells." In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-3561.

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Abdul-Aziz, Amina, Francis Burrows, Ning Yu, Nigel H. Russell, Claire H. Seedhouse, and Monica Pallis. "Abstract 4536: ABT-737 and ABT-199 complement the multikinase inhibitor TG02 to induce apoptosis in acute myeloid leukemia cells." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-4536.

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Lum, Ronnie, Mojib Javadi, Tiffany Cheng, et al. "Abstract 4544: Induction of KLF4 by LOR-253 as an innovative therapeutic approach to induce apoptosis in acute myeloid leukemia." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-4544.

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Roberts, Michael, Lauren Kageler, Kayla Bendinelli, Shannon Bonner, Ashir Borah, and Jeffrey Forrester. "Abstract 4678: The role of EGR1 and AP1 in acute myeloid leukemia cell reprogramming toward cell cycle arrest and apoptosis." In Proceedings: AACR Annual Meeting 2020; April 27-28, 2020 and June 22-24, 2020; Philadelphia, PA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.am2020-4678.

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Rapports d'organisations sur le sujet "Apoptosis. Acute myeloid leukemia"

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Zhang, Chengcheng. Dissecting the Role of IGFBP-2 in Development of Acute Myeloid Leukemia. Defense Technical Information Center, 2011. http://dx.doi.org/10.21236/ada555017.

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Sorror, Mohamed L., Barry E. Storer, and Elihu H. Estey. Comparing Hematopoietic Cell Transplant versus Other Treatments for Adults with Acute Myeloid Leukemia. Patient-Centered Outcomes Research Institute (PCORI), 2021. http://dx.doi.org/10.25302/01.2021.ce.13047451.

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Gong, Jun. Diminishing oncometabolic havoc: Approved IDH1 and IDH2 inhibitors in relapsed or refractory acute myeloid leukemia. Science Repository OU, 2018. http://dx.doi.org/10.31487/j.aco.2018.01.004.

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Getz, Kelly D., Julia E. Szymczak, Farah Contractor, Brian T. Fisher, and Richard Aplenc. Comparing Chemotherapy Recovery at Home versus in the Hospital for Children with Acute Myeloid Leukemia. Patient-Centered Outcomes Research Institute (PCORI), 2021. http://dx.doi.org/10.25302/01.2021.cer.140922827.

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Fan, Junjie, Li Gao, Jing Chen, and Shaoyan Hu. Influence of KIT mutations on prognosis of pediatric patients with core-binding factor acute myeloid leukemia: systematic review and meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, 2020. http://dx.doi.org/10.37766/inplasy2020.9.0019.

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Yin, Xuewei, Yi Ding, Liming Yu, et al. Efficacy and safety of chemotherapy combined with different doses of IL-2 maintenance therapies for acute myeloid leukemia: A protocol for a Bayesian network meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, 2021. http://dx.doi.org/10.37766/inplasy2021.4.0106.

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