Relevant bibliographies by topics / Apoptosis. Acute myeloid leukemia

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Academic literature on the topic 'Apoptosis. Acute myeloid leukemia'

Author: Grafiati
Published: 4 June 2021
Last updated: 13 February 2022

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

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Dimitroulakos, Jim, Dana Nohynek, Karen L. Backway, David W. Hedley, Herman Yeger, Melvin H. Freedman, Mark D. Minden, and Linda Z. Penn. "Increased Sensitivity of Acute Myeloid Leukemias to Lovastatin-Induced Apoptosis: A Potential Therapeutic Approach." Blood 93, no. 4 (February 15, 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 breast and prostate carcinomas. Because of the increased sensitivity of neuroblastoma cells to lovastatin-induced apoptosis, we examined the effect of this agent on a variety of tumor cells, including leukemic cell lines and primary patient samples. Based on a variety of cytotoxicity and apoptosis assays, the 6 acute lymphocytic leukemia cell lines tested displayed a weak apoptotic response to lovastatin. In contrast, the majority of the acute myeloid leukemic cell lines (6/7) and primary cell cultures (13/22) showed significant sensitivity to lovastatin-induced apoptosis, similar to the neuroblastoma cell response. Of significance, in the acute myeloid leukemia, but not the acute lymphocytic leukemia cell lines, lovastatin-induced cytotoxicity was pronounced even at the physiological relevant concentrations of this agent. Therefore, our study suggests the evaluation of HMG-CoA reductase inhibitors as a therapeutic approach in the treatment of acute myeloid leukemia.
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Dimitroulakos, Jim, Dana Nohynek, Karen L. Backway, David W. Hedley, Herman Yeger, Melvin H. Freedman, Mark D. Minden, and Linda Z. Penn. "Increased Sensitivity of Acute Myeloid Leukemias to Lovastatin-Induced Apoptosis: A Potential Therapeutic Approach." Blood 93, no. 4 (February 15, 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 and prostate carcinomas. Because of the increased sensitivity of neuroblastoma cells to lovastatin-induced apoptosis, we examined the effect of this agent on a variety of tumor cells, including leukemic cell lines and primary patient samples. Based on a variety of cytotoxicity and apoptosis assays, the 6 acute lymphocytic leukemia cell lines tested displayed a weak apoptotic response to lovastatin. In contrast, the majority of the acute myeloid leukemic cell lines (6/7) and primary cell cultures (13/22) showed significant sensitivity to lovastatin-induced apoptosis, similar to the neuroblastoma cell response. Of significance, in the acute myeloid leukemia, but not the acute lymphocytic leukemia cell lines, lovastatin-induced cytotoxicity was pronounced even at the physiological relevant concentrations of this agent. Therefore, our study suggests the evaluation of HMG-CoA reductase inhibitors as a therapeutic approach in the treatment of acute myeloid leukemia.
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Xiong, Jie, Xingyi Kuang, Tingting Lu, Bingqing Cheng, Danna Wei, Xinyao Li, Weili Wang, Zhaoyuan Zhang, and Jishi Wang. "The Crucial Role of NR4A1 Dependent Apoptosis Induced By Fenretinide in Acute Myeloid Leukemia." Blood 132, Supplement 1 (November 29, 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 / MPN, and even acute myeloid leukemia. This indicates that NR4A1 is an important tumor suppressor in acute myeloid leukemia. The present study was to investigate the effect of drug-induced NR4A1 expression on apoptosis in acute myeloid leukemia and its related mechanisms. The results suggested that NR4A1 may become a new target for the treatment of acute myeloid leukemia. METHODS: In vitro, on the one hand, bone marrow mononuclear cells from patients with newly diagnosed or relapsed acute myeloid leukemia were extracted as samples, and the expression of NR4A1 mRNA and protein was detected by Real-time PCR and Western blot. Acute myeloid leukemia cell lines HL60 and Kasumi-1 were tested for fenretinide activity and apoptosis, as well as NR4A1 and mitochondrial apoptosis pathway-related protein expression. We used siNR4A1 to knockdown NR4A1 expression and LMB to inhibit nuclear export, the apoptosis rate and apoptosis protein were detected. The mechanism of anti-apoptotic effect of NR4A1 was verified by western blot, immunofluorescence and co-immunoprecipitation. AML mice model were established and fenretinide was injected into the tail veins to observe the effects of NR4A1 expression on survival time, blood routine, bone marrow and important organs. Results: 1. NR4A1 expression in patients with acute myeloid leukemia was significantly higher than normal. 2. The expression of NR4A1 increased in a time- and concentration-dependent manner under the action of fenretinide. 3. After siNR4A1, the apoptosis of acute myeloid leukemia cells was significantly decreased, and the expression of apoptotic proteins was decreased. 4. The expression of apoptotic proteins was decreased after fenretinide combined with leptomycin treatment. After fenretinide treatment, the expression of NR4A1 was decreased in nuclear extracts, and the expression of mitochondrial extract was increased. After drug treatment, NR4A1 interacted with Bcl-2, and the bcl-2 BH3 domain in cytoplasm was exposed to play an anti-apoptotic effect. After successful modeling of AML mice, the survival rate of the fenretinide treatment group was significantly prolonged compared with the control group. The peripheral blood leukocytes, hemoglobin and platelet values were significantly different. The liver and spleen volume of the treatment group were significantly smaller than that of the control group. The mRNA and protein levels of NR4A1 in the spleen were significantly higher than those in the control group. Conclusion: The effect of fenretinide on acute myeloid leukemia cells induces NR4A1 expression and plays a pro-apoptotic effect. This apoptosis effect depends on the nuclear export of NR4A1. NR4A1 is located from the nucleus to the mitochondria, and binds to the Bcl-2 BH3 domain. Key words: NR4A1, fenretinide, acute myeloid leukemia, apoptosis, nuclear export Disclosures No relevant conflicts of interest to declare.
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Testa, U., and R. Riccioni. "Deregulation of apoptosis in acute myeloid leukemia." Haematologica 92, no. 1 (January 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, Francesco Buccisano, Luca Maurillo, Carla Mazzone, Antonio Bruno, et al. "Apoptosis and immaturity in acute myeloid leukemia." Hematology 10, no. 1 (February 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 (December 1, 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 hematologic diseases, such as Acute Myeloid Leukemia (AML) and their effects on responsiveness to anticancer therapy have been recently described. Thus, this review aims to discuss apoptosis and the role of the Bcl-2 family of proteins in chemoresistance when overexpressed in patients committed with Acute Myeloid Leukemia submitted to chemotherapy treatment.
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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 (December 3, 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 prevent incorporation of these damaged bases in the DNA. MTH1 is thought to be non-essential for normal cells but crucial for neoplastic cells in order to avoid incorporation of oxidized dNTPs into DNA, thereby evading DNA damage and cell death. Whether MTH1 inhibitors have any activity against AML is not known. METHODS: Neoplastic myeloid cell lines HL-60, HEL, K562, KG1A, ML1, MV-4-11, SET2, and U937 were treated with varying concentrations of TH588 for a total of 48 hours. In experiments using the pan-caspase inhibitor Q-VD-OPh (Qvd), cells were pre-treated with 5µM Qvd for 1 hour followed by TH588. Cells were washed and stained with annexin, propidium iodide (PI), or MitoTracker (Life Technologies, Carlsbad, CA) for flow cytometry. To evaluate the potential impact of MTH1 inhibition on chemorefractory AML, HL-60/VCR cells were treated with vehicle control or TH588 in culture medium with or without vincristine (1µg/ml). Percentage apoptosis was calculated by normalizing to vehicle only control. With IRB approval, bone marrow aspirate samples were obtained from patients with untreated AML or healthy controls. Mononuclear cells were analyzed using colony-forming unit (CFU) assays. The total number of erythroid (CFU-E) and myeloid (CFU-G, CFU-GM) colonies containing ≥50 cells were read on day 14 and reported as percentage colonies compared to vehicle control. RESULTS: TH588 induced dose-dependent cell death in each of the neoplastic cell lines tested except HEL. In particular, treatment with TH588 resulted in a dose-dependent increase in the number of cells undergoing apoptosis as indicated by annexin V and/or PI staining (IC50 3.1-21.3µM, Figure 1). Pre-treatment with Qvd significantly inhibited TH588-induced cell death in all the cell lines studied except KG1A and SET2, suggesting a caspase-dependent mechanism of cell death. In further studies, cells treated with TH588 exhibited decreased MitoTracker staining; and Qvd pretreatment increased the number of MitoTrackerLow cells at the same time apoptotic cells decreased, suggesting that mitochondrial damage is upstream of caspase activation in TH588-induced apoptosis. Treatment with TH588 not only induced apoptosis in HL-60/VCR cells, but also facilitated further apoptosis in cells co-treated with vincristine and TH588 (Figure 2). Treatment with TH588 also diminished colony formation in a primary AML sample (IC50 6µM, Figure 3). Analysis of additional primary AML samples is ongoing. DISCUSSION: Our results show that the MTH1 inhibitor TH588 induces apoptosis in most neoplastic myeloid cells. MTH1 causes mitochondrial damage that, in turn, leads to caspase-dependent apoptosis in these cells. In HL-60/VCR cells representing chemorefractory phenotype, TH588 induces apoptosis as a single agent and resensitizes cells to vincristine. Moreover, TH588 significantly diminished colony formation in primary AML ex vivo. Further preclinical and possible clinical study of this class of agent appears warranted. Figure 1. Induction of cell death by MTH1 inhibitor TH588 in neoplastic myeloid cell lines. Figure 1. Induction of cell death by MTH1 inhibitor TH588 in neoplastic myeloid cell lines. Figure 2. TH588 induces apoptosis in HL-60/VCR cells and resensitizes cells to vincristine. Figure 2. TH588 induces apoptosis in HL-60/VCR cells and resensitizes cells to vincristine. Figure 3. TH588 significantly diminished colony formation in primary AML ex vivo indose-dependent manner. Figure 3. TH588 significantly diminished colony formation in primary AML ex vivo indose-dependent manner. Disclosures No relevant conflicts of interest to declare.
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Garzon, Ramiro, Catherine E. A. Heaphy, Violaine Havelange, Muller Fabbri, Stefano Volinia, Twee Tsao, Nicola Zanesi, et al. "MicroRNA 29b functions in acute myeloid leukemia." Blood 114, no. 26 (December 17, 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 that miR-29b target apoptosis, cell cycle, and proliferation pathways. A significant enrichment for apoptosis genes, including MCL-1, was found among the mRNAs inversely correlated with miR-29b expression in 45 primary AML samples. Together, the data support a tumor suppressor role for miR-29 and provide a rationale for the use of synthetic miR-29b oligonucleotides as a novel strategy to improve treatment response in AML.
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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 (February 7, 2018): 1353–60. http://dx.doi.org/10.1021/acs.molpharmaceut.7b01151.

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Dissertations / Theses on the topic "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 apoptotic pathway. Priming is measured by determining the sensitivity of mitochondria to perturbation by peptides derived from the BH3 domains of pro-apoptotic proteins. Using BH3 profiling, we now have a functional readout that can quantify priming and assess its contribution to drug sensitivity. Here we show that priming affects the sensitivity of acute myeloid leukemia (AML) cell lines to various standard chemotherapeutics, especially topoisomerase II inhibitors. Priming predicts clinical response to conventional induction chemotherapy as well as the long term maintenance of remission in AML patients. Interestingly, the priming of normal hematopoietic stem cells (HSCs) sits at the boundary line between the priming of cured and refractory patient AML. This HSC priming likely defines the therapeutic index since AML that are lower primed than HSCs are often refractory and cannot be cured without transplantation. Additionally, our BH3 profiles revealed that AML cells are more sensitive to BCL-2 antagonism than normal HSCs, which are primarily dependent on MCL-1. Indeed, we were able to kill primary refractory AML cells in vitro with the BCL-2 antagonist ABT-737 at doses that left HSCs unharmed. Cumulatively, these findings show that priming is a major mechanistic determinant of AML response in vitro and in the clinic to standard induction chemotherapy. With the ability to predict outcome, BH3 profiling may offer physicians and patients a promising tool for treatment decision-making.
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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 quelques mois. La compréhension des mécanismes d’action des agents hypométhylants, la mise en évidence des facteurs biologiques impliqués dans la résistance à l’Aza ou encore l’identification de nouvelles associations de molécules constitue donc un enjeu majeur. Plusieurs équipes, dont la nôtre, ont démontré que l’erlotinib (Erlo) (inhibiteur de l’activité kinase de l’EGFR (Epidermal Growth Factor Receptor)) possède des effets antinéoplasiques dans les SMD/LAM. Compte tenu de sa toxicité modérée, cet inhibiteur de tyrosine kinase est actuellement en essai clinique en France et aux États-Unis dans les SMD en échec d’Aza. Dans ce travail, nous avons tenté de comprendre les mécanismes d’action impliqués dans l’activité de l’Aza et de l’Erlo seuls ou en association. Nous avons observé que l’Aza et la décitabine (un autre agent hypométhylant) induisent la déphosphorylation et la translocation dans le noyau du facteur de transcription FOXO3A où il réactive l’expression de gènes cibles tels que les facteurs pro apoptotiques PUMA et BIM. Cet effet observé rapidement, suggère un effet « off target » non lié à une reprogrammation épigénétique. La phosphorylation constitutive de FOXO3A étant considérée comme un facteur de mauvais pronostic dans les LAM, cette observation soulève l’intérêt potentiel des agents hypométhylants dans cette pathologie. Nous avons également identifié deux nouvelles cibles de l’Erlo : les SRC-kinases et la voie mTOR/p70S6K dont l’inhibition par des inhibiteurs biochimiques induit un arrêt du cycle cellulaire en G0/G1 sans apoptose ni différenciation confirmant l’hypothèse d’une action « multikinase » de l’Erlo. Par ailleurs, nous avons mis en évidence une activité synergique sur l’apoptose de l’association Aza et Erlo sur des lignées cellulaires de SMD/LAM et sur des cellules de patients. Cet effet n’a pas été retrouvé avec la décitabine ni les autres inhibiteurs de tyrosine kinase testés. La potentialisation de l’apoptose semble liée à plusieurs mécanismes associant l’augmentation de la concentration intracellulaire d’Aza via l’inhibition des transporteurs ABC, un arrêt de la prolifération, une activation des voies apoptotiques caspases-dépendantes et indépendantes et une activation des dommages à l’ADN. En conclusion, ce travail a permis l’identification de nouvelles cibles de l’Erlo et de l’AZA et a révélé un effet synergique entre ces deux molécules. Ces résultats précliniques encourageants suggèrent que cette association pourrait apporter un potentiel bénéfice chez les patients atteints de SMD/LAM, notamment ceux devenus réfractaires à l’Aza
Myelodysplasic syndromes (MDS) constitute a diverse group of malignant clonal disorders that typically occur in elderly people. MDS are characterized by ineffective hematopoiesis, refractory cytopenias, morphologic dysplasia and increased potential to transform into acute myeloid leukemia (AML). Treatment of MDS has progressed considerably in recent years with the emergence of new approval agents such as azacytidine (aza)(a hypomethylating agent (HMA)) in higher-risk MDS. However, there are still a significant proportion of patients who do not respond to therapy with aza. Therefore, understanding the mechanisms of action of HMAs, identifying predictive factors for aza resistance and combining HMAs with other active compounds in MDS represent a challenging area to improve MDS/AML treatment. Previous works showed that erlotinib (an inhibitor of the epidermal growth factor receptor (EGFR)) exhibits antineoplastic effects in MDS/AML. Due to its limited toxicity profile, this tyrosine kinase inhibitor is currently being evaluated after failure of aza in two clinical trials. In this project, we aimed at understanding the molecular mechanisms involved in the activity of aza and erlo alone or in combination. We observed that aza and decitabine (another HMA related to aza) induces dephosphorylation and translocation to nucleus of the transcriptional regulator FOXO3A promoting the upregulation of the pro-apoptotic factors PUMA and BIM. This effect could be an “off target” effect and could contribute the bebenfical role of HMA in AML as constitutive phosphorylation of FOXO3A has been shown to be an adverse prognostic factor. We discovered new target for erlo, Src-kinase kinases and mTOR that are implicated in the cell-cycle arrest but not in the induction of apoptosis or differentiation confirming the “multikinase” activity of erlo. We found that the combination of aza and erlo demonstrated synergistic induction of apoptosis in MDS/AML cell lines and in some patient cells. This effect was not observed with decitabine or other tyrosine kinase inhibitors frequently used in onco-hematology. We demonstrated that potentiation of cell death is associated with different mechanisms such as intracellular accumulation of aza (via inhibition of ABC transporters), cell cycle arrest with inhibition of leukemic cells growth, caspase-dependent and -independent induction of apoptosis and DNA damage level. In conclusion, this work identified new targets of aza and erlo and revealed a synergistic induction of apoptosis upon co-treatment suggesting that this drug combination might be promising for SMD/AML treatment SMD/AML, especially the resistant patients
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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 (ainsi que dans les LAM post-SMD), les cellules souches hématopoïétiques et leurs produits de différenciation montrent une translocation activatrice des sous-unités p50/p65 de NF-κB. L’utilisation d’antagonistes de IKK provoque une inhibition de NF-κB conduisant à une apoptose accélérée, ainsi l’activation de NF-κB serait responsable de la suppression progressive de l’apoptose et donc de la transformation maligne. Ce projet de thèse a consisté à comprendre les mécanismes impliqués dans la dérégulation de l’apoptose dans les SMD/LAM ; ainsi qu’à utiliser des technologies de criblage pour permettre une meilleure compréhension des voies de signalisation impliquées, et à adapter de nouveaux outils d’analyse. Au cours d’une première étude, nous avons montré que les inhibiteurs de méthyltransférase de l’ADN et les inhibiteurs d’histones déacétylases induisent efficacement l’apoptose dans la lignée cellulaire SMD/LAM P39, parallèlement à une inhibition de la translocation de NF-κB du cytoplasme au noyau. Dans une seconde étude, nous avons montré que l’inhibition pharmacologique du récepteur Flt3 induit une inhibition de la voie NF-κB, et pourrait être une cible thérapeutique pertinente. Dans une troisième étude, nous avons montré que l’auto-activation d’ATM chez les patients atteints de SMD/LAM joue un rôle dans l’activation constitutive de NF-κB suggérant qu’ATM serait également une bonne cible thérapeutique dont l’inhibition pourrait réduire le défaut d’apoptose des cellules SMD et LAM. Et enfin, grâce à l’optimisation d’une technique d’analyse d’images à haut débit, nous avons identifié deux composés capables d’induire la mort cellulaire des lignées cellulaires LAM in vitro : le zinc pyrithione et la ouabain. Leurs effets d’inhibition du signal de survie NF-κB, conduisant à une réduction de l’expression de protéines anti-apoptotiques, suggèrent que ces composés pharmaceutiques pourraient être utilisés comme des agents anti-leucémiques. Ce projet de thèse nous a permis de mettre en évidence le potentiel anti-leucémique de différents agents impliqués dans les principales voies de signalisation de l’apoptose dérégulées dans les SMD/LAM, qui pourraient prochainement servir de cibles pour de nouveaux essais thérapeutiques
Myelodysplastic syndrome (MDS) is a group of hematopoietic stem cell disorders that is characterized by an ineffective hematopoiesis (finaly leading to blood cytopenias) and by a high risk of progression to acute myeloid leukemia (AML). It can therefore be viewed as a preleukemic condition in which apoptosis aborts the differentiation products of potentially malignant mutated (stem) cells. The progression of MDS into AML is associated with progressive inhibition of apoptotsis (by e.g. the expression of antiapoptotic proteins) and a negative prognostic value, suggesting that loss of the apoptotic program could favor the MDS-to-AML transition. Therefore the present project aimed at understanding the mechanisms involved in the deregulation of apoptosis in MDS and AML and the characterization of their underlying signaling pathways by means of standard biochemical and high throughput screening approaches. Our previous work showed that inhibitors of DNA methyltransferases and histone deacetylases effectively induced apoptosis in AML cells in vivo which was associated with an inhibition of NF-κB-dependent transactivation of survival signals. We further found that the pharmacological inhibition of the Flt3 receptor in AML cells decreased NF-κB activation and might therefore constitute a relevant therapeutic target for the treatment of AML. In line with these findings we demonstrated that the constitutive activation of ATM in high-risk MDS and AML patients accounts for the activation of NF-κB suggesting ATM as yet another drugable target for antileukemic therapy. Finally we generated a high throughput image based screening platform, which enabled us to perform large scale drug screening approaches and to identify two compounds with antileukemic properties. Both agent, pyrithione zinc (PZ) and Ouabain (OUA) efficiently induced cell death in AML cells in vitro associated with the inhibition of NF-κB. PZ and OUA exerted significant anticancer effects in vivo, on human AML cells xenografts as well as ex vivo, on CD34+ (but not CD34-) malignant myeloblasts from AML patients. Summarizing this project allowed us to shed some light on the importance of NF-κB during MDS to AML progression and at the same time it helped to identify drugable targets and agents with potential anticancer properties for the treatment of leukemia
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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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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 %.

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.

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 profiles in order to better understand why treatment fails in some patients and how therapy may be improved.

Blood samples were analysed to study the pharmacokinetics of doxorubicin (n=41), etoposide (n=45) and 6-thioguanine (n=50). Doxorubicin plasma concentration and total body clearance were correlated to the effect of induction therapy, and doxorubicin plasma concentration was an independent factor for complete remission, both in univariate and multivariate analysis including sex, age, and white blood cell count at diagnosis. For etoposide and 6-thioguanine no correlation was found between pharmacokinetics and clinical effect. Children with Down syndrome (DS) tended to reach higher blood concentrations of etoposide and thioguanine nucleotides, indicating that dose reduction may be reasonable to reach the same drug exposure as in children without DS.

Leukemic cells from 201 children with newly diagnosed AML, 15 of whom had DS, were successfully analysed for in vitro drug sensitivity by the fluorometric microculture cytotoxicity assay (FMCA). We found that samples from children with DS were highly sensitive to most drugs used in AML treatment. In non-DS children, the t(9;11) samples were significantly more sensitive to cytarabine (p=0.03) and doxorubicin (p=0.035) than other samples. The findings might explain the very favorable outcome reported in children with DS and t(9;11)-positive AML. A specific drug resistance profile was found for several other genetic subgroups as well. A detailed study of MLL-rearranged leukemia showed that cellular drug sensitivity is correlated both to partner genes and cell lineage, findings that support the strategy of contemporary protocols to include high-dose cytarabine in the treatment of patients with MLL-rearrangement, both in AML and acute lymphoblastic leukemia (ALL).

Our results indicate that drug resistance and pharmacokinetic studies may yield important information regarding drug response in different sub-groups of childhood AML, helping us to optimize future chemotherapy in childhood AML.

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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. Loss of hematopoietic autophagy following deletion of key gene Atg5 resulted in increased HSC proliferation, leading to HSC exhaustion and bone marrow failure. Although erythrocyte and lymphocyte populations were negatively impacted by autophagy loss, myeloid cells showing immature characteristics were expanded. Deletion of Atg5 in an AML model resulted in increased proliferation under metabolic stress, dependent on the glycolytic pathway, and aberrant upstream mTOR signaling. Moreover, modulation of Atg5 altered leukemic response to culture with stromal cells. Finally, primary AML cells displayed multiple markers of decreased autophagy. These data suggest a role for autophagy in preserving HSC function, partially through suppression of HSPC proliferation, and indicate that decreased autophagy may benefit AML cells. We postulate that modulation of autophagy could help maintain stem cell function, for example during transplantation, and aid AML therapy in a setting-specific manner.
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Books on the topic "Apoptosis. Acute myeloid leukemia"

1

Fortina, Paolo, Eric Londin, Jason Y. Park, and Larry J. Kricka, eds. Acute Myeloid Leukemia. New York, NY: 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. Cham: 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. New York, NY: Springer New York, 2015. http://dx.doi.org/10.1007/978-1-4939-1393-0.

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Mertzlufft, Nancy. Gift of life. Kansas City, Mo: Sheed & Ward, 1985.

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

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National Institute for Clinical Excellence. Guidance on the use of imatinib for chronic myeloid leukaemia. London: 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. London: 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. Berlin, Heidelberg: 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. New York: Riverhead Books, 2008.

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

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Book chapters on the topic "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, 47–65. New York, NY: 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, 151–73. New York, NY: 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, 122–30. Berlin, Heidelberg: 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, 121–28. Boca Raton : Taylor & Francis, a CRC title, part of the Taylor & Francis imprint, a member of the Taylor & Francis Group, the academic division of T&F Informa plc, 2018. | Series: Pocket guides to biomedical sciences: 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, 173–91. New York, NY: 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, 527–59. Cham: 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, 61–85. Singapore: 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, 89–96. Chichester, UK: 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, 89–100. Hoboken, NJ, USA: 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, 45–139. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2010. http://dx.doi.org/10.1002/9781118010136.ch5.

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Conference papers on the topic "Apoptosis. Acute myeloid leukemia"

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Rosen, David B., Mark D. Minden, Santosh Putta, Todd Covey, Ying-Wen Huang, Alessandra Cesano, Garry P. Nolan, and Wendy J. Fantl. "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, Gautam Borthakur, Steven M. Kornblau, Michael Andreeff, and Marina Konopleva. "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, Dhruv Chachad, Hiroaki Kitamura, Jo Ishizawa, Michael Andreeff, and Shinya Kimura. "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, Dominik Heimann, Peter Teriete, Carol Burian, James Mason, Nicholas D. Cosford, and Kristiina Vuori. "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 therapeutic effects of this drug. To solve this problem, several new drugs similar to imatinib have been developed in search for a new revolutionary molecule, with the same therapeutic potential. In this work, we study two second-generation inhibitors, dasatinib and afatinib, and compare their interactions with those of imatinib. Furthermore, we calculated the inhibition constant of afatinib, which is currently not used in this particular protein.
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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, Robert Peralta, Howard Cukier, Jeff Lightfoot, Yoon Lee, Aiping Young, and William G. Rice. "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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Reports on the topic "Apoptosis. Acute myeloid leukemia"

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Zhang, Chengcheng. Dissecting the Role of IGFBP-2 in Development of Acute Myeloid Leukemia. Fort Belvoir, VA: Defense Technical Information Center, June 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), January 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, December 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), January 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, September 2020. http://dx.doi.org/10.37766/inplasy2020.9.0019.

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Yin, Xuewei, Yi Ding, Liming Yu, Chenchen Guo, Yanyan Cui, Xixi Zhai, Yan wang, 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, April 2021. http://dx.doi.org/10.37766/inplasy2021.4.0106.

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