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Journal articles on the topic 'Metabolic CD34+ cells'

Author: Grafiati

Published: 6 July 2024

Last updated: 31 July 2025

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1

Kochi, Yu, Yoshikane Kikushige, Toshihiro Miyamoto, and Koichi Akashi. "Identification of ASCT1 As a Candidate Molecule Enhancing Antioxidant Activity in Primary Human AML Cells." Blood 128, no. 22 (2016): 1674. http://dx.doi.org/10.1182/blood.v128.22.1674.1674.

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Abstract Introduction: Recent studies have shown that the specific alteration of metabolic pathways are involved in the regulation of function of normal hematopoietic stem cells (HSCs) and leukemic stem cells (LSCs) in acute myeloid leukemia (AML). However, little is known about the features of metabolic activity in human HSCs and LSCs. To reveal the metabolic pathway alterations in primary AML cells, we performed the comprehensive metabolome analysis by comparing normal human CD34+ hematopoietic stem/progenitor cells (HSPCs)(n=5) and CD34+ primitive AML cells containing LSCs (n=16) using high

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Fadini, G. P. "Circulating CD34+ cells, metabolic syndrome, and cardiovascular risk." European Heart Journal 27, no. 18 (2006): 2247–55. http://dx.doi.org/10.1093/eurheartj/ehl198.

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Nakasone, Hideki, Misato Kikuchi, Yu Akahoshi, et al. "The Expression of CD83 Would be Increased in CD34-Positive Monocytes Detected in Peripheral Blood Mobilized By G-CSF in Humans." Blood 132, Supplement 1 (2018): 2063. http://dx.doi.org/10.1182/blood-2018-99-112084.

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Abstract [Background] CD34-positive monocytes (CD34+mono) have recently been identified following mobilization by granulocyte-colony stimulating factor (G-CSF), and have been suggested to have a potential to modulate immune functions in animal models. However, the biological feature of CD34+mono in humans still remains unclear. Thus, we explored the difference between CD34+mono, CD34+cells, and monocytes through the analyses of gene expression profiles (GEP). [Methods] CD34+mono (Lin-CD34+CD33+CD14+CD11b+, Figure1), CD34+cells (Lin-CD34+CD33-CD14-CD11b- ), and monocytes (Lin-CD34-CD33+CD14+CD1

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Desterke, Christophe, Estelle Balducci, Xavier Fund, Claire Borie, Annelise Bennaceur-Griscelli, and Ali G. Turhan. "A Novel Metabolic Transcriptome Identified in Myelodysplastic Syndromes (MDS) Correlates with OMS Classification and Poor Prognosis." Blood 132, Supplement 1 (2018): 5495. http://dx.doi.org/10.1182/blood-2018-99-110678.

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Abstract Myelodysplastic syndromes (MDS) are clonal malignancies of the hematopoietic stem cell leading to an ineffective hematopoiesis with a complex and poorly understood pathophysiology combining increased apoptosis and propensity to transformation associated with immune dysregulation. Despite a major improvement of the classification of MDS in terms of diagnosis and prognosis according to OMS recommendations, a significant fraction of MDS remains unclassified. In this study, we wished to determine if the integrative analysis of global MDS transcriptome associated with single cell experimen

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Perrone, Olivia, Tiziana Coppola, James Bartram, Waseem Nasr, Juying Xu, and Marie-Dominique Filippi. "The Effect of SCD-1 Inhibition on Human Hematopoietic Stem Cell Mitochondrial Metabolism, Cell Proliferation, and Differentiation Potential." Blood 142, Supplement 1 (2023): 1308. http://dx.doi.org/10.1182/blood-2023-185260.

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Hematopoietic stem cells (HSC) give rise to all blood lineages and sustain the production of blood cells throughout life. Due to their inherently high regenerative potential, HSC are used in a variety of clinical settings, including bone marrow transplantation (BMT) directly to cure a variety of hematologic and oncologic disorders often with gene therapy. During regeneration, HSC are activated into cycle. For this, HSC undergo drastic mitochondrial and metabolic remodeling to meet the bioenergetic and biosynthetic needs of activated HSC. A growing body of evidence indicates that HSC sustain in

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Poulaki, Aikaterini, Theodora Katsila, Emilia S. Hatziyannis, et al. "Metabolic Reprogramming in Myelodysplastic Syndromes." Blood 144, Supplement 1 (2024): 6694. https://doi.org/10.1182/blood-2024-211216.

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Myelodysplastic syndromes (MDS), lie at the interface of normal differentiation and leukemic transformation, being characterised by polymorphic presentation and elusive pathophysiology. Failure to establish a pathogenic relationship with specific genetic aberrations, along with general paucity in innovative and effective treatment strategies, led us to seek the possible role of a dysregulated metabolism in the disease pathobiology. Plasma and CD34+ progenitors isolated from 19 previously untreated MDS patients (WHO 2022 LB#9, IB1#8, IB2#2 - CD34+ pellet purity 97-99%) and 10 age-sex matched co

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Devaraj, Sridevi, and Ishwarlal Jialal. "Dysfunctional Endothelial Progenitor Cells in Metabolic Syndrome." Experimental Diabetes Research 2012 (2012): 1–5. http://dx.doi.org/10.1155/2012/585018.

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The metabolic syndrome (MetS) is highly prevalent and confers an increased risk of diabetes and cardiovascular disease. A key early event in atherosclerosis is endothelial dysfunction. Numerous groups have reported endothelial dysfunction in MetS. However, the measurement of endothelial function is far from optimum. There has been much interest recently in a subtype of progenitor cells, termed endothelial progenitor cells (EPCs), that can circulate, proliferate, and dfferentiate into mature endothelial cells. EPCs can be characterized by the assessment of surface markers, CD34 and vascular end

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Dalloul, Ali H., Claire Patry, Jean Salamero, Bruno Canque, Fernanda Grassi, and Christian Schmitt. "Functional and Phenotypic Analysis of Thymic CD34+CD1a− Progenitor-Derived Dendritic Cells: Predominance of CD1a+ Differentiation Pathway." Journal of Immunology 162, no. 10 (1999): 5821–28. http://dx.doi.org/10.4049/jimmunol.162.10.5821.

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Abstract Whether thymic dendritic cells (DC) are phenotypically and functionally distinct from the monocyte lineage DC is an important question. Human thymic progenitors differentiate into T, NK, and DC. The latter induce clonal deletion of autoreactive thymocytes and therefore might be different from their monocyte-derived counterparts. The cytokines needed for the differentiation of DC from thymic progenitors were also questioned, particularly the need for GM-CSF. We show that various cytokine combinations with or without GM-CSF generated DC from CD34+CD1a− but not from CD34+CD1a+ thymocytes

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Nishida, Yuki, Edward Ayoub, Darah Scruggs, et al. "Stem-Cell Enriched Cellular Hierarchy of TP53 Mutant Acute Myeloid Leukemia Is Vulnerable to Targeted Protein Degradation of c-MYC." Blood 142, Supplement 1 (2023): 583. http://dx.doi.org/10.1182/blood-2023-174938.

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Deregulation of MYC genes occurs in up to 70% of all human cancers and is associated with hallmarks of cancer including mitochondrial and ribosomal biogenesis, cell cycle progression, and metabolic abnormalities. TP53 regulates MYC while MYC suppresses TP53, suggesting counteracting negative feedback loops. Therefore, MYC or its function can be activated when TP53 is not functional. TP53 mutations occur in 30% of relapsed/refractory acute myeloid leukemias (AMLs) patients' survival is dismal, and there are no effective therapies for these patients. Compared to TP53 wild-type (TP53wt), TP53 mut

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Rai, Richa, Foramben Patel, Stella Melana, et al. "Rigosertib in Combination with Azacitidine Impacts Metabolic and Differentiation Pathways in the MDS-L Cell Line." Blood 136, Supplement 1 (2020): 35–36. http://dx.doi.org/10.1182/blood-2020-142908.

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Background Myelodysplastic Syndrome (MDS) is characterized by ineffective clonal hematopoiesis with peripheral blood cytopenias, leading to death from infection or bleeding. Azacitidine (AZA), a hypomethylating agent (HMA) is the standard of care for treatment of MDS patients (pts) with higher-risk MDS [Silverman LR, The Myelodysplastic Syndrome in Cancer Medicine, Editors: R.J. Bast, et al. 2017]. Responses to AZA occur in 50% of pts with significant effects on hematopoiesis ranging from improvement in a single lineage to complete restoration of blood counts and transfusion independence [Silv

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Forte, Dorian, Roberto Maria Pellegrino, Francesco Fabbri, et al. "Circulating Extracellular Vesicles from Acute Myeloid Leukemia Patients Drive Distinct Metabolic Profile of Leukemic Cells and Reveal Crucial Lipidomic Biomarkers." Blood 138, Supplement 1 (2021): 3471. http://dx.doi.org/10.1182/blood-2021-150339.

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Abstract Background. Extracellular vesicles (EVs) are submicron vesicles released from various cell types including blood cells with pleiotropic effects on cell signalling and metabolism. EV cargos are enriched in nucleic acids, proteins, and lipids that can be delivered to target cells to influence surrounding microenvironment. Thus, EVs represent a powerful tool for liquid biopsy in hematological malignancies including acute myeloid leukemia (AML). AML is an aggressive disease with high relapse rate and less invasive tools are urgently needed to investigate disease (metabolic) dynamics. Accu

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Rattazzi, Marcello, Sabina Villalta, Silvia Galliazzo, et al. "Low CD34+ cells, high neutrophils and the metabolic syndrome are associated with an increased risk of venous thromboembolism." Clinical Science 125, no. 4 (2013): 211–22. http://dx.doi.org/10.1042/cs20120698.

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The relationship between MetS (metabolic syndrome), levels of circulating progenitor/immune cells and the risk of VTE (venous thromboembolism) has not yet been investigated. We studied 240 patients with previous VTE and 240 controls. The presence of MetS was identified according to NCEP ATP III guidelines and flow cytometry was used to quantify circulating CD34+ cells. VTE patients showed higher BMI (body mass index), waist circumference, triacylglycerol (triglyceride) levels, blood glucose, hs-CRP (high-sensitivity C-reactive protein) and lower HDL-C (high-density lipoprotein cholesterol) lev

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Kuntz, Elodie Marie, Pablo Baquero, Tessa L. Holyoake, Eyal Gottlieb, and G. Vignir Helgason. "Therapy Resistant CML Stem Cells Are Dependent on Mitochondrial Oxidative Metabolism for Their Survival." Blood 128, no. 22 (2016): 932. http://dx.doi.org/10.1182/blood.v128.22.932.932.

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Abstract We and others have shown that tyrosine kinase inhibitors (TKIs), such as imatinib, fail to eliminate primitive chronic myeloid leukaemia (CML) stem cells (LSCs), suggesting that combination of TKIs with other targeted agents will be required to eradicate the LSC-pool. Therefore, identification of targetable pathways that selectively maintain CML LSC survival is critical. Metabolic reprogramming is a core feature of cancer cells making them susceptible to manipulation in a selective manner. Indeed, in recent years numerous studies have shown that targeting abnormal aspects of metabolis

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Wu, Andrew, Katharina Rothe, Min Chen, et al. "Inhibition of the MiR-185-PAK6-Mediated Survival and Metabolic Pathways Selectively Targets Drug-Resistant CML Stem/Progenitor Cells." Blood 134, Supplement_1 (2019): 4138. http://dx.doi.org/10.1182/blood-2019-127826.

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Overcoming drug resistance and targeting leukemic stem cells (LSCs) remain major challenges for curative treatment of human leukemia, including chronic myeloid leukemia (CML). Indeed, most patients with CML require life-long therapy with ABL1 tyrosine kinase inhibitors (TKIs), due to the persistence of residual LSCs that maintain the potential for relapse. Increasing evidence also indicates that LSCs are susceptible to cellular metabolic changes and seem to have a greater dependence on mitochondrial oxidative phosphorylation (OXPHOS) for survival. Previously, through global transcriptome profi

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Díaz-Flores, Lucio, Ricardo Gutiérrez, Maria Pino García, et al. "Cd34+ Stromal Cells/Telocytes in Normal and Pathological Skin." International Journal of Molecular Sciences 22, no. 14 (2021): 7342. http://dx.doi.org/10.3390/ijms22147342.

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We studied CD34+ stromal cells/telocytes (CD34+SCs/TCs) in pathologic skin, after briefly examining them in normal conditions. We confirm previous studies by other authors in the normal dermis regarding CD34+SC/TC characteristics and distribution around vessels, nerves and cutaneous annexes, highlighting their practical absence in the papillary dermis and presence in the bulge region of perifollicular groups of very small CD34+ stromal cells. In non-tumoral skin pathology, we studied examples of the principal histologic patterns in which CD34+SCs/TCs have (1) a fundamental pathophysiological r

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Thomas, Geethu, Laura Garcia Prat, Marcela Gronda, et al. "The Metabolic Enzyme Hexokinase 2 Localizes to the Nucleus in AML and Normal Hematopoietic Stem/Progenitor Cells to Maintain Stemness." Blood 132, Supplement 1 (2018): 2795. http://dx.doi.org/10.1182/blood-2018-99-110021.

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Abstract Hematopoietic cells are arranged in a hierarchy where stem and progenitor cells differentiate into mature blood cells. Likewise, AML (Acute Myeloid Leukemia) is also hierarchical with leukemic stem and progenitor cells giving rise to more mature and differentiated blasts. Recent studies have shown that mitochondrial enzymes such as IDH2 can regulate AML stemness by altering metabolites that affect epigenetic marks. However, it is unknown whether mitochondrial metabolic enzymes can directly localize to the nucleus to regulate stemness in AML and normal hematopoietic cells. Here, we sho

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Subedi, Amit, Qiang Liu, David Sharon, et al. "Nicotinamide Phosphoribosyltransferase Inhibitors Induce Apoptosis of AML Stem Cells through Dysregulation of Lipid Metabolism." Blood 136, Supplement 1 (2020): 25–26. http://dx.doi.org/10.1182/blood-2020-142404.

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Current chemotherapeutic regimens for acute myeloid leukemia (AML) often fail to eliminate leukemic stem cells (LSCs) which contribute to disease relapse. A key step towards the development of more effective therapies is the identification of vulnerabilities that are unique to LSCs. Here, we sought to identify LSC-specific metabolic dependencies by performing a flow cytometry-based screen of 110 metabolically-focused drugs against a primary human AML sample. This sample harbored distinct subsets defined by CD34 and CD38 expression, and LSC activity assayed by xenotransplantation was restricted

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Pershina, Pakhomova, Widera, et al. "Gender Differences in the Pharmacological Actions of Pegylated Glucagon-Like Peptide-1 on Endothelial Progenitor Cells and Angiogenic Precursor Cells in a Combination of Metabolic Disorders and Lung Emphysema." International Journal of Molecular Sciences 20, no. 21 (2019): 5414. http://dx.doi.org/10.3390/ijms20215414.

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In clinical practice, the metabolic syndrome (MetS) is often associated with chronic obstructive pulmonary disease (COPD). Although gender differences in MetS are well documented, little is known about sex-specific differences in the pathogenesis of COPD, especially when combined with MetS. Consequently, it is not clear whether the same treatment regime has comparable efficacy in men and women diagnosed with MetS and COPD. In the present study, using sodium glutamate, lipopolysaccharide, and cigarette smoke extract, we simulated lipid metabolism disorders, obesity, hyperglycemia, and pulmonary

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Krüger, Karsten, Rainer Klocke, Julia Kloster, Sigrid Nikol, Johannes Waltenberger, and Frank C. Mooren. "Activity of daily living is associated with circulating CD34+/KDR+ cells and granulocyte colony-stimulating factor levels in patients after myocardial infarction." Journal of Applied Physiology 116, no. 5 (2014): 532–37. http://dx.doi.org/10.1152/japplphysiol.01254.2013.

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The study aimed to investigate whether the extent of activities of daily living (ADL) of patients after myocardial infarction affect numbers of circulating CD34+/KDR+ and CD45+/CD34+ cells, which are supposed to protect structural and functional endothelial integrity. In a cross-sectional study, 34 male coronary artery disease patients with a history of myocardial infarction were assessed for times spent per week for specific physical ADL, including basic activities (instrumental ADL), leisure time activities, and sport activities, using a validated questionnaire. Individual specific activity

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Michurova, Marina Sergeevna, Victor Yur'evich Kalashnikov, Olga Michailovna Smirnova, Olga Nikolaevna Ivanova, and Sergey Anatol'evich Terekhin. "Mobilization of endothelial progenitor cells after endovascular interventions in patients with type 2 diabetes mellitus." Diabetes mellitus 17, no. 4 (2014): 35–42. http://dx.doi.org/10.14341/dm2014435-42.

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Aim. To investigate the mobilisation of endothelial progenitor cells (EPC) in patients with type 2 diabetes mellitus (T2DM) after endovascular interventions for coronary and peripheral arteries. Materials and Methods. The levels of EPC in peripheral blood were determined by flow cytometry in 42 patients prior to endovascular intervention and 2?4 days after surgery. EPC were defined as CD34+ VEGFR2+ CD45- and CD34+ CD133+CD45- cells. Twenty-three patients with T2DM were included in group 1, and 19 patients without metabolic disorders were included in group 2. Results. The levels of EPC in the p

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Guo, Bin, Xinxin Huang та Hal E. Broxmeyer. "Antagonizing PPARγ Expands Human Hematopoietic Stem and Progenitor Cells By Switching on FBP1-Repressed Glycolysis and Preventing Differentiation". Blood 130, Suppl_1 (2017): 709. http://dx.doi.org/10.1182/blood.v130.suppl_1.709.709.

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Abstract Allogeneic hematopoietic cell transplantation (HCT) is widely used as a life-saving treatment for malignant and non-malignant blood disorders. Hematopoietic stem cells (HSCs) are a major contributing cell population for a successful HCT. While cord blood (CB) is an acceptable source of HSCs for clinical HCTbecause of its many advantages including prompt availability, lower incidence of GvHD and virus infection, CB HCT is usually associated with slower time to engraftment especially in adult patients when compared with other cell sources; this is partly due to limiting numbers of HSCs

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Pierre-Louis, Olivier, Denis Clay, Bernadette Guerton, et al. "A New Multiparametric Flow Cytometry Technique Based on Combined Side Population (SP) and Aldehyde Deshydrogenase (ALDH) Functionalities Identifies a Hierarchy within the Human Hematopoietic Stem/Progenitor Compartment." Blood 110, no. 11 (2007): 2226. http://dx.doi.org/10.1182/blood.v110.11.2226.2226.

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Abstract Hematopoietic stem cells (HSC) are characterized by their potential to reconstitute in vivo haematopoiesis in NOD/SCID mice and to give rise to differentiated cells of all haematopoietic lineages. They are usually defined by a CD34+CD38−CD90+ antigenic profile; however taking into account the versatility of antigen membrane expression (Lataillade et al., J. Leukoc. Biol. 2005), more reliable methods based on their selective functional/metabolic activities such as ABCG2 activity and Aldehyde Deshydrogenase expression have been developed. Actually, HSC can be purified on basis of Hoechs

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Forte, Dorian, Filippo Maltoni, Samantha Bruno, et al. "Single-Cell Metabolic Profiling Integrated with Extracellular Vesicle Analysis Reveals Novel Metabolic Vulnerabilities and Prognostic Biomarkers in Acute Myeloid Leukemia." Blood 142, Supplement 1 (2023): 1598. http://dx.doi.org/10.1182/blood-2023-185909.

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Introduction Acute myeloid leukemia (AML) is an aggressive disease for which less invasive tools are needed to explore disease dynamics. Changes in cell metabolism and metabolic adaptation are hallmark features for AML, thus emerging as promising therapeutic targets. However, it is still poorly elucidated whether and which extrinsic microenvironment signals may regulate the metabolic reprogramming occurring in AML. In this regard, Extracellular Vesicles (EVs) represent a promising tool for non-invasive liquid biopsy and may reveal a novel role in energy metabolism as well as clinically relevan

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Kikushige, Yoshikane, Toshihiro Miyamoto, Takahiro Maeda, and Koichi Akashi. "Human Acute Leukemia Is Addicted to Branched-Chain Amino Acid Metabolism to Maintain Leukemia Stemness." Blood 134, Supplement_1 (2019): 2516. http://dx.doi.org/10.1182/blood-2019-129372.

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Hematopoietic stem cells (HSCs) have capabilities to self-renew, maintaining an undifferentiated status, as well as to proliferate and mature into blood cells. Similarly, cancer stem cells (CSCs) self-renew and propagate to form cancer tissues. In human acute myeloid leukemia (AML) and acute lymphoblastic leukemia (ALL), CSC-like populations that can reconstitute human leukemia in immuno-deficient mice have been found, and are called leukemic stem cells or leukemia-initiating cells (LICs). In order to obtain "cure" by eradicating LICs, it should be critical to understand molecular machineries

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Mendler, Jason H., Marlene Balys, Umayal Sivagnanalingam, et al. "Distinct Properties of Leukemia Stem Cells in Primary Refractory Acute Myeloid Leukemia." Blood 126, no. 23 (2015): 685. http://dx.doi.org/10.1182/blood.v126.23.685.685.

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Abstract Introduction: Acute Myeloid Leukemia (AML) patients who are refractory to induction chemotherapy (RF) have a dismal prognosis. Properties of AML cell populations that cause the refractory phenotype are poorly understood. It is postulated that the leukemia stem cell (LSC) pool promotes chemotherapy resistance in AML; yet whether differences exist in this pool as a function of eventual remission status, and thus may account for induction failure, is unknown. Our group has recently found that in AML patients who initially achieve complete remission (CR) and then relapse, the LSC pool evo

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Qiu, Jiajing, Jana Gjini, Tasleem Arif, Kateri Moore, Miao Lin, and Saghi Ghaffari. "Using mitochondrial activity to select for potent human hematopoietic stem cells." Blood Advances 5, no. 6 (2021): 1605–16. http://dx.doi.org/10.1182/bloodadvances.2020003658.

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Abstract Hematopoietic cell transplantation is a critical curative approach for many blood disorders. However, obtaining grafts with sufficient numbers of hematopoietic stem cells (HSCs) that maintain long-term engraftment remains challenging; this is due partly to metabolic modulations that restrict the potency of HSCs outside of their native environment. To address this, we focused on mitochondria. We found that human HSCs are heterogeneous in their mitochondrial activity as measured by mitochondrial membrane potential (MMP) even within the highly purified CD34+CD38−CD45RA−CD90+CD49f+ HSC po

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Antonova, E. I., D. I. Omarova, N. V. Firsova, and K. A. Krasnikova. "The Role of Liver Progenitor Cells in Postembryonic Development of <i>Rana terrestris</i> under Normal Physiological Conditions." Uchenye Zapiski Kazanskogo Universiteta Seriya Estestvennye Nauki 166, no. 1 (2024): 38–65. http://dx.doi.org/10.26907/2542-064x.2024.1.38-65.

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The liver plays an essential role in the metabolism of animals, acting as a central hub for metabolic reactions. It serves as a “peripheral integrator” and balances the body’s energy needs. Its regenerative capacity is remarkably high and is maintained by the proliferation of hepatocytes, as well as hematopoietic and regional liver progenitor cells (LPC). This study investigated LPC-driven liver regeneration during postembryonic development in Rana terrestris under normal physiological conditions. The analysis of intrahepatic and hematopoietic markers by immunohistochemistry and flow cytometry

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Chu, Su, Tinisha McDonald, and Ravi Bhatia. "Enhanced Phosphorylation and Altered Localization Lead to Impairment of p27kip Activity in CML Progenitor Cells Despite Enhanced Protein Translation and Expression." Blood 110, no. 11 (2007): 999. http://dx.doi.org/10.1182/blood.v110.11.999.999.

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Abstract The cyclin-dependent kinase inhibitor p27kip is a key regulator of hematopoietic progenitor proliferation and pool size. The activity of p27 can be regulated by modulation of its expression and localization in different cellular compartments. The levels of p27 protein expression are reported to be reduced in BCR-ABL expressing cell lines. In contrast p27 levels have been reported to be elevated in BCR/ABL expressing CML progenitor cells. However, CML progenitors paradoxically demonstrate enhanced proliferation despite having elevated levels of p27. Therefore the regulation of p27 prot

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Mantel, Charlie, Steven Messina-Graham, Akira Moh, Xin-Yuan Fu, and Hal E. Broxmeyer. "The Earliest Stages of Loss of Stem Cell Self-Renewal in-Vivo Is Linked to Upregulated Biosynthesis of “Quiet” Mitochondria and Is Influenced by CXCR4 Activation and STAT3 Gene Deletion." Blood 114, no. 22 (2009): 2546. http://dx.doi.org/10.1182/blood.v114.22.2546.2546.

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Abstract Abstract 2546 Poster Board II-523 One attribute of all stem cells is self-renewal (SR). Progress has been made in identifying genes/proteins involved in stem cell SR mechanisms, especially in embryonic stem cells, but very little is known in adult stem cells such as hematopoietic stem cells (HSCs). Mitochondria (Mt) have recently been considered more than an ATP generator and mediator of apoptosis. They act as a kind of scaffold for integrating numerous signals to and from the nucleus and from the extracellular environment, and signals involved in differentiation and cell cycle. They

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Irifune, Hidetoshi, Yu Kochi, Masayasu Hayashi, Yoshikane Kikushige, Toshihiro Miyamoto, and Koichi Akashi. "Identification of GPAT1 As a Novel Therapeutic Target for Acute Leukemia By Inhibiting Leukemia Specific Metabolism." Blood 134, Supplement_1 (2019): 1384. http://dx.doi.org/10.1182/blood-2019-125661.

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With the development of mass spectrometer technology, recent studies revealed the critical roles of cancer-specific metabolism for tumor propagation in several types of cancers. In leukemia, many studies have been conducted to elucidate a leukemia-specific metabolism, and several effective treatments such as IDH1/2 inhibitors targeting acute myeloid leukemia (AML) with IDH1/2 mutation have been developed. To identify the new metabolic pathways on which acute leukemia cells depend, we purified water-soluble metabolites from CD34+ hematopoietic stem and progenitor cells (HSPCs) of healthy donors

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Peng, Ching-Tien. "Metabolic Reprogramming of Human Mitochondrial NAD(P)+-Dependent-Malic Enzyme 2 in Acute Myeloid Leukemia." Blood 134, Supplement_1 (2019): 5168. http://dx.doi.org/10.1182/blood-2019-123339.

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Yu-Nan Huang1, Kang-Hsi Wu4, Te-fu Weng4, Su-Ching Liu4, Hui-Chih Hung1*, Ching-Tien Peng4,5* FLT3 internal tandem duplication (FLT3-ITD) mutations in patients with acute myeloid leukemia (AML) are usually associated with other mutations resulting in unfavorable outcome. Tyrosine kinase inhibitors (TKI) have shown promising responses, however, these responses are almost transient in therapy-resistant AML. Here, we show that human mitochondrial NAD(P)+-dependent-malic enzyme 2 (ME2) have significantly increased in CD34+ cell of patients with AML. To determine how ME2 establish metabolic reprogr

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Gueller, Saskia, Martina Komor, Julian C. Desmond, et al. "Identification of Putative New Tumor Suppressor Genes in Highly Purified CD34+ Bone Marrow Cells from Patients with Myelodysplastic Syndromes." Blood 104, no. 11 (2004): 204. http://dx.doi.org/10.1182/blood.v104.11.204.204.

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Abstract Activation of transcription of DNA by demethylation and hyperacetylation is known to cause hematologic improvement in patients with myelodysplastic syndromes (MDS). In this study we discriminated genes not expressed in CD34+ cells from untreated patients with MDS but activated by in vitro demethylation (2-aza-5-deoxycytidine, Decitabine) and hyperacetylation (suberoylanilide hydroxamic acid, SAHA). Highly purified CD34+ cells from normal individuals (n=3) and patients with low (n=3) and high (n=3) risk MDS were cultured with SCF (50 ng/ml), IL-3 (10 ng/ml) and GM-CSF (10 ng/ml). The c

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Zarou, Martha M., Kevin Rattigan, Zuzana Brabcova, et al. "Inhibition of Folate Metabolism Drives Autophagy-Dependent Differentiation and Reduces Survival of Therapy-Resistant Leukaemic Stem Cells." Blood 138, Supplement 1 (2021): 2543. http://dx.doi.org/10.1182/blood-2021-149664.

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Abstract Metabolic rewiring is an important hallmark of cancer. The folate metabolism pathway, also known as one-carbon (1C) metabolism, allows for transfer of 1C units through folate intermediates for biosynthetic processes, including precursors for DNA synthesis. Recent studies have shown that enzymes involved in the mitochondrial arm of 1C metabolism are overexpressed in a subset of aggressive cancers and that their expression affects responses to anti-metabolite drug treatments. However, the role of 1C metabolism in therapy resistant leukemic stem cells (LSCs) is currently unknown. Therefo

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Bosman, Matthieu C. J., Jan J. Schuringa, Wim J. Quax та Edo Vellenga. "Identification of the TAK1-NF-κB Axis As Critical Regulator of AML Stem and Progenitor Cell Survival." Blood 120, № 21 (2012): 2982. http://dx.doi.org/10.1182/blood.v120.21.2982.2982.

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Abstract Abstract 2982 A small population of leukemic stem cells is resistant to chemotherapy and is responsible for the leukemic out-growth and relapse in acute myeloid leukemia (AML) patients. Evasion of apoptosis might be one of the essential mechanisms involved in this process. In order to gain more insight into the differences in the apoptotic programming between normal and leukemic (stem) cells, we recently performed gene array analysis by comparing CD34+ AML cells versus CD34+ normal bone marrow (NBM) cells. Gene ontology (GO) analysis of the differentially expressed genes between AML a

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Redondo Monte, Enric, Anja Wilding, Georg Leubolt, et al. "Loss of ZBTB7A Facilitates RUNX1/RUNX1T1-Dependent Clonal Expansion and Sensitizes for Metabolic Inhibition." Blood 132, Supplement 1 (2018): 1499. http://dx.doi.org/10.1182/blood-2018-99-114789.

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Abstract ZBTB7A is a transcription factor involved in the regulation of metabolism and hematopoietic linage fate decisions. Recently, we found ZBTB7A mutated in 23% of Acute Myeloid Leukemia (AML) patients with t(8;21) translocation (Hartmann et al., 2016, Nat Commun). However, the oncogenic collaboration between ZBTB7A alterations and the RUNX1/RUNX1T1 fusion in AML t(8;21) remains poorly understood. To study ZBTB7A mutations in the context of RUNX1/RUNX1T1-dependent transformation, we used human CD34+ cells co-transduced with a truncated form of RUNX1/RUNX1T1 and ZBTB7A wild-type (WT) or its

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Carter, Bing Z., Po Yee Mak, Wenjing Tao, et al. "Mcl-1/CDK9 Targeting By AZD5991/AZD4573 Overcomes Intrinsic and Acquired Venetoclax Resistance in Vitro and In Vivo in PDX Model of AML through Modulation of Cell Death and Metabolic Functions." Blood 132, Supplement 1 (2018): 768. http://dx.doi.org/10.1182/blood-2018-99-113491.

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Abstract Mcl-1 and Bcl-2 are two major anti-apoptotic Bcl-2 proteins frequently overexpressed in malignant cells. They cooperatively support cell survival and are associated with therapy resistance. ABT-199 (venetoclax), a highly selective Bcl-2 inhibitor, showed potent preclinical activity but limited clinical efficacy in AML as a single agent. Mcl-1 is induced by and a major resistance factor to ABT-199. Mcl-1 was recently found to also positively regulate mitochondrial oxidative phosphorylation that induces cancer stem cells and promotes chemoresistance. Mcl-1 is essential for the developme

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Reiman, Lauren T., My H. Vu, Michael Cotez-Bacolot, Brent L. Wood, and Alexandra E. Kovach. "Flow Cytometric Quantitation of CD34+ Progenitors in Peripheral Blood: An Underutilized Tool in Diagnostic Evaluation of Pancytopenia." Blood 144, Supplement 1 (2024): 1316. https://doi.org/10.1182/blood-2024-205737.

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Aplastic anemia (AA) is a type of immune-mediated bone marrow (BM) failure characterized by peripheral pancytopenia and marrow hypocellularity. The disease demonstrates decreased to absent CD34+ progenitors, including hematopoietic stem cells (HSCs), due to their diminished production. In normal healthy individuals, small numbers of CD34+ progenitors are detectable in peripheral blood (PB) by flow cytometry. In patients with pancytopenia due to AA, other BM failure syndromes (genetic etiologies) and/or transient bone marrow suppression (viral or other reactive etiologies), PB CD34+ progenitors

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Orchard, Paul, Glen D. Raffel, Carolyn H. Condon, et al. "Preliminary Phase 2 Results Demonstrate Engraftment with Minimal Neutropenia with MGTA-456, a CD34+ Expanded Cord Blood (CB) Product in Patients Transplanted for Inherited Metabolic Disorders (IMD)." Blood 132, Supplement 1 (2018): 3467. http://dx.doi.org/10.1182/blood-2018-99-115102.

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Abstract Background: IMDs including mucopolysaccharidosis type IH (MPS1/Hurler Syndrome), metachromatic leukodystrophy (MLD), globoid cell leukodystrophy (GLD) and cerebral adrenoleukodystrophy (cALD) are progressive, fatal diseases affecting the central nervous system which are treatable through allogeneic hematopoietic stem cell transplantation (HSCT). CB, in the absence of a matched donor, is the preferred source of stem cells as it is rapidly available and allows greater flexibility in allele matching. As a result of low cell doses, CB transplants in IMD are associated with prolonged perio

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Lahey, Ryan, Jesper Bonde, and Jan A. Nolta. "Uptake of Protamine Sulphate Complexed Fluorescent Nano-Particles Is Defined by Cell Cycle Status in Primary Human CD34+ Cells: Use of a Multi-Color p27 kip1 Based Flow Cytometric Assay." Blood 106, no. 11 (2005): 1363. http://dx.doi.org/10.1182/blood.v106.11.1363.1363.

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Abstract The use of iron based nano-particles for multi-modal imaging is gaining interest, since it allows high resolution non-invasive in vivo imaging of human hematopoietic homing and engraftment events in xenograft models. The uptake of ferridex nano-particles complexed to cationic protamine sulphate is believed to be non-specific through mechanisms like endocytosis, but this has not been well defined for hematopoietic stem cells (HSC). In defining ex vivo cultivation strategies for manipulation of human HSC, a key factor is the responsiveness of the most primitive cells to the in vitro con

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Mistry, Jayna J., Charlotte Hellmich, Jamie A. Moore, et al. "Daratumumab Inhibits AML Metabolic Capacity and Tumor Growth through Inhibition of CD38 Mediated Mitochondrial Transfer from Bone Marrow Stromal Cells to Blasts in the Leukemic Microenvironment." Blood 134, Supplement_1 (2019): 1385. http://dx.doi.org/10.1182/blood-2019-128592.

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Background Acute myeloid leukemia (AML) is dependent on the bone marrow microenvironment, where bone marrow stromal cells (BMSCs) are an important tumor supporting cell type. We have previously demonstrated that, contrary to the Warburg hypothesis, AML blasts rely on oxidative phosphorylation for survival and are dependent on increased mitochondrial levels compared to non-malignant CD34+ progenitor cells. Moreover, we found that AML blasts meet their high metabolic demands by transferring in mitochondria from surrounding BMSC. We have also recently described how mitochondria are transferred fr

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Thomas, Geethu Emily, Grace Egan, Laura Garcia Prat, et al. "The Metabolic Enzyme Hexokinase 2 Localizes to the Nucleus in AML and Normal Hematopoietic Stem/Progenitor Cells to Maintain Stemness." Blood 136, Supplement 1 (2020): 1–2. http://dx.doi.org/10.1182/blood-2020-135858.

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Abstract Mitochondrial metabolites affect epigenetic marks, but it is largely unknown whether mitochondrial metabolic enzymes can directly localize to the nucleus to regulate stem cell function in AML. Here, we discovered that the mitochondrial enzyme, Hexokinase 2 (HK2), localizes to the nucleus in AML and normal hematopoietic stem cells to maintain stem cell function. We searched for mitochondrial enzymes moonlighting in the nucleus using 8227 AML cells, a low passage primary AML culture model arranged in a hierarchy with functionally defined stem cells in the CD34+CD38-fraction. By immunobl

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Woolthuis, Carolien M., Hendrik JM de Jonge, Annet Z. Vos, et al. "Gene Expression Profiling In Leukemic Stem Cell-Enriched AML CD34+ Cell Fraction Identifies Target Genes That Predict Prognosis In Normal Karyotype AML." Blood 116, no. 21 (2010): 952. http://dx.doi.org/10.1182/blood.v116.21.952.952.

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Abstract Abstract 952 Acute myeloid leukemia (AML) is clinically, cytogenetically and molecularly a heterogeneous disease which makes it challenging to classify it properly. In recent years major advances have been achieved in predicting outcome. However, there is still need for more powerful and independent prognostic factors that can guide treatment decisions, especially for the large subgroup of patients presenting with normal karyotype AML. In order to improve the identification of prognostic markers, gene expression studies have been performed. However, most of these studies have analyzed

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Alt, Ruediger, Thomas Riemer, Oliver Fiehn, Dietger Niederwieser, and Michael Cross. "Evidence for Restricted Glycolytic Metabolism in Primary CD133+ Cells." Blood 106, no. 11 (2005): 1726. http://dx.doi.org/10.1182/blood.v106.11.1726.1726.

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Abstract The slow cycling, location and hypoxia-resistance of hematopoietic stem cells are suggestive of a restricted metabolism. We propose that HSC metabolism is adapted to unique metabolic conditions supplied by the stem cell niche, and that a combination of the metabolic and signalling environments acts to support stem cell amplification and to limit it to a narrowly-defined and physiologically rare set of sites. To investigate this possibility, we have established moderate throughput, small scale cultures to examine the metabolic characteristics of primary CD133+ cells isolated from umbil

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Xiang, Wei, Yi Hui Lam, Collin Sng, et al. "Mefloquine Effectively Targets Blast Phase Chronic Myeloid Leukemia through Inducing Oxidative Stress and Lysosomal Disruption." Blood 128, no. 22 (2016): 5426. http://dx.doi.org/10.1182/blood.v128.22.5426.5426.

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Abstract Despite the remarkable clinical responses achieved with BCR-ABL tyrosine kinase inhibitors (TKIs) in the treatment of chronic phase-chronic myeloid leukemia (CML), these TKIs have been less effective as single agents in blast phase (BP) CML. Identification of new therapeutic strategies is needed for the better clinical management of BP-CML. It is well known that the mitochondrial metabolic properties of tumor cells are different from those of normal cells, making this as an attractive target for cancer treatment. Previously, we screened a number of antimicrobial drugs with possible me

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Majidi, Fatemeh, Oumaima Stambouli, Ron-Patrick Cadeddu, et al. "Effect of the Neddylation Inhibitor Pevonedistat on Normal Hematopoietic Stem Cell Subsets and Immune Cell Composition." Blood 138, Supplement 1 (2021): 4787. http://dx.doi.org/10.1182/blood-2021-150095.

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Abstract Introduction: Antitumor activity of the neddylation inhibitor pevonedistat has been documented in several hematologic and non-hematologic malignancies. Unexpectedly, Zhou et al (PNAS, 2016) discovered a dose-dependent biphasic effect of pevonedistat in solid tumor cell lines. While micromolar concentrations inhibited tumor cell growth, low nanomolar concentrations significantly increased cell proliferation and tumor stem cell self-renewal both in vitro and in vivo. The effect of low-dose pevonedistat has not yet been explored in the field of hematopoietic stem cell transplantation. Th

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Wang, DaQuan, Bo Qiu, Qianwen Liu, et al. "Value of Patlak-Ki from ultra-high sensitivity dynamic total body [¹⁸F]FDG PET/CT for evaluation of treatment response to induction immuno-chemotherapy in locally advanced non-small cell lung cancer (LA-NSCLC) patients." Journal of Clinical Oncology 41, no. 16_suppl (2023): e20508-e20508. http://dx.doi.org/10.1200/jco.2023.41.16_suppl.e20508.

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e20508 Background: This study aimed to explore the value of metabolic features in predicting the response to induction immuno-chemotherapy in locally advanced NSCLC, using dynamic total body [18F]FDG PET/CT. Methods: The LA-NSCLC patients who received two cycles of induction immuno-chemotherapy were analyzed in the study. The 60-minute dynamic total body [18F]FDG PET/CT scan was administered before treatment. The primary tumors (PTs) were manually delineated. The metabolic features including the Patlak-Ki, Patlak-Intercept, the SUVmax, metabolic tumor volume (MTV) and total lesion glycolysis (

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Bayraktar, Ulas D., and Maricer Escalon. "An Unusual Presentation of Acute Biphenotypic Leukemia without Bone Marrow Involvement." Blood 112, no. 11 (2008): 3995. http://dx.doi.org/10.1182/blood.v112.11.3995.3995.

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Abstract Acute biphenotypic leukemia (ABL) represents a minority of acute leukemia cases (around 5%) in which blasts co-express markers of different lineages (myeloid, T-cell or B-cell). ABL without bone marrow involvement is exceedingly rare. Case report: An 18-year-old man presented with slowly enlarging, non-tender cervical lymph nodes. He had no other symptoms. Family history included Hodgkin’s disease in his mother and maternal great aunt, histiocytosis X in his maternal cousin, and non-Hodgkin’s lymphoma in his paternal grandfather. Physical exam revealed multiple small cervical and axil

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Song, Byung Hoo, Su Young Son, Hyun Kyu Kim, et al. "Profiling of Metabolic Differences between Hematopoietic Stem Cells and Acute/Chronic Myeloid Leukemia." Metabolites 10, no. 11 (2020): 427. http://dx.doi.org/10.3390/metabo10110427.

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Although many studies have been conducted on leukemia, only a few have analyzed the metabolomic profiles of various leukemic cells. In this study, the metabolomes of THP-1, U937, KG-1 (acute myelogenous leukemia, AML), K562 (chronic myelogenous leukemia, CML), and cord blood-derived CD34-positive hematopoietic stem cells (HSC) were analyzed using gas chromatography-mass spectrometry, and specific metabolic alterations were found using multivariate statistical analysis. Compared to HSCs, leukemia cell metabolomes were found to have significant alterations, among which three were related to amin

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49

Goncalves, Kevin A., Shuping Li, Melissa L. Brooks, Sharon L. Hyzy, Anthony E. Boitano, and Michael P. Cooke. "MGTA-456, a First-in-Class Cell Therapy Produced from a Single Cord Blood Unit, Enables a Reduced Intensity Conditioning Regimen and Enhances Speed and Level of Human Microglia Engraftment in the Brains of NSG Mice." Blood 132, Supplement 1 (2018): 115. http://dx.doi.org/10.1182/blood-2018-99-118258.

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Abstract Background. Allogeneic bone marrow transplant (BMT) is a promising, curative approach for patients with inherited metabolic disorders (IMDs), a class of pediatric diseases characterized by a single enzyme deficiency. The goal of transplant is to provide cells that produce functional enzymes otherwise deficient in these patients, and thereby prevent or ameliorate neurological complications associated with selected IMDs. Donor-derived microglial cells are protective, limiting neurological disease progression. For IMD patients who do not have an HLA matched, non-carrier related donor, co

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Ganan-Gomez, Irene, Kelly S. Chien, Feiyang Ma, et al. "The Transcriptional and Epigenetic Reprogramming of Aged Hematopoietic Stem Cells Drives Myeloid Rewiring in Clonal Hematopoiesis-Associated Cytopenias." Blood 138, Supplement 1 (2021): 3273. http://dx.doi.org/10.1182/blood-2021-150663.

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Abstract Patients (pts) with myelodysplastic syndromes (MDS) have few therapy options. Interventions to improve outcomes should consider strategies that arrest MDS in its early phases, when symptoms are minimal and prolonged survival is expected. To develop prevention strategies that arrest MDS before the disease outcomes become irreversibly dismal, we dissected the molecular and biological mechanisms that maintain MDS in one of its premalignant phases, clonal cytopenia of undetermined significance (CCUS). Recognizing that CCUS is an aging-related disease, we first sought to determine, at the

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