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Relevant bibliographies by topics / Chronic Myeloid Leukaemia, Leukaemic Stem Cells, Metabolism, Glutamine

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Journal articles
Dissertations / Theses

Academic literature on the topic 'Chronic Myeloid Leukaemia, Leukaemic Stem Cells, Metabolism, Glutamine'

Author: Grafiati

Published: 14 March 2023

Last updated: 31 July 2025

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Journal articles on the topic "Chronic Myeloid Leukaemia, Leukaemic Stem Cells, Metabolism, Glutamine"

1

Khalaf, Ahmed, Lucie de Beauchamp, Eric Kalkman, et al. "Nutrient-Sensitising Drug Repurposing Screen Identifies Lomerizine As a Mitochondrial Metabolism Inhibitor in Chronic Myeloid Leukaemia." Blood 142, Supplement 1 (2023): 862. http://dx.doi.org/10.1182/blood-2023-186405.

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In chronic myeloid leukaemia (CML), the persistence of leukaemic stem cells (LSCs) following first line treatment with tyrosine kinase inhibitors (TKIs) such as imatinib, can lead to disease relapse. We have previously demonstrated that therapy-resistant CML LSCs rely on oxidative phosphorylation (OXPHOS) for survival and that targeting mitochondrial metabolism sensitises CML LSCs to imatinib treatment. However, current OXPHOS inhibitors have demonstrated limited efficacy, or are associated with adverse effects in clinical trials, highlighting that identification of clinically safe oxidative p

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2

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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3

Zarou, Martha M., Kevin Rattigan, Daniele Sarnello, et al. "Novel Role of Mitochondrial Folate Metabolism in Cell Fate Decisions and Leukaemogenesis." Blood 142, Supplement 1 (2023): 1369. http://dx.doi.org/10.1182/blood-2023-185915.

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Folate-mediated one carbon (1C) metabolism sustains proliferation of rapidly dividing cells through its direct contribution to nucleotide biosynthesis. In brief, new 1C units are donated from the amino acid serine (the primary source of 1C units), while folate molecules function as 1C unit carriers. Accordingly, antifolates have been used in the treatment of several malignancies, particularly in the field of haemato-oncology. Chronic myeloid leukaemia (CML) is a clonal myeloproliferative disorder that arises in a single haematopoietic stem cell with the introduction of the BCR::ABL1 oncoprotei

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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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5

de Beauchamp, Lucie, Ekaterini Himonas, and G. Vignir Helgason. "Mitochondrial metabolism as a potential therapeutic target in myeloid leukaemia." Leukemia, September 24, 2021. http://dx.doi.org/10.1038/s41375-021-01416-w.

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AbstractWhile the understanding of the genomic aberrations that underpin chronic and acute myeloid leukaemia (CML and AML) has allowed the development of therapies for these diseases, limitations remain. These become apparent when looking at the frequency of treatment resistance leading to disease relapse in leukaemia patients. Key questions regarding the fundamental biology of the leukaemic cells, such as their metabolic dependencies, are still unresolved. Even though a majority of leukaemic cells are killed during initial treatment, persistent leukaemic stem cells (LSCs) and therapy-resistan

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6

Rattigan, Kevin M., Zuzana Brabcova, Daniele Sarnello, et al. "Pyruvate anaplerosis is a targetable vulnerability in persistent leukaemic stem cells." Nature Communications 14, no. 1 (2023). http://dx.doi.org/10.1038/s41467-023-40222-z.

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AbstractDeregulated oxidative metabolism is a hallmark of leukaemia. While tyrosine kinase inhibitors (TKIs) such as imatinib have increased survival of chronic myeloid leukaemia (CML) patients, they fail to eradicate disease-initiating leukemic stem cells (LSCs). Whether TKI-treated CML LSCs remain metabolically deregulated is unknown. Using clinically and physiologically relevant assays, we generate multi-omics datasets that offer unique insight into metabolic adaptation and nutrient fate in patient-derived CML LSCs. We demonstrate that LSCs have increased pyruvate anaplerosis, mediated by i

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7

Zarou, Martha M., Kevin M. Rattigan, Daniele Sarnello, et al. "Inhibition of mitochondrial folate metabolism drives differentiation through mTORC1 mediated purine sensing." Nature Communications 15, no. 1 (2024). http://dx.doi.org/10.1038/s41467-024-46114-0.

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AbstractSupporting cell proliferation through nucleotide biosynthesis is an essential requirement for cancer cells. Hence, inhibition of folate-mediated one carbon (1C) metabolism, which is required for nucleotide synthesis, has been successfully exploited in anti-cancer therapy. Here, we reveal that mitochondrial folate metabolism is upregulated in patient-derived leukaemic stem cells (LSCs). We demonstrate that inhibition of mitochondrial 1C metabolism through impairment of de novo purine synthesis has a cytostatic effect on chronic myeloid leukaemia (CML) cells. Consequently, changes in pur

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Dissertations / Theses on the topic "Chronic Myeloid Leukaemia, Leukaemic Stem Cells, Metabolism, Glutamine"

1

POTETI, MARTINA. "The metabolic profile of Chronic Myeloid Leukaemia: stem cells as a target to overcome resistance to therapy." Doctoral thesis, Università di Siena, 2019. http://hdl.handle.net/11365/1071850.

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Chronic Myeloid Leukaemia (CML) is a stem cell-driven disorder treated with Tyrosine Kinase inhibitors (TKi) with impressive efficacy. However, TKi are unable in most cases to prevent the relapse of disease, as even a very successful response to treatment results in the persistence of a state of Minimal Residual Disease (MRD). Our hypothesis predicts that MRD is sustained by the persistence of Leukaemic Stem Cells (LSC) capable to survive and cycle independently of BCR/Abl kinase activity within Bone Marrow (BM) stem cell niches where severe oxygen and glucose shortage would result in BCR/Ablp

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