Pharmacologic inhibition of fatty acid oxidation sensitizes human leukemia cells to apoptosis induction.
By I. Samudio, R. Harmancey, M. Fiegl, H. Kantarjian, M. Konopleva, Borys Korchin, K. Kaluarachchi, W. Bornmann, S. Duvvuri, H. Taegtmeyer and 1 more. Journal of Clinical Investigation, 2010
678 citations recorded by the source corpus.
Subfields: Cancer Research, Molecular Biology
View Paper: https://www.semanticscholar.org/paper/792f248de514b20b9bc8be04f7b5946a035597d8
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Citations in the corpus
- ROS homeostasis and metabolism: a dangerous liason in cancer cells (2016, background): “Overexpression of the key FAO regulators, such as the carnitine palmitoyltransferase-1,(86) occurs in both solid tumors and leukemia cells,(87) whereas its pharmacological inhibition by etomoxir was found to impair NADPH production and promote oxidative stress-induced cell death in human glioblastom”
- Links between metabolism and cancer. (2012, background): “It is notable that certain cells could also take up free fatty acids from media to support their macromolecular needs, whether for fatty acid oxidation (FAO) or direct insertion into the growing cells’ membranes (Samudio et al. 2010; Zaugg et al. 2011).”
- INHIBITION OF MITOCHONDRIAL TRANSLATION AS A THERAPEUTIC STRATEGY FOR HUMAN ACUTE MYELOID LEUKEMIA (2011, background): “Recently, it was demonstrated that leukemia cells have increased rates of fatty acid oxidation (Samudio et al., 2010), and inhibition of fatty acid oxidation targeted both LSCs and their ‘‘mature’’ blast progeny.”
- Fatty acid uptake and lipid storage induced by HIF-1α contribute to cell growth and survival after hypoxia-reoxygenation. (2014, background): “Other studies have shown the importance of b-oxidation in the development of cancer (Khasawneh et al., 2009; Samudio et al., 2010).”
- CPT1A-mediated fat oxidation, mechanisms and therapeutic potential. (2020, background): “In fact, in leukemia cells, CPT1A was able to antagonize BAK-dependent apoptosis when the cells were challenged with the BCL2-targeted agent ABT-737 (now known as Navitoclax) (120).”
- MYC, Metabolism, and Cancer. (2015, background): “Additional studies to determine whether dormant cancer cells use this previously unsuspected memory T-cell futile cycle may reveal additional metabolic rewiring pathways used by cancer cells (73, 74).”
- Cancer Cell Metabolism: One Hallmark, Many Faces (2012, background): “While glucose and glutamine serve as the primary catabolic substrates of proliferative metabolism, fatty acid oxidation (FAO) can also be used as an additional (or alternative) energy source in some leukemia cells and lung tumors (77, 78).”