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dc.contributor.authorMahmood, K.
dc.contributor.authorEmadi, A.
dc.date.accessioned2021-04-12T16:48:43Z
dc.date.available2021-04-12T16:48:43Z
dc.date.issued2021-02-26
dc.identifier.urihttp://hdl.handle.net/10713/15202
dc.description.abstractMetabolic reprogramming contributes to tumor development and introduces metabolic liabilities that can be exploited to treat cancer. Studies in hematological malignancies have shown alterations in fatty acid, folate, and amino acid metabolism pathways in cancer cells. One-carbon (1-C) metabolism is essential for numerous cancer cell functions, including protein and nucleic acid synthesis and maintaining cellular redox balance, and inhibition of the 1-C pathway has yielded several highly active drugs, such as methotrexate and 5-FU. Glutamine depletion has also emerged as a therapeutic approach for cancers that have demonstrated dependence on glutamine for survival. Recent studies have shown that in response to glutamine deprivation leukemia cells upregulate key enzymes in the serine biosynthesis pathway, suggesting that serine upregulation may be a targetable compensatory mechanism. These new findings may provide opportunities for novel cancer treatments. Copyright 2021 by the authors. Licensee MDPI, Basel, Switzerland.en_US
dc.description.sponsorshipThis work was supported by the University of Maryland Greenebaum Comprehensive Cancer Center Support grant (P30CA134274).en_US
dc.description.urihttps://doi.org/10.3390/ph14030190en_US
dc.language.isoen_USen_US
dc.publisherMDPI AGen_US
dc.relation.ispartofPharmaceuticals
dc.subjectAmino acid metabolismen_US
dc.subjectAmino acid restriction in canceren_US
dc.subjectAmino-acid-degrading enzymesen_US
dc.subjectCancer therapyen_US
dc.subjectLeukemiaen_US
dc.title1-c metabolism-serine, glycine, folates-in acute myeloid leukemiaen_US
dc.typeArticleen_US
dc.identifier.doi10.3390/ph14030190


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