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dc.contributor.authorLee, Namgyu
dc.contributor.authorKim, Dohoon
dc.date2022-08-11T08:09:20.000
dc.date.accessioned2022-08-23T16:26:51Z
dc.date.available2022-08-23T16:26:51Z
dc.date.issued2016-12-01
dc.date.submitted2017-02-16
dc.identifier.citationMol Cells. 2016 Dec;39(12):847-854. doi: 10.14348/molcells.2016.0310. Epub 2016 Dec 29. <a href="https://doi.org/10.14348/molcells.2016.0310">Link to article on publisher's site</a>
dc.identifier.issn1016-8478 (Linking)
dc.identifier.doi10.14348/molcells.2016.0310
dc.identifier.pmid28030896
dc.identifier.urihttp://hdl.handle.net/20.500.14038/36652
dc.description.abstractThe early landmark discoveries in cancer metabolism research have uncovered metabolic processes that support rapid proliferation, such as aerobic glycolysis (Warburg effect), glutaminolysis, and increased nucleotide biosynthesis. However, there are limitations to the effectiveness of specifically targeting the metabolic processes which support rapid proliferation. First, as other normal proliferative tissues also share similar metabolic features, they may also be affected by such treatments. Secondly, targeting proliferative metabolism may only target the highly proliferating "bulk tumor" cells and not the slower-growing, clinically relevant cancer stem cell subpopulations which may be required for an effective cure. An emerging body of research indicates that altered metabolism plays key roles in supporting proliferation-independent functions of cancer such as cell survival within the ischemic and acidic tumor microenvironment, immune system evasion, and maintenance of the cancer stem cell state. As these aspects of cancer cell metabolism are critical for tumor maintenance yet are less likely to be relevant in normal cells, they represent attractive targets for cancer therapy.
dc.language.isoen_US
dc.relation<a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=28030896&dopt=Abstract">Link to Article in PubMed</a>
dc.relation.urlhttps://doi.org/10.14348/molcells.2016.0310
dc.rights.urihttp://creativecommons.org/licenses/by-nc-sa/3.0/
dc.subjectcancer
dc.subjectimmune evasion
dc.subjectmetabolism
dc.subjectmetabolites
dc.subjecttumor microenvironment
dc.subjectBiochemistry
dc.subjectCancer Biology
dc.subjectCell Biology
dc.subjectCellular and Molecular Physiology
dc.subjectMolecular Biology
dc.titleCancer Metabolism: Fueling More than Just Growth
dc.typeJournal Article
dc.source.journaltitleMolecules and cells
dc.source.volume39
dc.source.issue12
dc.identifier.legacyfulltexthttps://escholarship.umassmed.edu/cgi/viewcontent.cgi?article=1019&amp;context=metnet_pubs&amp;unstamped=1
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/metnet_pubs/20
dc.identifier.contextkey9698875
refterms.dateFOA2022-08-23T16:26:51Z
html.description.abstract<p>The early landmark discoveries in cancer metabolism research have uncovered metabolic processes that support rapid proliferation, such as aerobic glycolysis (Warburg effect), glutaminolysis, and increased nucleotide biosynthesis. However, there are limitations to the effectiveness of specifically targeting the metabolic processes which support rapid proliferation. First, as other normal proliferative tissues also share similar metabolic features, they may also be affected by such treatments. Secondly, targeting proliferative metabolism may only target the highly proliferating "bulk tumor" cells and not the slower-growing, clinically relevant cancer stem cell subpopulations which may be required for an effective cure. An emerging body of research indicates that altered metabolism plays key roles in supporting proliferation-independent functions of cancer such as cell survival within the ischemic and acidic tumor microenvironment, immune system evasion, and maintenance of the cancer stem cell state. As these aspects of cancer cell metabolism are critical for tumor maintenance yet are less likely to be relevant in normal cells, they represent attractive targets for cancer therapy.</p>
dc.identifier.submissionpathmetnet_pubs/20
dc.contributor.departmentUMass Metabolic Network
dc.contributor.departmentDepartment of Molecular, Cell and Cancer Biology
dc.source.pages847-854


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