Individualizing antimetabolic treatment strategies for head and neck squamous cell carcinoma based on TP53 mutational status
Sandulache VC, Skinner HD, Ow TJ, Zhang A, Xia X, Luchak JM, Wong L, Pickering CR, Zhou G, Myers JN. Individualizing antimetabolic treatment strategies for head and neck squamous cell carcinoma based on TP53 mutational status. Cancer 2011, 118: 711-721. PMID: 21720999, PMCID: PMC3188683, DOI: 10.1002/cncr.26321.Peer-Reviewed Original ResearchConceptsMitochondrial respirationGlycolytic dependenceHNSCC cellsAltered tumor cell metabolismGlycolytic inhibitionTumor suppressor geneTumor cell metabolismTP53 mutational statusMitochondrial reserveInhibition of respirationMetabolic shiftCell metabolismCellular resistanceSuppressor geneHNSCC cell linesMutational statusGlycolytic fluxCell linesRespirationNeck squamous cell carcinomaMutationsGlycolysisCellsClonogenic assayRadioresistanceGlucose, not glutamine, is the dominant energy source required for proliferation and survival of head and neck squamous carcinoma cells
Sandulache VC, Ow TJ, Pickering CR, Frederick MJ, Zhou G, Fokt I, Davis‐Malesevich M, Priebe W, Myers JN. Glucose, not glutamine, is the dominant energy source required for proliferation and survival of head and neck squamous carcinoma cells. Cancer 2011, 117: 2926-2938. PMID: 21692052, PMCID: PMC3135768, DOI: 10.1002/cncr.25868.Peer-Reviewed Original ResearchAdenosine TriphosphateCarcinomaCarcinoma, Squamous CellCell CycleCell Line, TumorCell ProliferationChromatography, LiquidDeoxyglucoseDisease ProgressionGenes, p53GlucoseGlutamineHead and Neck NeoplasmsHumansLactic AcidMass SpectrometryMetabolomicsMetforminNeoplasms, Squamous CellSquamous Cell Carcinoma of Head and NeckTreatment OutcomeTumor Suppressor Protein p53