2021
Cooperation between oncogenic Ras and wild-type p53 stimulates STAT non-cell autonomously to promote tumor radioresistance
Dong YL, Vadla GP, Lu J, Ahmad V, Klein TJ, Liu LF, Glazer PM, Xu T, Chabu CY. Cooperation between oncogenic Ras and wild-type p53 stimulates STAT non-cell autonomously to promote tumor radioresistance. Communications Biology 2021, 4: 374. PMID: 33742110, PMCID: PMC7979758, DOI: 10.1038/s42003-021-01898-5.Peer-Reviewed Original ResearchMeSH KeywordsA549 CellsAnimalsAnimals, Genetically ModifiedCell ProliferationCytokinesDrosophila melanogasterDrosophila ProteinsFemaleGene Expression Regulation, NeoplasticGenes, rasHumansJanus KinasesLung NeoplasmsMaleMice, NudeMice, TransgenicParacrine CommunicationRadiation ToleranceSignal TransductionSTAT Transcription FactorsTumor BurdenTumor Suppressor Protein p53Xenograft Model Antitumor AssaysConceptsTumor microenvironmentTumor radioresistanceRas clonesOncogenic Ras mutationsClinical outcomesRA tissuesCancer patientsJAK/STATRadiation therapyRobust tumorOncogenic RasTherapy outcomeTumor resistanceTumor tissueRas mutationsTumor cellsJAK/OutcomesRadioresistanceCellular responsesTissueCell-cell interactionsPatientsCytokinesRadiotherapy
2017
Clonal Evolution of Radioresistance in Esophageal Squamous Cell Carcinoma by Single-Cell Whole Exome Sequencing
Yang L, Zhang X, Wu H, Li Y, Zhang H, Jing Z, Hou Q, Jiang M, Hua Y, Vijay P, Mason C, Wu S. Clonal Evolution of Radioresistance in Esophageal Squamous Cell Carcinoma by Single-Cell Whole Exome Sequencing. International Journal Of Radiation Oncology • Biology • Physics 2017, 99: s198-s199. DOI: 10.1016/j.ijrobp.2017.06.493.Peer-Reviewed Original Research
2014
A Functional Screen Identifies miRs That Induce Radioresistance in Glioblastomas
Moskwa P, Zinn PO, Choi YE, Shukla SA, Fendler W, Chen CC, Lu J, Golub TR, Hjelmeland A, Chowdhury D. A Functional Screen Identifies miRs That Induce Radioresistance in Glioblastomas. Molecular Cancer Research 2014, 12: 1767-1778. PMID: 25256711, PMCID: PMC4386891, DOI: 10.1158/1541-7786.mcr-14-0268.Peer-Reviewed Original ResearchConceptsCell cycle checkpoint responsesFunctional screen identifiesTGFβ receptor inhibitorUnbiased functional screenCheckpoint responseScreen identifiesCancer Genome AtlasFunctional screenGlioblastoma patient specimensMolecular networksGlioblastoma datasetGlioblastoma cellsGenome AtlasSystematic identificationGlioblastoma radioresistanceTherapeutic resistanceMiR125aRadioresistanceTGFβNew roleTGFβ inhibitorsTherapeutic applicationsGlioblastomaMIR1MiR150
2011
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 assayRadioresistance
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