2020
Loss of p53 drives neuron reprogramming in head and neck cancer
Amit M, Takahashi H, Dragomir MP, Lindemann A, Gleber-Netto FO, Pickering CR, Anfossi S, Osman AA, Cai Y, Wang R, Knutsen E, Shimizu M, Ivan C, Rao X, Wang J, Silverman DA, Tam S, Zhao M, Caulin C, Zinger A, Tasciotti E, Dougherty PM, El-Naggar A, Calin GA, Myers JN. Loss of p53 drives neuron reprogramming in head and neck cancer. Nature 2020, 578: 449-454. PMID: 32051587, PMCID: PMC9723538, DOI: 10.1038/s41586-020-1996-3.Peer-Reviewed Original ResearchMeSH KeywordsAdrenergic AntagonistsAdrenergic NeuronsAnimalsCell DivisionCell TransdifferentiationCellular ReprogrammingDisease Models, AnimalDisease ProgressionFemaleHumansMaleMiceMice, Inbred BALB CMicroRNAsMouth NeoplasmsNerve FibersNeuritesReceptors, AdrenergicRetrospective StudiesSensory Receptor CellsTumor MicroenvironmentTumor Suppressor Protein p53Xenograft Model Antitumor AssaysConceptsOral cancerNerve fibersAdrenergic nerve fibersPoor clinical outcomeTrigeminal sensory neuronsLoss of TP53Sensory denervationAdrenergic nervesChemical sympathectomyNerve densitySensory nervesClinical outcomesSolid tumor microenvironmentLoss of p53Neck cancerPharmacological blockadeEndogenous neuronsRetrospective analysisMouse modelSensory neuronsAdrenergic phenotypeAdrenergic receptorsTumor growthTumor progressionTumor microenvironment
2017
Prevalence of promoter mutations in the TERT gene in oral cavity squamous cell carcinoma
Chang K, Wang C, Pickering CR, Huang Y, Tsai C, Tsang N, Kao H, Cheng M, Myers JN. Prevalence of promoter mutations in the TERT gene in oral cavity squamous cell carcinoma. Head & Neck 2017, 39: 1131-1137. PMID: 28230921, DOI: 10.1002/hed.24728.Peer-Reviewed Original ResearchMeSH KeywordsAdultAgedAged, 80 and overCarcinoma, Squamous CellCohort StudiesDisease ProgressionDisease-Free SurvivalFemaleGene Expression Regulation, NeoplasticHumansKaplan-Meier EstimateMaleMiddle AgedMouth NeoplasmsMutationPrevalencePromoter Regions, GeneticReal-Time Polymerase Chain ReactionRetrospective StudiesRisk AssessmentStatistics, NonparametricSurvival AnalysisTaiwanTelomeraseConceptsOral cavity squamous cell carcinomaSquamous cell carcinomaTERT promoter mutationsAdjacent normal tissuesPromoter mutationsSomatic TERT promoter mutationsNormal tissuesC228T mutationTelomerase reverse transcriptase (TERT) promoterT mutationSCC tumor tissuesHuman telomerase reverse transcriptase (hTERT) promoterC250T mutationsReverse transcriptase promoterCell carcinomaSCC tumorsC228TTumor tissueTERT activityBetel nutTERT promoterTissuePresent studyMutationsSanger method
2016
Cross-species identification of genomic drivers of squamous cell carcinoma development across preneoplastic intermediates
Chitsazzadeh V, Coarfa C, Drummond JA, Nguyen T, Joseph A, Chilukuri S, Charpiot E, Adelmann CH, Ching G, Nguyen TN, Nicholas C, Thomas VD, Migden M, MacFarlane D, Thompson E, Shen J, Takata Y, McNiece K, Polansky MA, Abbas HA, Rajapakshe K, Gower A, Spira A, Covington KR, Xiao W, Gunaratne P, Pickering C, Frederick M, Myers JN, Shen L, Yao H, Su X, Rapini RP, Wheeler DA, Hawk ET, Flores ER, Tsai KY. Cross-species identification of genomic drivers of squamous cell carcinoma development across preneoplastic intermediates. Nature Communications 2016, 7: 12601. PMID: 27574101, PMCID: PMC5013636, DOI: 10.1038/ncomms12601.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAntineoplastic AgentsCarcinogenesisCarcinoma, Squamous CellDisease ProgressionDNA Mutational AnalysisExome SequencingFemaleGene Expression ProfilingGenomicsHigh-Throughput Nucleotide SequencingHumansKeratosis, ActinicMiceMice, HairlessMolecular Targeted TherapyPrecancerous ConditionsSequence Analysis, RNASkinSkin NeoplasmsUltraviolet RaysConceptsCross-species genomic analysisCross-species identificationCross-species analysisKey genomic changesGenomic analysisGenomic changesTranscriptional driversDistinct precancerous lesionsGenomic driversPotential targetSquamous cell carcinoma developmentMolecular similarityActinic keratosisAccessible modelDiverse sitesCutaneous squamous cell carcinomaHuman samplesSquamous cell carcinomaHairless mouse modelProgression sequenceMouse modelCarcinoma developmentCell carcinomaPrecancerous lesionsCommon treatment
2015
New DNA Methylation Markers and Global DNA Hypomethylation Are Associated with Oral Cancer Development
Foy JP, Pickering CR, Papadimitrakopoulou VA, Jelinek J, Lin SH, William WN, Frederick MJ, Wang J, Lang W, Feng L, Zhang L, Kim ES, Fan YH, Hong WK, El-Naggar AK, Lee JJ, Myers JN, Issa JP, Lippman SM, Mao L, Saintigny P. New DNA Methylation Markers and Global DNA Hypomethylation Are Associated with Oral Cancer Development. Cancer Prevention Research 2015, 8: 1027-1035. PMID: 26342026, PMCID: PMC4777304, DOI: 10.1158/1940-6207.capr-14-0179.Peer-Reviewed Original ResearchConceptsGlobal DNA hypomethylationOral squamous cell carcinomaOral premalignant lesionsDNA hypomethylationOral cancer-free survivalCancer-free survivalDNA methylation changesDNA methylation profilesPromoter methylationDNA promoter methylationGlobal DNA methylationTumor suppressor geneNew DNA methylation markersPromoter CpG sitesOSCC developmentDNA methylationMethylation changesMethylation profilesFoxi2Degree of methylationSuppressor geneCpG sitesMethylationDNA methylation markersGenes
2014
Mutational Landscape of Aggressive Cutaneous Squamous Cell Carcinoma
Pickering CR, Zhou JH, Lee JJ, Drummond JA, Peng SA, Saade RE, Tsai KY, Curry JL, Tetzlaff MT, Lai SY, Yu J, Muzny DM, Doddapaneni H, Shinbrot E, Covington KR, Zhang J, Seth S, Caulin C, Clayman GL, El-Naggar AK, Gibbs RA, Weber RS, Myers JN, Wheeler DA, Frederick MJ. Mutational Landscape of Aggressive Cutaneous Squamous Cell Carcinoma. Clinical Cancer Research 2014, 20: 6582-6592. PMID: 25303977, PMCID: PMC4367811, DOI: 10.1158/1078-0432.ccr-14-1768.Peer-Reviewed Original ResearchConceptsAggressive cutaneous squamous cell carcinomaCutaneous squamous cell carcinomaSquamous cell carcinomaCell carcinomaCandidate tumor suppressorNeck squamous cell carcinomaNovel therapeutic targetNovel candidate tumor suppressorTumor suppressorWhole-exome sequencingBone invasionPoor outcomeTherapeutic targetLethal diseaseTumor suppressor geneCarcinomaKMT2C mutationsHigh mutational backgroundGene TP53Mutational landscapePutative linkDriver genesDiseaseMutational spectrumUV exposure
2011
Glucose, 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