2022
Mildly dysplastic oral lesions with optically-detectable abnormalities share genetic similarities with severely dysplastic lesions
Brenes D, Nipper A, Tan M, Gleber-Netto F, Schwarz R, Pickering C, Williams M, Vigneswaran N, Gillenwater A, Sikora A, Richards-Kortum R. Mildly dysplastic oral lesions with optically-detectable abnormalities share genetic similarities with severely dysplastic lesions. Oral Oncology 2022, 135: 106232. PMID: 36335817, PMCID: PMC9881670, DOI: 10.1016/j.oraloncology.2022.106232.Peer-Reviewed Original ResearchConceptsOral premalignant lesionsMild dysplasiaSevere dysplasiaOral lesionsPremalignant lesionsDysplastic oral lesionsHigh-grade pathologySubset of lesionsLoss of autofluorescenceDysplastic lesionsOptical imaging studiesOral surgeryDysplasiaDetectable abnormalitiesPatient careLesionsImaging studiesEpithelial cell nucleiPatientsGene expressionGene expression profilesMarkersGene expression analysisSimilar gene expressionExpression profilesGenetic Changes Driving Immunosuppressive Microenvironments in Oral Premalignancy
Rangel R, Pickering CR, Sikora AG, Spiotto MT. Genetic Changes Driving Immunosuppressive Microenvironments in Oral Premalignancy. Frontiers In Immunology 2022, 13: 840923. PMID: 35154165, PMCID: PMC8829003, DOI: 10.3389/fimmu.2022.840923.Peer-Reviewed Original ResearchMeSH KeywordsCarcinoma, Squamous CellHumansMouth NeoplasmsPrecancerous ConditionsTumor MicroenvironmentConceptsOral premalignant lesionsImmunosuppressive microenvironmentProgression of OPLsOral cavity cancerGenomic alterationsImmune microenvironmentOral cancerOSCC progressionInflammatory environmentPremalignant lesionsSpecific genomic changesOral premalignancyTherapeutic approachesNovel biomarkersMalignant transformationMicroenvironmental changesCancerProgressionGenomic changesMicroenvironmentAlterationsGenetic changesPremalignancyTherapyLesions
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
2010
DNA Damage Drives an Activin A–Dependent Induction of Cyclooxygenase-2 in Premalignant Cells and Lesions
Fordyce C, Fessenden T, Pickering C, Jung J, Singla V, Berman H, Tlsty T. DNA Damage Drives an Activin A–Dependent Induction of Cyclooxygenase-2 in Premalignant Cells and Lesions. Cancer Prevention Research 2010, 3: 190-201. PMID: 20028875, PMCID: PMC2954106, DOI: 10.1158/1940-6207.capr-09-0229.Peer-Reviewed Original ResearchMeSH KeywordsActivinsAtaxia Telangiectasia Mutated ProteinsBlotting, WesternBreast NeoplasmsCarcinoma in SituCarcinoma, Ductal, BreastCell Cycle ProteinsCyclin-Dependent Kinase Inhibitor p16Cyclooxygenase 2DNA DamageDNA-Binding ProteinsEnzyme-Linked Immunosorbent AssayFemaleGene ExpressionGene Expression ProfilingHumansImmunohistochemistryNeoplasm ProteinsOligonucleotide Array Sequence AnalysisPrecancerous ConditionsProtein Serine-Threonine KinasesRetinoblastoma ProteinReverse Transcriptase Polymerase Chain ReactionSignal TransductionTelomereTelomeric Repeat Binding Protein 2Tumor Suppressor Protein p53Tumor Suppressor ProteinsConceptsCOX-2 expressionCyclooxygenase-2Activin AEpithelial cellsHigh COX-2 expressionPoor clinical outcomeCOX-2 inhibitionCOX-2 inhibitorsTumor-promoting phenotypeSynthesis of prostaglandinsDNA damageDependent inductionVariant human mammary epithelial cellsBreast epithelial cellsHuman mammary epithelial cellsGastrointestinal complicationsSystemic complicationsClinical outcomesDuctal carcinomaCell cycle arrestSitu lesionsChemopreventative agentMammary epithelial cellsCancer metastasisPremalignant cells
2005
p38 Regulates Cyclooxygenase-2 in Human Mammary Epithelial Cells and Is Activated in Premalignant Tissue
Gauthier ML, Pickering CR, Miller CJ, Fordyce CA, Chew KL, Berman HK, Tlsty TD. p38 Regulates Cyclooxygenase-2 in Human Mammary Epithelial Cells and Is Activated in Premalignant Tissue. Cancer Research 2005, 65: 1792-1799. PMID: 15753376, DOI: 10.1158/0008-5472.can-04-3507.Peer-Reviewed Original ResearchMeSH KeywordsApoptosisBreastBreast NeoplasmsCarcinoma, Intraductal, NoninfiltratingCell NucleusCell ProliferationCyclooxygenase 2CytoplasmEnzyme ActivationEnzyme InhibitorsEpithelial CellsFemaleGene Expression Regulation, EnzymologicHumansMembrane ProteinsMiddle AgedP38 Mitogen-Activated Protein KinasesPhosphorylationPrecancerous ConditionsProstaglandin-Endoperoxide SynthasesProstaglandinsTranscription, GeneticConceptsVariant human mammary epithelial cellsCOX-2 expressionCyclooxygenase-2Human mammary epithelial cellsEpithelial cellsMammary epithelial cellsNormal tissuesOverexpress COX-2COX-2 transcriptsDecreases cell survivalCOX-2 transcriptionRegulates Cyclooxygenase-2Ductal carcinomaPremalignant lesionsReduction mammoplastyBreast cancerNeoplastic processTargeted preventionPremalignant tissuesImmediate early genesEarly carcinogenesisUpstream regulatory pathwaysLesionsCell survivalTissue