2001
Escaping the stem cell compartment: Sustained UVB exposure allows p53-mutant keratinocytes to colonize adjacent epidermal proliferating units without incurring additional mutations
Zhang W, Remenyik E, Zelterman D, Brash D, Wikonkal N. Escaping the stem cell compartment: Sustained UVB exposure allows p53-mutant keratinocytes to colonize adjacent epidermal proliferating units without incurring additional mutations. Proceedings Of The National Academy Of Sciences Of The United States Of America 2001, 98: 13948-13953. PMID: 11707578, PMCID: PMC61147, DOI: 10.1073/pnas.241353198.Peer-Reviewed Original ResearchTransgenic expression of survivin in keratinocytes counteracts UVB-induced apoptosis and cooperates with loss of p53
Grossman D, Kim P, Blanc-Brude O, Brash D, Tognin S, Marchisio P, Altieri D. Transgenic expression of survivin in keratinocytes counteracts UVB-induced apoptosis and cooperates with loss of p53. Journal Of Clinical Investigation 2001, 108: 991-999. PMID: 11581300, PMCID: PMC200956, DOI: 10.1172/jci13345.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsApoptosisChromosomal Proteins, Non-HistoneGene ExpressionHumansInhibitor of Apoptosis ProteinsKeratin-14KeratinocytesKeratinsMiceMice, KnockoutMice, TransgenicMicrotubule-Associated ProteinsNeoplasm ProteinsPhenotypePromoter Regions, GeneticSkinSurvivinTumor Suppressor Protein p53Ultraviolet Rays
2000
Regulation of TNFα production and release in human and mouse keratinocytes and mouse skin after UV‐B irradiation
Yarosh D, Both D, Kibitel J, Anderson C, Elmets C, Brash D, Brown D. Regulation of TNFα production and release in human and mouse keratinocytes and mouse skin after UV‐B irradiation. Photodermatology Photoimmunology & Photomedicine 2000, 16: 263-270. PMID: 11132130, DOI: 10.1034/j.1600-0781.2000.160606.x.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAtaxia Telangiectasia Mutated ProteinsCell Cycle ProteinsCell LineCell MembraneEnzyme-Linked Immunosorbent AssayGene Expression RegulationGenes, fosGenes, p53HomozygoteHumansInterleukin-1KeratinocytesMaleMiceMice, Inbred C57BLMice, KnockoutProtein Serine-Threonine KinasesRadiation DosageReceptors, Tumor Necrosis FactorReverse Transcriptase Polymerase Chain ReactionSignal TransductionSirolimusSkinTranscription Factor AP-1Tumor Necrosis Factor-alphaUltraviolet RaysConceptsP53 knockout miceKnockout miceMembrane-bound TNFalphaHomozygous p53 knockout miceC-Fos signalingWild-type miceGene knockout miceRelease of TNFalphaTNFalpha gene expressionAP-1Cultured human keratinocytesImmunosuppressive responseCell culture supernatantsAP-1 transcription factorCultured epidermal cellsIL-1alphaCytokine TNFalphaTNFα productionType micePrimary cytokineTNFalpha inductionTNFalphaBasal levelsMouse skinMice
1999
Induction of cyclin-dependent kinase inhibitors and G1 prolongation by the chemopreventive agent N-acetylcysteine
Liu M, Wikonkal N, Brash D. Induction of cyclin-dependent kinase inhibitors and G1 prolongation by the chemopreventive agent N-acetylcysteine. Carcinogenesis 1999, 20: 1869-1872. PMID: 10469636, DOI: 10.1093/carcin/20.9.1869.Peer-Reviewed Original ResearchMeSH KeywordsAcetylcysteineAnimalsAnticarcinogenic AgentsAntioxidantsCell CycleCell LineChromansCyclin-Dependent Kinase Inhibitor p16Cyclin-Dependent Kinase Inhibitor p21CyclinsFibroblastsFree Radical ScavengersG1 PhaseGene Expression RegulationGene Expression Regulation, NeoplasticGenes, p16GlutathioneHumansKeratinocytesMiceModels, BiologicalNeoplasm ProteinsPapillomaSkin NeoplasmsTumor Cells, CulturedTumor Suppressor Protein p53ConceptsCyclin-dependent kinase inhibitorNovel molecular basisCell cycle transitionKinase inhibitorsDNA replicationDNA repairCellular differentiationMolecular basisG1 prolongationGene expressionAntioxidant N-acetylcysteineN-acetylcysteineIntracellular glutathione levelsArrestAgent N-acetylcysteineInductionInhibitorsGlutathione levelsCyclinChemopreventive agentsChemopreventive activityDifferentiationUsual mechanismP53ReplicationUltraviolet Radiation Induced Signature Mutations in Photocarcinogenesis
Wikonkal N, Brash D. Ultraviolet Radiation Induced Signature Mutations in Photocarcinogenesis. Journal Of Investigative Dermatology Symposium Proceedings 1999, 4: 6-10. PMID: 10537000, DOI: 10.1038/sj.jidsp.5640173.Peer-Reviewed Reviews, Practice Guidelines, Standards, and Consensus StatementsConceptsSignature mutationsSkin cancerNon-melanoma skin cancerUV-signature mutationsClinical dataSubstantial burdenSkin carcinogenesisMurine epidermisNormal individualsNormal humansCancerCancer developmentTumor suppressor geneClonal expansionTumor promoterTP53Suppressor geneGenetic eventsMutationsCellsUV Induces p21WAF1/CIP1 Protein in Keratinocytes Without p53
Liu M, Wikonkal N, Brash D. UV Induces p21WAF1/CIP1 Protein in Keratinocytes Without p53. Journal Of Investigative Dermatology 1999, 113: 283-284. PMID: 10469320, DOI: 10.1046/j.1523-1747.1999.00657.x.Peer-Reviewed Original Research
1996
Frequent clones of p53-mutated keratinocytes in normal human skin
Jonason A, Kunala S, Price G, Restifo R, Spinelli H, Persing J, Leffell D, Tarone R, Brash D. Frequent clones of p53-mutated keratinocytes in normal human skin. Proceedings Of The National Academy Of Sciences Of The United States Of America 1996, 93: 14025-14029. PMID: 8943054, PMCID: PMC19488, DOI: 10.1073/pnas.93.24.14025.Peer-Reviewed Original ResearchConceptsP53-mutated keratinocytesNormal individualsSun-shielded skinSun-exposed skinNormal human skinHuman skinWhole-mount preparationsP53-mutated cellsCancer predictsDermal-epidermal junctionSubstantial burdenFrequent clonesClonal expansionHair folliclesGenetic hitsTumor promoterSkinKeratinocytesCells