2024
Chemiexcitation in preventing macular degeneration
Brash D, Gaillard E. Chemiexcitation in preventing macular degeneration. Frontiers In Photonics 2024, 5: 1451857. DOI: 10.3389/fphot.2024.1451857.Peer-Reviewed Original ResearchExcited statesGround-state chemical reactionsExcited-state wavefunctionsHigh-energy statesQuantum biologyMagnetic fieldEnergy statesChemiexcitation processEnergy barrierChemiexcitationElectronReaction productsChemical reactionsWavefunctionsEnergyQuantumStateTransient mixingReactionIntermediate moleculesMoleculesGroundField
2023
Reply to Pfeffer: Macular degeneration clues from comparative anatomy
Wang K, Lyu Y, Tschulakow A, Brash D, Schraermeyer U. Reply to Pfeffer: Macular degeneration clues from comparative anatomy. Proceedings Of The National Academy Of Sciences Of The United States Of America 2023, 120: e2315582120. PMID: 37871227, PMCID: PMC10622899, DOI: 10.1073/pnas.2315582120.Peer-Reviewed Original ResearchNext-generation sequencing methodologies to detect low-frequency mutations: “Catch me if you can”
Menon V, Brash D. Next-generation sequencing methodologies to detect low-frequency mutations: “Catch me if you can”. Mutation Research/Reviews In Mutation Research 2023, 792: 108471. PMID: 37716438, PMCID: PMC10843083, DOI: 10.1016/j.mrrev.2023.108471.Peer-Reviewed Original ResearchChemiexcitation and melanin in photoreceptor disc turnover and prevention of macular degeneration
Lyu Y, Tschulakow A, Wang K, Brash D, Schraermeyer U. Chemiexcitation and melanin in photoreceptor disc turnover and prevention of macular degeneration. Proceedings Of The National Academy Of Sciences Of The United States Of America 2023, 120: e2216935120. PMID: 37155898, PMCID: PMC10194005, DOI: 10.1073/pnas.2216935120.Peer-Reviewed Original ResearchConceptsRetinal pigment epitheliumIntravitreal injectionMacular degenerationMelanolipofuscin granulesLipofuscin accumulationAge-related macular degenerationAlbino micePigmented miceMouse modelStargardt diseasePigment epitheliumRetinal pathologyRetinal degenerationNitric oxideDegenerationMiceLipofuscinPigment lipofuscinPhotoreceptor disksAlbinoAccelerated accumulationInjectionDiseasePathologyChemiexcited Neurotransmitters and Hormones Create DNA Photoproducts in the Dark
Gonçalves L, Angelé-Martínez C, Premi S, Palmatier M, Prado F, Di Mascio P, Bastos E, Brash D. Chemiexcited Neurotransmitters and Hormones Create DNA Photoproducts in the Dark. ACS Chemical Biology 2023, 18: 484-493. PMID: 36775999, PMCID: PMC10276651, DOI: 10.1021/acschembio.2c00787.Peer-Reviewed Original ResearchConceptsSinglet molecular oxygenOxidation of serotoninMolecular oxygenElectron excitationTriplet stateAdjacent pyrimidine basesAbsence of lightEnergy transferDark processPyrimidine basesSkin pigment melaninBiochemical reactionsMoleculesEnergy levelsCatecholamine neurotransmittersBiomoleculesCycloadditionUltravioletMammalian metabolismCyclobutane pyrimidine dimersOxidationAminesPigment melaninRadicalsPeroxynitriteChemiexcitation: Mammalian Photochemistry in the Dark†
Brash D, Goncalves L. Chemiexcitation: Mammalian Photochemistry in the Dark†. Photochemistry And Photobiology 2023, 99: 251-276. PMID: 36681894, PMCID: PMC10065968, DOI: 10.1111/php.13781.Peer-Reviewed Original ResearchConceptsExcited statesMammalian cellsCyclobutane pyrimidine dimersEvolutionary selectionBond rearrangementUnoccupied orbitalsGround stateReaction productsPyrimidine dimersChemiexcitationRecent findingsBiologyPathogenic eventsRadicalsUltraviolet lightMoleculesDrug-induced deafnessPotential pathogenesisCellsMelaninAchilles heelMammalsBiomoleculesPhotochemistryDNA
2016
Carcinogenesis: UV Radiation
Brash D, Heffernan T, Nghiem P, Cho R. Carcinogenesis: UV Radiation. 2016, 887-902. DOI: 10.1007/978-3-662-47398-6_56.ChaptersLarge-scale sequencing projectsUV-damaged cellsSequencing projectsDNA repairTumor suppressorSomatic point mutationsSurveillance mechanismClonal growthLow-frequency mutationsDNA damageBase changesCell behaviorPoint mutationsMutationsSomatic mutationsFree radical clearanceHuman skin cancerFrequency mutationsSpecific somatic mutationsUltraviolet radiationPTCH mutationsGenetic factorsNOTCH1 mutationsCellsVast number
2015
Carcinogenesis: UV Radiation
Brash D, Heffernan T, Nghiem P, Cho R. Carcinogenesis: UV Radiation. 2015, 1-17. DOI: 10.1007/978-3-642-27814-3_56-2.ChaptersLarge-scale sequencing projectsUV-damaged cellsSequencing projectsDNA repairTumor suppressorSomatic point mutationsSurveillance mechanismClonal growthLow-frequency mutationsDNA damageBase changesCell behaviorPoint mutationsMutationsSomatic mutationsFree radical clearanceHuman skin cancerFrequency mutationsSpecific somatic mutationsUltraviolet radiationPTCH mutationsGenetic factorsNOTCH1 mutationsCellsVast number
2010
Carcinogenesis: UV Radiation*
Brash D, Heffernan T, Nghiem P. Carcinogenesis: UV Radiation*. 2010, 567-578. DOI: 10.1007/978-3-540-89656-2_56.Chapters
2004
Reply: Lymphomagenesis and female-specific lethality in p53-deficient mice occur independently of E2f1
Brash D. Reply: Lymphomagenesis and female-specific lethality in p53-deficient mice occur independently of E2f1. Nature Cell Biology 2004, 6: 567-568. DOI: 10.1038/ncb0704-567.Commentaries, Editorials and Letters
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 ResearchThe DNA Damage Signal for Mdm2 Regulation, Trp53 Induction, and Sunburn Cell Formation In Vivo Originates from Actively Transcribed Genes
Brash D, Wikonkal N, Remenyik E, van der Horst G, Friedberg E, Cheo D, van Steeg H, Westerman A, van Kranen H. The DNA Damage Signal for Mdm2 Regulation, Trp53 Induction, and Sunburn Cell Formation In Vivo Originates from Actively Transcribed Genes. Journal Of Investigative Dermatology 2001, 117: 1234-1240. PMID: 11710938, DOI: 10.1046/j.0022-202x.2001.01554.x.Peer-Reviewed Original ResearchConceptsDNA photoproductsDNA damage signalsUnrepaired DNA lesionsCell formationSpecific genome regionsTumor suppressor proteinCsb-/- miceUltraviolet-induced apoptosisNucleotide excision repair genesApoptosis signal pathwayExcision repair genesActive genesMutant cellsGenome regionsDNA repairSuppressor proteinDamage signalsMDM2 regulationWild typeDNA lesionsPrevents cellsHomozygous inactivationGenesRepair genesDNA signalsTransgenic 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
1998
Tumor necrosis factor-α gene expression is induced by cyclobutyl pyrimidine dimers in DNA
Yarosh D, Klein J, O'Connor A, Kibitel J, Brash D, Hejmadi V, Sutherland B. Tumor necrosis factor-α gene expression is induced by cyclobutyl pyrimidine dimers in DNA. Journal Of Dermatological Science 1998, 16: s177. DOI: 10.1016/s0923-1811(98)84055-3.Peer-Reviewed Original Research
1997
Sunlight and the onset of skin cancer
Brash D. Sunlight and the onset of skin cancer. Trends In Genetics 1997, 13: 410-414. PMID: 9351343, DOI: 10.1016/s0168-9525(97)01246-8.Peer-Reviewed Reviews, Practice Guidelines, Standards, and Consensus Statements
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