2022
Cyclobutane Pyrimidine Dimer Hyperhotspots as Sensitive Indicators of Keratinocyte UV Exposure†
Garcia‐Ruiz A, Kornacker K, Brash DE. Cyclobutane Pyrimidine Dimer Hyperhotspots as Sensitive Indicators of Keratinocyte UV Exposure†. Photochemistry And Photobiology 2022, 98: 987-997. PMID: 35944237, PMCID: PMC9802031, DOI: 10.1111/php.13683.Peer-Reviewed Original ResearchConceptsCyclobutane pyrimidine dimersGenomic averageSequence motifsHigh-throughput DNA sequencing methodsETS family transcription factorsNucleotide resolution analysisRNA processing genesNeonatal human epidermal keratinocytesDNA sequencing methodsTranscription factorsCpG islandsSites hundredsCell physiologyProcessing genesPromoter regionCell deathDNA damageSequencing methodsBiological importanceHuman epidermal keratinocytesPyrimidine dimersGenesMotifEpidermal keratinocytesMelanocytes
2019
Acetyl zingerone: An efficacious multifunctional ingredient for continued protection against ongoing DNA damage in melanocytes after sun exposure ends
Chaudhuri RK, Meyer T, Premi S, Brash D. Acetyl zingerone: An efficacious multifunctional ingredient for continued protection against ongoing DNA damage in melanocytes after sun exposure ends. International Journal Of Cosmetic Science 2019, 42: 36-45. PMID: 31538664, PMCID: PMC7004018, DOI: 10.1111/ics.12582.Peer-Reviewed Original ResearchConceptsSun exposureSolar-simulated ultraviolet radiationReactive oxygen speciesIntracellular levelsCyclobutane pyrimidine dimersΑ-tocopherolCPD formationTraditional sunscreensScavenge peroxynitriteUVR exposureOngoing DNA damageAntioxidant α-tocopherolUltraviolet radiationUVA radiationMelanocytesROS formationExposureQuench singlet oxygenUse of AZEfficacyOxygen speciesKeratinocytesDNA damageFree radicalsHours
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
Human Telomeres Are Hypersensitive to UV-Induced DNA Damage and Refractory to Repair
Rochette PJ, Brash DE. Human Telomeres Are Hypersensitive to UV-Induced DNA Damage and Refractory to Repair. PLOS Genetics 2010, 6: e1000926. PMID: 20442874, PMCID: PMC2861706, DOI: 10.1371/journal.pgen.1000926.Peer-Reviewed Original ResearchConceptsUV-induced DNA damageDNA damageTelomeric repeatsHuman telomeresExcision repairTelomeric repeat unitsNucleotide excision repairDouble-strand breaksUV-induced CPDGenome integrityGenomic integrityExcision repair sitesMitochondrial DNARegion of p53Opposite strandTelomeresCPD removalUnrepaired lesionsRepeatsPreeminent risk factorUV sensitivityPyrimidine dimersCancer developmentRepeat unitsCritical roleCarcinogenesis: UV Radiation*
Brash D, Heffernan T, Nghiem P. Carcinogenesis: UV Radiation*. 2010, 567-578. DOI: 10.1007/978-3-540-89656-2_56.Chapters
1994
Sunburn and p53 in the onset of skin cancer
Ziegler A, Jonason A, Leffellt D, Simon J, Sharma H, Kimmelman J, Remington L, Jacks T, Brash D. Sunburn and p53 in the onset of skin cancer. Nature 1994, 372: 773-776. PMID: 7997263, DOI: 10.1038/372773a0.Peer-Reviewed Original ResearchConceptsActinic keratosisP53 mutationsSquamous cell carcinomaP53 tumor suppressor geneP53-mutated cellsCell carcinomaApoptotic keratinocytesSkin cancerTumor initiatorTumor suppressor geneMouse skinClonal expansionPrecancerous cellsTumor promoterCarcinomaSkinTissue responseP53SunburnCell differentiationDNA damageAberrant cell differentiationCellsResponseKeratosis
1984
Target Organ Specificity: Diethylnitrosamine-and Dibenzylnitrosamine-induced Single-strand Breaks Plus Alkali-labile Bonds
Brash D, Su C, Nabi H, Reuter K, Ortman J, Sheikh Y, Hart R. Target Organ Specificity: Diethylnitrosamine-and Dibenzylnitrosamine-induced Single-strand Breaks Plus Alkali-labile Bonds. International Journal Of Toxicology 1984, 3: 207-216. DOI: 10.3109/10915818409018034.Peer-Reviewed Original Research
1982
Role of gene expression in mechanisms of toxicity/carcinogenicity relative to environmental cancer, heart, and lung disease
Brash D. Role of gene expression in mechanisms of toxicity/carcinogenicity relative to environmental cancer, heart, and lung disease. Journal Of Environmental Science And Health Part A 1982, 17: 589-598. DOI: 10.1080/10934528209375061.Peer-Reviewed Reviews, Practice Guidelines, Standards, and Consensus Statements