2008
Preneoplastic lesion growth driven by the death of adjacent normal stem cells
Chao DL, Eck JT, Brash DE, Maley CC, Luebeck EG. Preneoplastic lesion growth driven by the death of adjacent normal stem cells. Proceedings Of The National Academy Of Sciences Of The United States Of America 2008, 105: 15034-15039. PMID: 18815380, PMCID: PMC2567488, DOI: 10.1073/pnas.0802211105.Peer-Reviewed Original ResearchConceptsNormal stem cellsStem cellsClonal expansionCell replicationMutant cellsNormal cell replicationMutant clonesProliferative advantageDorsal epidermisCell mutationTissue architectureClonesClone growthBiological observationsCell killingApoptosis rateReplicationMutationsGrowth rateCellsGrowthNormal territoriesApoptosisExponential growth modelImportant stepProgressive apoptosis resistance prior to senescence and control by the anti-apoptotic protein BCL-xL
Rochette PJ, Brash DE. Progressive apoptosis resistance prior to senescence and control by the anti-apoptotic protein BCL-xL. Mechanisms Of Ageing And Development 2008, 129: 207-214. PMID: 18262222, PMCID: PMC2652169, DOI: 10.1016/j.mad.2007.12.007.Peer-Reviewed Original ResearchConceptsAnti-apoptotic protein Bcl-xLBcl-xLProtein Bcl-xLLevels of p53Pro-apoptotic protein BaxApoptosis reductionAnti-apoptotic proteinsPro-apoptotic BaxNormal balanceAnti-apoptotic Bcl-xLUV-induced apoptosisOld cellsApoptosis resistanceProgressive disruptionSenescent cellsApoptosisBaxProtein BaxHuman diploid fibroblastsCellsYoung cellsDiploid fibroblastsGenotoxic stressLevels
2007
Bcl-2 is the target of a UV-inducible apoptosis switch and a node for UV signaling
Knezevic D, Zhang W, Rochette PJ, Brash DE. Bcl-2 is the target of a UV-inducible apoptosis switch and a node for UV signaling. Proceedings Of The National Academy Of Sciences Of The United States Of America 2007, 104: 11286-11291. PMID: 17586682, PMCID: PMC2040891, DOI: 10.1073/pnas.0701318104.Peer-Reviewed Original Research
2006
Keratinocyte Apoptosis in Epidermal Development and Disease
Raj D, Brash DE, Grossman D. Keratinocyte Apoptosis in Epidermal Development and Disease. Journal Of Investigative Dermatology 2006, 126: 243-257. PMID: 16418733, PMCID: PMC2291295, DOI: 10.1038/sj.jid.5700008.Peer-Reviewed Reviews, Practice Guidelines, Standards, and Consensus StatementsConceptsEpidermal developmentNormal developmental programPre-malignant cellsDevelopmental programApoptosis controlMolecular mechanismsKeratinocyte apoptosisDysfunctional apoptosisKC apoptosisApoptosisCritical roleComplex roleNew insightsCorneum formationMouse modelCarcinogenesisSkin carcinogenesisPathwayRoleProliferationCells
2004
Melanin acts as a potent UVB photosensitizer to cause an atypical mode of cell death in murine skin
Takeuchi S, Zhang W, Wakamatsu K, Ito S, Hearing VJ, Kraemer KH, Brash DE. Melanin acts as a potent UVB photosensitizer to cause an atypical mode of cell death in murine skin. Proceedings Of The National Academy Of Sciences Of The United States Of America 2004, 101: 15076-15081. PMID: 15477596, PMCID: PMC524044, DOI: 10.1073/pnas.0403994101.Peer-Reviewed Original ResearchConceptsYellow miceTerminal deoxynucleotidyltransferase-mediated dUTP nickTUNEL-positive cellsActive caspase-3Sunburn cellsPositive cellsBlack miceSkin cancerCongenic miceMurine skinDUTP nickDNA strand breaksMiceEpidermal sheetsHair folliclesAbility of melaninCaspase-3Sensitivity of individualsApoptosisLesionsUVA radiationRed hairCell deathHair shaftSunlight UV radiationRole of E2F1 in Apoptosis: A case Study in Feedback Loops
Knezevic D, Brash DE. Role of E2F1 in Apoptosis: A case Study in Feedback Loops. Cell Cycle 2004, 3: 727-730. PMID: 15107604, DOI: 10.4161/cc.3.6.907.Peer-Reviewed Reviews, Practice Guidelines, Standards, and Consensus Statements
2003
Inactivating E2f1 reverts apoptosis resistance and cancer sensitivity in Trp53-deficient mice
Wikonkal NM, Remenyik E, Knezevic D, Zhang W, Liu M, Zhao H, Berton TR, Johnson DG, Brash DE. Inactivating E2f1 reverts apoptosis resistance and cancer sensitivity in Trp53-deficient mice. Nature Cell Biology 2003, 5: 655-660. PMID: 12833065, DOI: 10.1038/ncb1001.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsApoptosisCell Cycle ProteinsCell SurvivalCell Transformation, NeoplasticCells, CulturedDNA DamageDNA-Binding ProteinsE2F Transcription FactorsE2F1 Transcription FactorFemaleFibroblastsGene Expression Regulation, NeoplasticGenes, SuppressorKeratinocytesMaleMiceMice, KnockoutMutationSex RatioSkin NeoplasmsTranscription FactorsTumor Suppressor Protein p53Ultraviolet RaysConceptsUVB-induced apoptosisEarly-onset tumorsDouble knockout miceTrp53-deficient miceKnockout miceCancer sensitivityUVB exposureGenetic abnormalitiesMiceKeratinocyte apoptosisProtective mechanismApoptosis defectsApoptosis resistanceApoptosisDouble knockoutApoptosis pathwayE2F1 transcription factorE2F1 functionsPrimary fibroblastsE2F1Trp53S phase
1998
Antioxidant action via p53-mediated apoptosis.
Liu M, Pelling JC, Ju J, Chu E, Brash DE. Antioxidant action via p53-mediated apoptosis. Cancer Research 1998, 58: 1723-9. PMID: 9563490.Peer-Reviewed Original ResearchMeSH KeywordsAcetylcysteineAnimalsAntioxidantsApoptosisBlotting, NorthernBlotting, WesternButhionine SulfoximineCells, CulturedDimercaprolDose-Response Relationship, DrugGene Expression Regulation, NeoplasticGlutathioneMiceOxidation-ReductionPyrrolidonecarboxylic AcidSulfhydryl CompoundsThiazolesThiazolidinesTumor Cells, CulturedTumor Suppressor Protein p53Vitamin EConceptsP53 inductionCellular redox potentialP53-dependent apoptosisNormal cellsP53-mediated apoptosisTumor suppressor geneP53 mRNA translationCellular thiol levelsMRNA translationRedox sensorProtein stabilitySuppressor geneP53 tumor suppressor geneNontoxic antioxidantsApoptosisCell linesSulfur-containing antioxidantsBiological effectsPrimary culturesElevated p53 expressionCellsInductionN-acetylcysteineGlutathione levelsRedox potential