2017
Fluorouracil Enhances Photodynamic Therapy of Squamous Cell Carcinoma via a p53-Independent Mechanism that Increases Protoporphyrin IX levels and Tumor Cell Death
Anand S, Rollakanti KR, Brankov N, Brash DE, Hasan T, Maytin EV. Fluorouracil Enhances Photodynamic Therapy of Squamous Cell Carcinoma via a p53-Independent Mechanism that Increases Protoporphyrin IX levels and Tumor Cell Death. Molecular Cancer Therapeutics 2017, 16: 1092-1101. PMID: 28336806, PMCID: PMC5497500, DOI: 10.1158/1535-7163.mct-16-0608.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBiosynthetic PathwaysCarcinoma, Squamous CellCell DeathCell Line, TumorCell ProliferationCombined Modality TherapyDisease Models, AnimalFluorouracilGene Expression Regulation, EnzymologicGene Expression Regulation, NeoplasticHemeHumansMicePhotochemotherapyProtoporphyrinsTumor Suppressor Protein p53Xenograft Model Antitumor AssaysConceptsSquamous cell carcinomaActinic keratosesPhotodynamic therapyP53-null tumorsNew therapeutic approachesMol Cancer TherCell deathCell carcinomaTherapeutic responsePpIX levelsTherapeutic approachesMouse modelSkin cancerSCC precursorsHeme synthesis pathwayTumorsKeratosesDeathP53PDT efficacyInductionPretreatmentNeoadjuvantCombination approachSurgery
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
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 mechanismP53Replication
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