2012
Langerhans Cells Facilitate Epithelial DNA Damage and Squamous Cell Carcinoma
Modi BG, Neustadter J, Binda E, Lewis J, Filler RB, Roberts SJ, Kwong BY, Reddy S, Overton JD, Galan A, Tigelaar R, Cai L, Fu P, Shlomchik M, Kaplan DH, Hayday A, Girardi M. Langerhans Cells Facilitate Epithelial DNA Damage and Squamous Cell Carcinoma. Science 2012, 335: 104-108. PMID: 22223807, PMCID: PMC3753811, DOI: 10.1126/science.1211600.Peer-Reviewed Original ResearchMeSH Keywords9,10-Dimethyl-1,2-benzanthraceneAnimalsAryl Hydrocarbon HydroxylasesCarcinogensCarcinoma, Squamous CellCell Transformation, NeoplasticCells, CulturedCytochrome P-450 CYP1A1Cytochrome P-450 CYP1B1DNA DamageGenes, rasHumansKeratinocytesLangerhans CellsMiceMice, TransgenicSkin NeoplasmsT-LymphocytesConceptsLangerhans cellsDendritic cellsDMBA-induced DNA damageCutaneous chemical carcinogenesisEpidermal dendritic cellsLC-deficient miceT cell immunitySquamous cell carcinomaChemical carcinogenesisDMBA-transHras mutationsCell immunityCell carcinomaImmune cellsDNA damageTumor resistanceDMBAPrior incubationHuman keratinocytesCarcinogenesisUnderlying mechanismMicePotent carcinogenSkinPAH metabolism
2008
Skint1, the prototype of a newly identified immunoglobulin superfamily gene cluster, positively selects epidermal γδ T cells
Boyden LM, Lewis JM, Barbee SD, Bas A, Girardi M, Hayday AC, Tigelaar RE, Lifton RP. Skint1, the prototype of a newly identified immunoglobulin superfamily gene cluster, positively selects epidermal γδ T cells. Nature Genetics 2008, 40: 656-662. PMID: 18408721, PMCID: PMC4167720, DOI: 10.1038/ng.108.Peer-Reviewed Original Research
2007
Promotion of Hras-induced squamous carcinomas by a polymorphic variant of the Patched gene in FVB mice
Wakabayashi Y, Mao JH, Brown K, Girardi M, Balmain A. Promotion of Hras-induced squamous carcinomas by a polymorphic variant of the Patched gene in FVB mice. Nature 2007, 445: 761-765. PMID: 17230190, DOI: 10.1038/nature05489.Peer-Reviewed Original ResearchMeSH KeywordsAmino Acid SequenceAnimalsApoptosisCarcinoma, Squamous CellCell LineCell Transformation, NeoplasticCrosses, GeneticFemaleGene Expression Regulation, NeoplasticGenes, rasHSP40 Heat-Shock ProteinsHumansKruppel-Like Transcription FactorsMaleMiceMice, Inbred C57BLMice, TransgenicMolecular Sequence DataPatched ReceptorsPatched-1 ReceptorPolymorphism, GeneticRas ProteinsReceptors, Cell SurfaceZinc Finger Protein Gli2ConceptsSquamous carcinomaTumor suppressor geneFVB/N miceSonic hedgehogSuppressor geneFVB/N strainBasal cell carcinomaPTCH geneSame target cellsCell lineage commitmentPatched geneHuman patched geneHost genetic backgroundClassical tumor suppressor geneCell carcinomaPtch alleleFVB miceN miceCarcinogen exposureC57BL/6 strainTumor typesLineage commitmentMouse homologueHybrid miceGenetic basis
2005
Sustained localized expression of ligand for the activating NKG2D receptor impairs natural cytotoxicity in vivo and reduces tumor immunosurveillance
Oppenheim DE, Roberts SJ, Clarke SL, Filler R, Lewis JM, Tigelaar RE, Girardi M, Hayday AC. Sustained localized expression of ligand for the activating NKG2D receptor impairs natural cytotoxicity in vivo and reduces tumor immunosurveillance. Nature Immunology 2005, 6: 928-937. PMID: 16116470, DOI: 10.1038/ni1239.Peer-Reviewed Original ResearchMeSH Keywords9,10-Dimethyl-1,2-benzanthraceneAnimalsCarcinomaCell Line, TumorDisease SusceptibilityDown-RegulationFemaleImmunologic SurveillanceKiller Cells, NaturalLigandsMaleMembrane ProteinsMiceMice, Inbred C57BLMice, KnockoutMice, TransgenicNK Cell Lectin-Like Receptor Subfamily KPapillomaReceptors, ImmunologicReceptors, Natural Killer CellSkin NeoplasmsTetradecanoylphorbol AcetateT-LymphocytesTumor BurdenConceptsNKG2D downregulationNK cell-mediated cytotoxicityNatural killer cellsCell-mediated cytotoxicityInnate immune activationT cell defectsNKG2D engagementNatural cytotoxicityKiller cellsImmune activationReceptor NKG2DTumor immunosurveillanceCutaneous carcinogenesisTumor surveillanceT cellsReversible defectsRAE-1Normal epitheliumLigand expressionTumor resistanceCell defectsSustained expressionNKG2DImmunosurveillanceDownregulation