2011
Genome-wide methylation changes in night working women in Denmark: same altered promoter methylation of CLOCK and CRY2 as in breast cancer cases
Zhu Y, Stevens R, Hoffman A, Tjonneland A, Vogal U, Zheng T, Hansen J. Genome-wide methylation changes in night working women in Denmark: same altered promoter methylation of CLOCK and CRY2 as in breast cancer cases. Occupational And Environmental Medicine 2011, 68: a18. DOI: 10.1136/oemed-2011-100382.56.Peer-Reviewed Original ResearchGenome-wide methylation analysisMethylation patternsGenome-wide methylation changesMethylation analysisDifferential promoter methylationCore circadian genesPromoter methylationIngenuity Pathway AnalysisCancer-related pathwaysAltered promoter methylationMethylation chipDNA replicationEpigenetic impactMethylation changesEpigenetic changesGene promoterMethylation alterationsEpigenetic effectsCancer relevanceGene expressionPathway analysisCircadian genesRelevant transcriptsAssociation analysisPromoter hypomethylation
2009
Cancer-related transcriptional targets of the circadian gene NPAS2 identified by genome-wide ChIP-on-chip analysis
Yi CH, Zheng T, Leaderer D, Hoffman A, Zhu Y. Cancer-related transcriptional targets of the circadian gene NPAS2 identified by genome-wide ChIP-on-chip analysis. Cancer Letters 2009, 284: 149-156. PMID: 19457610, PMCID: PMC3182267, DOI: 10.1016/j.canlet.2009.04.017.Peer-Reviewed Original ResearchMeSH KeywordsAdenocarcinomaBasic Helix-Loop-Helix Transcription FactorsBreast NeoplasmsCell Line, TumorCell Transformation, NeoplasticChromatin ImmunoprecipitationCircadian RhythmFemaleGene Expression ProfilingGene Expression Regulation, NeoplasticGene Regulatory NetworksGenome-Wide Association StudyHumansNeoplasm ProteinsNerve Tissue ProteinsOligonucleotide Array Sequence AnalysisRNA InterferenceRNA, Small InterferingTranscription, GeneticConceptsDirect transcriptional targetTranscriptional targetsCircadian genesGenome-wide mapping approachChip analysisGenome-wide ChIPCancer-related gene expressionCore circadian genesRelevant biological pathwaysTranscriptional profilesGene expressionReal-time PCR assaysBiological processesCell cycleBiological pathwaysNPAS2Biological involvementGenesHuman cancersMCF-7 cellsCancer developmentTumorigenesisPCR assaysCircadian rhythmTarget
2001
A single nucleotide polymorphism in the matrix metalloproteinase-1 promoter enhances lung cancer susceptibility.
Zhu Y, Spitz M, Lei L, Mills G, Wu X. A single nucleotide polymorphism in the matrix metalloproteinase-1 promoter enhances lung cancer susceptibility. Cancer Research 2001, 61: 7825-9. PMID: 11691799.Peer-Reviewed Original ResearchConceptsSingle nucleotide polymorphismsLung cancer riskNucleotide polymorphismsLung cancer susceptibilityCancer susceptibilityG genotypeCancer riskLung cancerMatrix metalloproteinase-1 promoterTranscriptional activityGene expressionPromoter regionCurrent smokersCellular invasionCellular microenvironmentOncogenic mutationsMMP-1 promoter polymorphismTumor initiationTumor formationCancer developmentFrequency-matched controlsMMP-1 genotypesCase-control studyLung cancer casesMolecular epidemiological evidence