2022
N-nitrosamines-mediated downregulation of LncRNA-UCA1 induces carcinogenesis of esophageal squamous by regulating the alternative splicing of FGFR2
Wang X, Sun M, Gao Z, Yin L, Pu Y, Zhu Y, Wang X, Liu R. N-nitrosamines-mediated downregulation of LncRNA-UCA1 induces carcinogenesis of esophageal squamous by regulating the alternative splicing of FGFR2. The Science Of The Total Environment 2022, 855: 158918. PMID: 36169023, DOI: 10.1016/j.scitotenv.2022.158918.Peer-Reviewed Original ResearchMeSH KeywordsAlternative SplicingCarcinogenesisCell Line, TumorCell MovementCell ProliferationDown-RegulationEpigenesis, GeneticEsophageal NeoplasmsEsophageal Squamous Cell CarcinomaGene Expression Regulation, NeoplasticHeterogeneous-Nuclear Ribonucleoprotein Group F-HHumansMicroRNAsNitrosaminesPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktReceptor, Fibroblast Growth Factor, Type 2RNA, Long NoncodingConceptsFibroblast growth factor receptor 2Alternative splicingEsophageal squamous cell carcinomaExact molecular mechanismsHet-1A cellsDownregulation of UCA1Epithelial-mesenchymal transitionPI3K-AKT axisFGFR2-IIIcMolecular mechanismsPI3K-AktF proteinUnknown mechanismESCC cellsESCC progressionSplicingN-nitrosamine exposureGrowth factor receptor 2Squamous cell carcinomaDigestive system tumorsRegulation levelESCC tissuesFactor receptor 2High incidence areaLncRNA UCA1
2021
Co-distribution of Light At Night (LAN) and COVID-19 incidence in the United States
Meng Y, Zhu V, Zhu Y. Co-distribution of Light At Night (LAN) and COVID-19 incidence in the United States. BMC Public Health 2021, 21: 1509. PMID: 34348695, PMCID: PMC8335974, DOI: 10.1186/s12889-021-11500-6.Peer-Reviewed Original Research
2018
Detection of heterozygous mutation in hook microtubule-tethering protein 1 in three patients with decapitated and decaudated spermatozoa syndrome
Chen H, Zhu Y, Zhu Z, Zhi E, Lu K, Wang X, Liu F, Li Z, Xia W. Detection of heterozygous mutation in hook microtubule-tethering protein 1 in three patients with decapitated and decaudated spermatozoa syndrome. Journal Of Medical Genetics 2018, 55: 150. PMID: 29330334, DOI: 10.1136/jmedgenet-2016-104404.Peer-Reviewed Original ResearchConceptsAssisted reproduction treatmentFertilization rateClinical studiesReproduction treatmentWhole genomic DNAPatientsTeratozoospermia patientsControl individualsNovel missense mutationAbnormal junctionProtein 1 geneHeterozygous mutationsIntramanchette transportUnreported mutationsHeadless tailsGenetic cuesPopulation-matched control individualsReduced fertilization ratesGenomic therapyMorphological observationsProtein 1Genomic DNADysfunctional proteinsFurther studiesMolecular mechanisms
2014
Epigenome-wide analysis of piRNAs in gene-specific DNA methylation
Fu A, Jacobs D, Zhu Y. Epigenome-wide analysis of piRNAs in gene-specific DNA methylation. RNA Biology 2014, 11: 1301-1312. PMID: 25590657, PMCID: PMC4615395, DOI: 10.1080/15476286.2014.996091.Peer-Reviewed Original ResearchConceptsPIWI-interacting RNAsGene-specific DNA methylationDNA methylationGenic lociTransposable elementsCpG sitesSilencing of transposable elementsGenome-wide methylation profilingDifferentially methylated CpG sitesGenome-wide effortsTarget CpG sitesInduce DNA methylationTransposon classesEpigenome-wide analysisIntergenic regionGenomic regionsNascent mRNAHuman genomeMethylation changesGenomic DNAMethylation profilesHuman somatic cellsUnique speciesGenome copiesSomatic cells
2009
microRNA miR-196a-2 and Breast Cancer: A Genetic and Epigenetic Association Study and Functional Analysis
Hoffman AE, Zheng T, Yi C, Leaderer D, Weidhaas J, Slack F, Zhang Y, Paranjape T, Zhu Y. microRNA miR-196a-2 and Breast Cancer: A Genetic and Epigenetic Association Study and Functional Analysis. Cancer Research 2009, 69: 5970-5977. PMID: 19567675, PMCID: PMC2716085, DOI: 10.1158/0008-5472.can-09-0236.Peer-Reviewed Original ResearchMeSH KeywordsAdultAgedAged, 80 and overBase SequenceBreast NeoplasmsCell CycleCell Line, TumorCpG IslandsDNA MethylationEpigenesis, GeneticGene Expression ProfilingGene Regulatory NetworksGenetic Predisposition to DiseaseHumansMicroRNAsMiddle AgedModels, BiologicalMolecular Sequence DataOligonucleotide Array Sequence AnalysisPolymorphism, Single NucleotideRisk FactorsTransfectionConceptsMiR-196a-2Cancer-relevant networkWhole-genome expression microarraysEpigenetic association studiesPathway-based analysisGenetic variantsCpG island upstreamCancer-related biological pathwaysCell cycle responseMiRNA genesFunctional genetic variantsMiRNA precursorsCommon sequence variantsTranscriptional regulatorsGenetic association analysisMutant precursorMutagenesis analysisTarget genesMature regionBreast cancer riskExpression microarraysFunctional analysisTumor suppressorBiological pathwaysAssociation studiesCancer-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 rhythmTargetClock-Cancer Connection in Non–Hodgkin's Lymphoma: A Genetic Association Study and Pathway Analysis of the Circadian Gene Cryptochrome 2
Hoffman AE, Zheng T, Stevens RG, Ba Y, Zhang Y, Leaderer D, Yi C, Holford TR, Zhu Y. Clock-Cancer Connection in Non–Hodgkin's Lymphoma: A Genetic Association Study and Pathway Analysis of the Circadian Gene Cryptochrome 2. Cancer Research 2009, 69: 3605-3613. PMID: 19318546, PMCID: PMC3175639, DOI: 10.1158/0008-5472.can-08-4572.Peer-Reviewed Original ResearchConceptsCryptochrome 2Single nucleotide polymorphismsCircadian genesWhole-genome expression microarraysPathway-based analysisCore circadian genesCancer-related biological pathwaysCRY2 knockdownTranscriptional repressorGenetic association analysisGenetic association studiesExpression microarraysFunctional analysisPathway analysisAssociation studiesBiological pathwaysAssociation analysisGenesNucleotide polymorphismsGenetic associationCircadian biomarkersDNA samplesFunctional effectsImportant roleRepressor
2007
Variants in circadian genes and prostate cancer risk: a population-based study in China
Chu LW, Zhu Y, Yu K, Zheng T, Yu H, Zhang Y, Sesterhenn I, Chokkalingam AP, Danforth KN, Shen MC, Stanczyk FZ, Gao YT, Hsing AW. Variants in circadian genes and prostate cancer risk: a population-based study in China. Prostate Cancer And Prostatic Diseases 2007, 11: 342-348. PMID: 17984998, DOI: 10.1038/sj.pcan.4501024.Peer-Reviewed Original ResearchConceptsProstate cancer riskLess insulin resistanceInsulin resistanceCancer riskGG genotypePopulation-based case-control studyGreater insulin resistancePopulation-based studyCase-control studyVariant C alleleCircadian genesProstate tumorigenesisC alleleNeed of confirmationMenRiskGenotypesVariantsGenes
2006
E‐cadherin promoter polymorphism (C‐160A) and risk of recurrence in patients with superficial bladder cancer
Lin J, Dinney C, Grossman H, Jhamb M, Zhu Y, Spitz, Wu X. E‐cadherin promoter polymorphism (C‐160A) and risk of recurrence in patients with superficial bladder cancer. Clinical Genetics 2006, 70: 240-245. PMID: 16922727, DOI: 10.1111/j.1399-0004.2006.00666.x.Peer-Reviewed Original ResearchConceptsSuperficial bladder cancerBladder cancer recurrenceBladder cancerCancer recurrencePromoter polymorphismHazard ratioCaucasian patientsMedian recurrence-free survivalMedical chart reviewRecurrence-free survivalRisk of recurrencePeripheral blood lymphocytesProportional hazards modelHomozygous CC genotypeChart reviewDisease recurrenceSmoking statusTumor recurrenceTumor stageBlood lymphocytesClinical dataCC genotypeHazards modelPatientsRecurrence riskDoes “Clock” Matter in Prostate Cancer?
Zhu Y, Zheng T, Stevens RG, Zhang Y, Boyle P. Does “Clock” Matter in Prostate Cancer? Cancer Epidemiology Biomarkers & Prevention 2006, 15: 3-5. PMID: 16434577, PMCID: PMC2366206, DOI: 10.1158/1055-9965.epi-05-0631.Peer-Reviewed Original ResearchConceptsProstate cancerSex hormone levelsFemale breast cancerCommon cancer typesEvening shift workHormone levelsPrognostic biomarkerBreast cancerAndrogen expressionProstate tumorigenesisCancerCancer typesShift workDaily biochemicalIndividual riskEtiologyCircadian rhythmGenetic variantsRiskCircadian clockCircadian cycleBiomarkersPhysiologicProfound effect
2005
Occupation and Risk of Pancreatic Cancer: A Population-Based Case–Control Study in Iowa
Zhang Y, Cantor KP, Lynch CF, Zhu Y, Zheng T. Occupation and Risk of Pancreatic Cancer: A Population-Based Case–Control Study in Iowa. Journal Of Occupational And Environmental Medicine 2005, 47: 392-398. PMID: 15824631, DOI: 10.1097/01.jom.0000158707.88801.f5.Peer-Reviewed Original ResearchNucleotide Excision Repair Gene Polymorphisms and Recurrence after Treatment for Superficial Bladder Cancer
Gu J, Zhao H, Dinney C, Zhu Y, Leibovici D, Bermejo C, Grossman H, Wu X. Nucleotide Excision Repair Gene Polymorphisms and Recurrence after Treatment for Superficial Bladder Cancer. Clinical Cancer Research 2005, 11: 1408-1415. PMID: 15746040, DOI: 10.1158/1078-0432.ccr-04-1101.Peer-Reviewed Original ResearchMeSH KeywordsAgedAllelesBCG VaccineDisease ProgressionDNA HelicasesDNA RepairDNA Repair EnzymesDNA-Binding ProteinsFemaleFollow-Up StudiesGene FrequencyGenotypeHumansMaleMiddle AgedMultivariate AnalysisNeoplasm Recurrence, LocalPoly-ADP-Ribose Binding ProteinsPolymorphism, GeneticSurvival AnalysisTime FactorsUrinary Bladder NeoplasmsXeroderma Pigmentosum Group A ProteinConceptsBacillus Calmette-Guerin treatmentRecurrence-free survival timeSuperficial bladder cancerShorter recurrence-free survival timeHigh recurrence riskDNA repair capacityHigh-risk allelesRecurrence riskPutative high-risk alleleVariant allelesClinical outcomesBladder cancerSurvival timeIntravesical bacillus Calmette-Guerin treatmentGene polymorphismsSuperficial bladder cancer recurrenceRepair capacityNucleotide excision repair gene polymorphismsRisk allelesCancer treatmentBladder cancer outcomesBladder cancer recurrenceBladder cancer treatmentMore risk allelesEnd of observationPeriod3 Structural Variation: A Circadian Biomarker Associated with Breast Cancer in Young Women
Zhu Y, Brown HN, Zhang Y, Stevens RG, Zheng T. Period3 Structural Variation: A Circadian Biomarker Associated with Breast Cancer in Young Women. Cancer Epidemiology Biomarkers & Prevention 2005, 14: 268-270. PMID: 15668506, DOI: 10.1158/1055-9965.268.14.1.Peer-Reviewed Original ResearchConceptsCircadian genesCell cycle regulationCycle regulationCircadian biologyBiological pathwaysGenesHuman cancersCell proliferationLength variationTumor developmentStructural variationsCircadian rhythmNovel panelNovel findingsBreast cancerCircadian disruptionPotential biomarkersBiologyMutationsCaucasian controlsApoptosisBiomarkers AssociatedPathwayRegulationDeregulation
2004
Re: No Increased Risk of non-Hodgkin's Lymphoma with Steroids, Estrogens and Psychotropics (Netherlands)
Zheng T, Zhang Y, Morton L, Zhu Y. Re: No Increased Risk of non-Hodgkin's Lymphoma with Steroids, Estrogens and Psychotropics (Netherlands). Cancer Causes & Control 2004, 15: 433-434. PMID: 15248307, DOI: 10.1023/b:caco.0000027551.90202.5a.Commentaries, Editorials and LettersMethyl‐CpG‐binding domain 2
Zhu Y, Spitz M, Zhang H, Grossman H, Frazier M, Wu X. Methyl‐CpG‐binding domain 2. Cancer 2004, 100: 1853-1858. PMID: 15112265, DOI: 10.1002/cncr.20199.Peer-Reviewed Original ResearchMeSH KeywordsBase SequenceCase-Control StudiesDNA MethylationDNA-Binding ProteinsFemaleGene Expression Regulation, NeoplasticGenetic Predisposition to DiseaseHumansLogistic ModelsMaleMolecular Sequence DataOdds RatioProbabilityPrognosisPromoter Regions, GeneticReference ValuesReverse Transcriptase Polymerase Chain ReactionRisk FactorsRNA, MessengerSensitivity and SpecificityUrinary Bladder NeoplasmsConceptsMBD2 expressionCarcinoma riskCurrent case-control studyReverse transcription polymerase chain reaction assaysCase-control studyPeripheral blood lymphocytesQuantitative reverse transcription-polymerase chain reaction assaysTranscription-polymerase chain reaction assaysMessenger RNA expressionReal-time quantitative reverse transcription-polymerase chain reaction assaysControl patientsLight smokersCase patientsHeavy smokersUnderlying molecular mechanismsTumor tissue typesBlood lymphocytesChain reaction assaysProtective effectProtective roleQuartile distributionDomain 2 proteinOlder individualsTumor developmentYoung individualsAn Evolutionary Perspective on Single-Nucleotide Polymorphism Screening in Molecular Cancer Epidemiology
Zhu Y, Spitz MR, Amos CI, Lin J, Schabath MB, Wu X. An Evolutionary Perspective on Single-Nucleotide Polymorphism Screening in Molecular Cancer Epidemiology. Cancer Research 2004, 64: 2251-2257. PMID: 15026370, DOI: 10.1158/0008-5472.can-03-2800.Peer-Reviewed Original ResearchConceptsSingle nucleotide polymorphismsAmino acidsConservation levelDifferent cancer-related genesHuman DNA repair genesTolerance indexMolecular evolutionary approachEntire human genomeNonsynonymous single nucleotide polymorphismsSingle nucleotide polymorphism (SNP) screeningTarget single nucleotide polymorphismsDNA repair genesAmino acid changesEvolutionary conservationHuman genomeCancer-related genesMolecular epidemiological studiesSelective pressureMolecular cancer epidemiologyDifferent speciesPhenotypic functionsAcid changesRepair genesEvolutionary perspectivePolymorphism screening
2003
Telomere Dysfunction: A Potential Cancer Predisposition Factor
Wu X, Amos C, Zhu Y, Zhao H, Grossman B, Shay J, Luo S, Hong W, Spitz M. Telomere Dysfunction: A Potential Cancer Predisposition Factor. Journal Of The National Cancer Institute 2003, 95: 1211-1218. PMID: 12928346, DOI: 10.1093/jnci/djg011.Peer-Reviewed Original ResearchMeSH KeywordsAdultAgedBlotting, SouthernCarcinoma, Renal CellCase-Control StudiesDNA DamageDNA RepairDNA, NeoplasmFemaleFlow CytometryGenetic Predisposition to DiseaseHead and Neck NeoplasmsHumansIn Situ Hybridization, FluorescenceKidney NeoplasmsLung NeoplasmsLymphocytesMaleMiddle AgedNeoplasmsOdds RatioRisk AssessmentRisk FactorsSmokingTelomereUrinary Bladder NeoplasmsConceptsControl subjectsTelomere lengthNeck cancerOdds ratioCancer riskShort telomeresOngoing case-control studyPercent of patientsRenal cell cancerCase-control studyPeripheral blood lymphocytesLongest quartileCase patientsCell cancerSmoking statusDisease characteristicsBladder cancerBlood lymphocytesStratified analysisGenetic instabilityHuman bladderRenal cellsStudy participantsCancerPredisposition factorsFrom genotype to phenotype: correlating XRCC1 polymorphisms with mutagen sensitivity
Wang Y, Spitz M, Zhu Y, Dong Q, Shete S, Wu X. From genotype to phenotype: correlating XRCC1 polymorphisms with mutagen sensitivity. DNA Repair 2003, 2: 901-908. PMID: 12893086, DOI: 10.1016/s1568-7864(03)00085-5.Peer-Reviewed Original Research
2002
A case‐control analysis of lymphocytic chromosome 9 aberrations in lung cancer
Zhu Y, Spitz M, Strom S, Tomlinson G, Amos C, Minna J, Wu X. A case‐control analysis of lymphocytic chromosome 9 aberrations in lung cancer. International Journal Of Cancer 2002, 102: 536-540. PMID: 12432559, DOI: 10.1002/ijc.10762.Peer-Reviewed Original ResearchConceptsPeripheral blood lymphocytesChromosome 9 aberrationsLung cancerOdds ratioFamily historyPrimary lung tumorsLung cancer casesElevated odds ratiosCase-control analysisLung carcinoma specimensLung cancer predispositionFamily history analysisFrequent genetic changesEpidemiologic profileBlood lymphocytesLung tumorigenesisLung tumorsCancer casesCarcinoma specimensChromosome 9 abnormalitiesControl individualsCancerCytogenetic aberrationsFamilial aggregationChromosomal alterationsBPDE‐induced lymphocytic 3p21.3 aberrations may predict head and neck carcinoma risk
Zhu Y, Spitz M, Zheng Y, Hong W, Wu X. BPDE‐induced lymphocytic 3p21.3 aberrations may predict head and neck carcinoma risk. Cancer 2002, 95: 563-568. PMID: 12209748, DOI: 10.1002/cncr.10689.Peer-Reviewed Original ResearchMeSH Keywords7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxideAgedCarcinogensCarcinoma, Squamous CellChromosome AberrationsChromosomes, Human, Pair 3FemaleGenetic Predisposition to DiseaseGenetic TestingHead and Neck NeoplasmsHumansIn Situ Hybridization, FluorescenceLymphocytesMaleMiddle AgedPredictive Value of TestsConceptsPeripheral blood lymphocytesIndividual genetic susceptibilityGenetic susceptibilityTobacco carcinogensNeck squamous cell carcinomaNeck carcinoma riskSquamous cell carcinomaChromosomal aberrationsTobacco smoke constituentsDose-response relationshipTobacco exposureSpecific molecular targetsCell carcinomaHNSCC riskBlood lymphocytesRisk factorsOdds ratioCarcinoma riskPBL culturesCutoff pointLymphocytic cellsHNSCCBPDE sensitivityMolecular targetsSmoke constituents