2004
Methyl‐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 factors