2019
Aging-like Spontaneous Epigenetic Silencing Facilitates Wnt Activation, Stemness, and Braf V600E-Induced Tumorigenesis
Tao Y, Kang B, Petkovich DA, Bhandari YR, In J, Stein-O'Brien G, Kong X, Xie W, Zachos N, Maegawa S, Vaidya H, Brown S, Yen R, Shao X, Thakor J, Lu Z, Cai Y, Zhang Y, Mallona I, Peinado MA, Zahnow CA, Ahuja N, Fertig E, Issa JP, Baylin SB, Easwaran H. Aging-like Spontaneous Epigenetic Silencing Facilitates Wnt Activation, Stemness, and Braf V600E-Induced Tumorigenesis. Cancer Cell 2019, 35: 315-328.e6. PMID: 30753828, PMCID: PMC6636642, DOI: 10.1016/j.ccell.2019.01.005.Peer-Reviewed Original ResearchMeSH KeywordsAdenocarcinomaAge FactorsAgingAnimalsCell Transformation, NeoplasticColonic NeoplasmsDNA MethylationGene Expression Regulation, NeoplasticGene SilencingGenetic Predisposition to DiseaseHumansMice, Inbred NODMice, Mutant StrainsMice, SCIDMutationPhenotypeProto-Oncogene Proteins B-rafStem CellsTime FactorsTissue Culture TechniquesWnt Signaling PathwayConceptsCell fate changesPromoter DNA hypermethylationStem-like stateAging-like phenotypesCpG island methylationFate changesDifferentiation defectsEpigenetic abnormalitiesDNA hypermethylationSimultaneous inactivationWnt pathwayWnt activationPromoter hypermethylationTumorigenesisGenesHypermethylationMethylator phenotypeColon tumorigenesisPhenotypeOrganoidsPrecursor roleCRISPRMethylationSupStemness
2016
DNA methylation changes in extracellular remodeling pathway genes during the transformation of human mesenchymal stem cells
Kim T, Park S, Kim H, Ahuja N, Yi J. DNA methylation changes in extracellular remodeling pathway genes during the transformation of human mesenchymal stem cells. Genes & Genomics 2016, 38: 611-617. DOI: 10.1007/s13258-016-0402-x.Peer-Reviewed Original ResearchTranscriptional silencingPathway genesECM genesMesenchymal compartmentStem cell model systemPromoter DNA hypermethylationPromoter hypermethylationDNA methylation changesGene expression profile dataEssential structural componentKey cellular eventsExpression profile dataImportant functional roleExtracellular matrix moleculesColon cancer cell linesCell model systemHuman mesenchymal stem cellsMethylation patternsMethylation changesTranscription-polymerase chain reaction analysisDNA hypermethylationEpigenetic alterationsReverse transcription-polymerase chain reaction analysisHuman malignancesCellular events
2012
Biomarkers for detection and prognosis of breast cancer identified by a functional hypermethylome screen
Jeschke J, Van Neste L, Glöckner SC, Dhir M, Calmon MF, Deregowski V, Van Criekinge W, Vlassenbroeck I, Koch A, Chan TA, Cope L, Hooker CM, Schuebel KE, Gabrielson E, Winterpacht A, Baylin SB, Herman JG, Ahuja N. Biomarkers for detection and prognosis of breast cancer identified by a functional hypermethylome screen. Epigenetics 2012, 7: 701-709. PMID: 22647880, DOI: 10.4161/epi.20445.Peer-Reviewed Original ResearchConceptsPoor overall survivalBreast cancerOverall survivalPrognosis predictionEffective biomarkersClinical prognostic variablesPrimary breast cancerDetection of BCFrequent methylated genesStrongest single markersSignificant prognosticatorBC patientsValidation cohortPrognostic variablesPrognostic signatureEarly detectionCancerBiomarkersPromoter hypermethylationMethylation changesTumor heterogeneityPrognosisSingle markerGene expression approachSurvival
1998
Incidence and functional consequences of hMLH1 promoter hypermethylation in colorectal carcinoma
Herman J, Umar A, Polyak K, Graff J, Ahuja N, Issa J, Markowitz S, Willson J, Hamilton S, Kinzler K, Kane M, Kolodner R, Vogelstein B, Kunkel T, Baylin S. Incidence and functional consequences of hMLH1 promoter hypermethylation in colorectal carcinoma. Proceedings Of The National Academy Of Sciences Of The United States Of America 1998, 95: 6870-6875. PMID: 9618505, PMCID: PMC22665, DOI: 10.1073/pnas.95.12.6870.Peer-Reviewed Original ResearchConceptsCpG islandsMismatch repair genesCell linesDNA mismatch repairMMR-deficient cell linesDNA methylationSuch methylationSporadic primary colorectal cancerEpigenetic inactivationMMR capacityMismatch repairRepair genesMethylationFunctional consequencesColorectal cancer cell linesCancer cell linesPromoter hypermethylationHypermethylationMicrosatellite instabilityProtein expressionHMLH1 proteinGenesColorectal cancerHMLH1 protein expressionInactivation
1997
Association between CpG island methylation and microsatellite instability in colorectal cancer.
Ahuja N, Mohan AL, Li Q, Stolker JM, Herman JG, Hamilton SR, Baylin SB, Issa JP. Association between CpG island methylation and microsatellite instability in colorectal cancer. Cancer Research 1997, 57: 3370-4. PMID: 9269998.Peer-Reviewed Original ResearchConceptsDe novo methylationNovo methylationPromoter region CpG islandsThrombospondin-1 genesCpG island methylationDeficient DNA repairCancer 1 geneMethylation patternsTranscriptional inactivationCpG islandsDNA repairImportant genesHypermethylation eventsColorectal cancerGenetic instabilityExtensive methylationIsland methylationGenesMethylationAberrant methylationRepair genesInsulin-like growth factor IIPromoter hypermethylationMicrosatellite instabilityGrowth factor II