2013
CHFR silencing or microsatellite instability is associated with increased antitumor activity of docetaxel or gemcitabine in colorectal cancer
Pelosof L, Yerram SR, Ahuja N, Delmas A, Danilova L, Herman JG, Azad NS. CHFR silencing or microsatellite instability is associated with increased antitumor activity of docetaxel or gemcitabine in colorectal cancer. International Journal Of Cancer 2013, 134: 596-605. PMID: 23873170, PMCID: PMC3830586, DOI: 10.1002/ijc.28390.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAntineoplastic AgentsBase SequenceCell Cycle ProteinsCell Line, TumorColorectal NeoplasmsDeoxycytidineDNA MethylationDNA PrimersDocetaxelFemaleGemcitabineGene SilencingHumansMiceMicrosatellite InstabilityNeoplasm ProteinsPoly-ADP-Ribose Binding ProteinsPromoter Regions, GeneticReal-Time Polymerase Chain ReactionTaxoidsUbiquitin-Protein LigasesXenograft Model Antitumor AssaysConceptsTumor growth inhibitionColorectal cancerCombination therapyCHFR methylationCell linesAdditive tumor growth inhibitionBiomarker-selected patient populationsMicrosatellite instabilityGrowth inhibitionOngoing clinical trialsCRC cell linesCell line xenograftsMSI-H cell linesCRC patientsChemotherapy responsePatient populationPredictive markerClinical trialsDifferential sensitivityTherapeutic effectHuman xenograftsVivo treatmentMSI statusChemotherapy sensitivityGemcitabine
2001
Accelerated age-related CpG island methylation in ulcerative colitis.
Issa JP, Ahuja N, Toyota M, Bronner MP, Brentnall TA. Accelerated age-related CpG island methylation in ulcerative colitis. Cancer Research 2001, 61: 3573-7. PMID: 11325821.Peer-Reviewed Original ResearchMeSH KeywordsAdaptor Proteins, Signal TransducingAdultAge FactorsAgedCarrier ProteinsChondroitin Sulfate ProteoglycansColitis, UlcerativeColonic NeoplasmsCpG IslandsDNA MethylationGenes, p16HumansIntestinal MucosaLectins, C-TypeMiddle AgedMutL Protein Homolog 1MyoD ProteinNeoplasm ProteinsNuclear ProteinsPrecancerous ConditionsReceptors, EstrogenVersicansConceptsMechanism of geneP16 exon 1Exon 1CpG island hypermethylationCpG island methylationMethylation marksMethylation patternsUndesirable genesColorectal epithelial cellsIsland hypermethylationIsland methylationGenesMethylationPremature agingMyoDColon cancerHigh-grade dysplasiaEpithelial cellsCell turnoverHypermethylationNon-UC controlsNormal appearing epitheliumUlcerative colitisHigh levelsCSPG2
1999
Aberrant methylation in gastric cancer associated with the CpG island methylator phenotype.
Toyota M, Ahuja N, Suzuki H, Itoh F, Ohe-Toyota M, Imai K, Baylin SB, Issa JP. Aberrant methylation in gastric cancer associated with the CpG island methylator phenotype. Cancer Research 1999, 59: 5438-42. PMID: 10554013.Peer-Reviewed Original ResearchMeSH KeywordsAdaptor Proteins, Signal TransducingAllelesCarrier ProteinsCpG IslandsCyclin-Dependent Kinase Inhibitor p16Gene Expression Regulation, NeoplasticHumansMethylationModels, GeneticMucous MembraneMutL Protein Homolog 1Neoplasm ProteinsNuclear ProteinsPhenotypePolymerase Chain ReactionStomach NeoplasmsCpG island methylator phenotype in colorectal cancer
Toyota M, Ahuja N, Ohe-Toyota M, Herman J, Baylin S, Issa J. CpG island methylator phenotype in colorectal cancer. Proceedings Of The National Academy Of Sciences Of The United States Of America 1999, 96: 8681-8686. PMID: 10411935, PMCID: PMC17576, DOI: 10.1073/pnas.96.15.8681.Peer-Reviewed Original ResearchMeSH KeywordsAdaptor Proteins, Signal TransducingAge FactorsCarrier ProteinsCloning, MolecularColorectal NeoplasmsCpG IslandsDNA MethylationDNA RepairGenes, p16Genes, Tumor SuppressorHumansMicrosatellite RepeatsMutL Protein Homolog 1Neoplasm ProteinsNuclear ProteinsPhenotypePolymerase Chain ReactionSulfitesTumor Cells, CulturedConceptsCpG island methylator phenotypeColorectal cancerMethylator phenotypeSporadic colorectal cancerMismatch repair deficiencyCpG islandsAge-dependent mannerNormal colonic cellsCpG island amplificationHigh incidenceColon cancerTHBS1 methylationNormal colonPromoter region CpG islandsSporadic tumorsCancerMicrosatellite instabilityColonic cellsTumor suppressor geneCpG island methylationRepair deficiencyCancer-specific mannerHMLH1 methylationCell linesTranscriptional inactivation
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