2017
Hypomethylating agents synergize with irinotecan to improve response to chemotherapy in colorectal cancer cells
Sharma A, Vatapalli R, Abdelfatah E, McMahon K, Kerner Z, Guzzetta A, Singh J, Zahnow C, Baylin S, Yerram S, Hu Y, Azad N, Ahuja N. Hypomethylating agents synergize with irinotecan to improve response to chemotherapy in colorectal cancer cells. PLOS ONE 2017, 12: e0176139. PMID: 28445481, PMCID: PMC5405959, DOI: 10.1371/journal.pone.0176139.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAntineoplastic AgentsATP-Binding Cassette TransportersAzacitidineCaco-2 CellsCamptothecinCell AdhesionCell Line, TumorCell ProliferationColorectal NeoplasmsDNA MethylationDNA RepairGene ExpressionGene Expression ProfilingHCT116 CellsHumansIrinotecanLong Interspersed Nucleotide ElementsMiceMice, Inbred NODMice, SCIDConceptsCRC cell linesColorectal cancerMultiple CRC cell linesPhase 1/2 clinical trialCell linesMetastatic colorectal cancerMajority of patientsNOD-SCID miceColorectal cancer cellsSoft agar assayInitial therapyMetastatic settingCytotoxic chemotherapyCRC treatmentClinical efficacyCancer deathTumor regressionClinical trialsDNA demethylating agentVivo xenograftsChemotherapeutic agentsCancer cellsHCT116 cell linesAgar assayChemotherapy
2015
A phase I study of investigational agent SGI-110 combined with irinotecan in previously treated metastatic colorectal cancer patients.
Wang J, Gootjes E, Uram J, Zahurak M, El-Khoueiry A, Verheul H, Ahuja N, Azad N. A phase I study of investigational agent SGI-110 combined with irinotecan in previously treated metastatic colorectal cancer patients. Journal Of Clinical Oncology 2015, 33: tps797-tps797. DOI: 10.1200/jco.2015.33.3_suppl.tps797.Peer-Reviewed Original ResearchDose level 1SGI-110Colorectal cancerPhase ITumor biopsiesDay 1Metastatic colorectal cancer patientsRandomized phase II studyMajor eligibility criteriaPeriodic CT scansPhase II studyGrowth factor supportColorectal cancer patientsM2 days 1Metastatic colon adenocarcinomaMetastatic colon cancerCRC cell linesAdditional dose levelsEvaluation of biomarkersMeasureable diseaseTotal therapyII studyIrinotecan therapyDose escalationFactor support
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 sensitivityGemcitabineA phase II study of combination epigenetic therapy in metastatic colorectal cancer (mCRC): A phase II consortium (P2C)/Stand Up 2 Cancer (SU2C) study.
Azad N, El-Khoueiry A, Mahoney M, Adkins D, Flynn P, Bahary N, Kim G, Pitot H, Erlichman C, Donehower R, Herman J, Baylin S, Ahuja N. A phase II study of combination epigenetic therapy in metastatic colorectal cancer (mCRC): A phase II consortium (P2C)/Stand Up 2 Cancer (SU2C) study. Journal Of Clinical Oncology 2013, 31: 3539-3539. DOI: 10.1200/jco.2013.31.15_suppl.3539.Peer-Reviewed Original ResearchMetastatic colorectal cancerPrior regimensGood end-organ functionCombination epigenetic therapyECOG PS 0End-organ functionPhase II studyUrinary tract obstructionSerial tumor biopsiesInitial eligibility criteriaCRC cell linesMulti-institutional studyMCRC ptsChest painPrimary endpointPrior therapyRECIST criteriaTract obstructionII studyPS 0Cohort BCohort ALiver diseaseSubsequent therapyColorectal cancer
2007
Methylation-induced silencing of ASC/TMS1, a pro-apoptotic gene, is a late-stage event in colorectal cancer
Riojas MA, Guo M, Glöckner SC, Machida EO, Baylin SB, Ahuja N. Methylation-induced silencing of ASC/TMS1, a pro-apoptotic gene, is a late-stage event in colorectal cancer. Cancer Biology & Therapy 2007, 6: 1710-1716. PMID: 17986858, DOI: 10.4161/cbt.6.11.4829.Peer-Reviewed Original ResearchConceptsASC/TMS1Normal colorectal tissue samplesCRC cell linesColorectal tissue samplesColorectal cancerColorectal adenomasMethylation-specific PCRCell linesMRNA expressionPro-apoptotic genesPrimary colorectal cancer specimensStage 1 cancerStage 2 cancerStage 3 cancerRight-sided tumorsPrimary colorectal cancerStage 4 cancerColorectal cancer specimensTissue samplesColorectal cancer cell linesNormal colorectal tissuesUnmethylated cell linesDifferent human neoplasmsCancer cell linesLate-stage event