2011
MRE11 Deficiency Increases Sensitivity to Poly(ADP-ribose) Polymerase Inhibition in Microsatellite Unstable Colorectal Cancers
Vilar E, Bartnik C, Stenzel S, Raskin L, Ahn J, Moreno V, Mukherjee B, Iniesta M, Morgan M, Rennert G, Gruber S. MRE11 Deficiency Increases Sensitivity to Poly(ADP-ribose) Polymerase Inhibition in Microsatellite Unstable Colorectal Cancers. Cancer Research 2011, 71: 2632-2642. PMID: 21300766, PMCID: PMC3407272, DOI: 10.1158/0008-5472.can-10-1120.Peer-Reviewed Original ResearchMeSH KeywordsAcid Anhydride HydrolasesBenzimidazolesCell Line, TumorColorectal NeoplasmsDNA DamageDNA Repair EnzymesDNA-Binding ProteinsEnzyme InhibitorsGene Expression ProfilingGene Expression Regulation, NeoplasticGene Knockdown TechniquesHumansMicrosatellite InstabilityMRE11 Homologue ProteinMutationPoly (ADP-Ribose) Polymerase-1Poly(ADP-ribose) Polymerase InhibitorsPoly(ADP-ribose) PolymerasesRad51 RecombinaseRecombination, GeneticConceptsPoly(ADP-riboseDouble strand breaksColorectal cancer cell linesPARP-1 inhibitionCell linesPARP-1ABT-888PARP-1 inhibitorsColorectal cancerPoly(ADP-ribose) polymeraseRepetitive DNA sequencesWild-type cell linesMSI cell linesMicrosatellite instabilityConcept of synthetic lethalityMicrosatellite instability colorectal tumorsSensitivity to poly(ADP-riboseMutant Mre11Short hairpin RNAPoly(ADP-ribose) polymerase inhibitionDNA sequencesDNA mismatch repairCell line modelsSecondary to mutationsSynthetic lethality
2009
Preclinical testing of the PARP inhibitor ABT-888 in microsatellite instable colorectal cancer
Vilar Sanchez E, Chow A, Raskin L, Iniesta M, Mukherjee B, Gruber S. Preclinical testing of the PARP inhibitor ABT-888 in microsatellite instable colorectal cancer. Journal Of Clinical Oncology 2009, 27: 11028-11028. DOI: 10.1200/jco.2009.27.15_suppl.11028.Peer-Reviewed Original ResearchMSI cell linesDouble strand breaksMSS cell linesPARP inhibitor ABT-888ABT-888Cell linesInhibitor ABT-888Genetic instabilityDouble strand break repair pathwaysColorectal cancerMutation statusDouble strand break repairPARP inhibitorsMicrosatellite instable colorectal cancerSystems biology studiesSystems biology toolsMicrosatellite instabilitySensitivity to PARP inhibitionPreclinical activityStrand breaksMicrosatellite instability colorectal tumorsRepetitive sequencesColorectal cancer cell linesRAD50 geneMutator phenotypeGene Expression Patterns in Mismatch Repair-Deficient Colorectal Cancers Highlight the Potential Therapeutic Role of Inhibitors of the Phosphatidylinositol 3-Kinase-AKT-Mammalian Target of Rapamycin Pathway
Vilar E, Mukherjee B, Kuick R, Raskin L, Misek D, Taylor J, Giordano T, Hanash S, Fearon E, Rennert G, Gruber S. Gene Expression Patterns in Mismatch Repair-Deficient Colorectal Cancers Highlight the Potential Therapeutic Role of Inhibitors of the Phosphatidylinositol 3-Kinase-AKT-Mammalian Target of Rapamycin Pathway. Clinical Cancer Research 2009, 15: 2829-2839. PMID: 19351759, PMCID: PMC3425357, DOI: 10.1158/1078-0432.ccr-08-2432.Peer-Reviewed Original ResearchMeSH KeywordsAlgorithmsAntineoplastic AgentsBenzoquinonesCell CycleCell Line, TumorChromonesColorectal NeoplasmsComputational BiologyDNA Mismatch RepairDrug Evaluation, PreclinicalEnzyme InhibitorsGene Expression ProfilingHumansHydroxamic AcidsImmunosuppressive AgentsLactams, MacrocyclicMicrosatellite InstabilityMorpholinesPhosphoinositide-3 Kinase InhibitorsProto-Oncogene Proteins c-aktSirolimusConceptsGene expression informationColorectal cancerCell linesExpression informationGene expression dataSystems biology toolsLY-294002Gene expression patternsLow molecular weight compoundsPhosphatidylinositol 3-kinase-Akt-mammalian target of rapamycin pathwayMutant cellsBioinformatics approachTarget of rapamycin pathwayExpression dataMismatch repair-deficient colorectal cancerMolecular weight compoundsGroup of patientsCell cycleBiology toolsApoptosis effectExpression patternsPotential therapeutic roleTrichostatin AMSI-HWeight compounds