2019
Targeted Assessment of G0S2 Methylation Identifies a Rapidly Recurrent, Routinely Fatal Molecular Subtype of Adrenocortical Carcinoma
Mohan D, Lerario A, Else T, Mukherjee B, Almeida M, Vinco M, Rege J, Mariani B, Zerbini M, Mendonca B, Latronico A, Marie S, Rainey W, Giordano T, Fragoso M, Hammer G. Targeted Assessment of G0S2 Methylation Identifies a Rapidly Recurrent, Routinely Fatal Molecular Subtype of Adrenocortical Carcinoma. Clinical Cancer Research 2019, 25: 3276-3288. PMID: 30770352, PMCID: PMC7117545, DOI: 10.1158/1078-0432.ccr-18-2693.Peer-Reviewed Original ResearchConceptsUpregulation of cell cycleDNA damage response programsAdrenocortical carcinomaTargeted bisulfite sequencingCancer Genome Atlas projectBisulfite sequencingCpG island hypermethylation phenotypeHypermethylation phenotypeAggressive adrenocortical carcinomasCell cycleMolecular markersBiological processesHypermethylationMolecular diagnosticsShorter disease-freeCancers of patientsBiomarker methylationAtlas projectEfficacious adjuvant therapyLocoregional diseaseOverall survivalAdjuvant therapyAdrenocortical tumorsDismal outcomeSilencing
2014
No effect of acute exposure to coarse particulate matter air pollution in a rural location on high-density lipoprotein function
Maiseyeu A, Yang H, Ramanathan G, Yin F, Bard R, Morishita M, Dvonch J, Wang L, Spino C, Mukherjee B, Badgeley M, Barajas-Espinosa A, Sun Q, Harkema J, Rajagopalan S, Araujo J, Brook R. No effect of acute exposure to coarse particulate matter air pollution in a rural location on high-density lipoprotein function. Inhalation Toxicology 2014, 26: 23-29. PMID: 24417404, PMCID: PMC4445365, DOI: 10.3109/08958378.2013.850761.Peer-Reviewed Original ResearchConceptsRural locationsParticulate matter air pollutionHDL dysfunctionHDL anti-oxidative capacityRandomized double-blind crossover studyDouble-blind crossover studyHDL functionHDL-mediated cholesterol efflux capacityParaoxonase activityFiltered airVascular protective functionCholesterol efflux capacityHigh-density lipoprotein (HDL) particlesMetrics of HDL functionHDL-mediated effluxConcentrated ambient particlesCrossover studyImpact of PMEfflux capacityPM exposureVenous bloodAnimal studiesHealthy humansCoarse PMWilcoxon test
2013
Transcriptome Profiling Identifies HMGA2 as a Biomarker of Melanoma Progression and Prognosis
Raskin L, Fullen D, Giordano T, Thomas D, Frohm M, B. K, Ahn J, Mukherjee B, Johnson T, Gruber S. Transcriptome Profiling Identifies HMGA2 as a Biomarker of Melanoma Progression and Prognosis. Journal Of Investigative Dermatology 2013, 133: 2585-2592. PMID: 23633021, PMCID: PMC4267221, DOI: 10.1038/jid.2013.197.Peer-Reviewed Original ResearchConceptsAmerican Joint Committee on CancerOverall survivalTissue microarrayPrimary melanomaMelanoma pathogenesisMelanoma progressionAssociated with disease-free survivalAnalysis of tissue microarraysMetastases-free survivalDisease-free survivalHMGA2 overexpressionCox proportional hazards regression modelsLog-rank testPredictors of survivalProportional hazards regression modelsHazards regression modelsBRAF/NRAS mutationsPrimary tumorPrognostic featuresMelanoma metastasesClinicopathological characteristicsReal-time PCRGenetic alterationsAQUA analysisMelanoma development
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
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
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