Featured Publications
To weight or not to weight? The effect of selection bias in 3 large electronic health record-linked biobanks and recommendations for practice
Salvatore M, Kundu R, Shi X, Friese C, Lee S, Fritsche L, Mondul A, Hanauer D, Pearce C, Mukherjee B. To weight or not to weight? The effect of selection bias in 3 large electronic health record-linked biobanks and recommendations for practice. Journal Of The American Medical Informatics Association 2024, 31: 1479-1492. PMID: 38742457, PMCID: PMC11187425, DOI: 10.1093/jamia/ocae098.Peer-Reviewed Original ResearchEHR-linked biobanksNational Health Interview Survey dataHealth Interview Survey dataPhenome-wide association studyMichigan Genomics InitiativeElectronic health record-linked biobankTarget populationInterview Survey dataColorectal cancerUS adult populationSelection biasUK BiobankAssociation estimatesBiobank dataRecruitment strategiesEffect of selection biasICD codesLog odds ratioUKBSelection weightsEffect sizeAssociation studiesAdult populationBiobankImpact prevalence
2023
COVID-19 outcomes by cancer status, site, treatment, and vaccination
Salvatore M, Hu M, Beesley L, Mondul A, Pearce C, Friese C, Fritsche L, Mukherjee B. COVID-19 outcomes by cancer status, site, treatment, and vaccination. Cancer Epidemiology Biomarkers & Prevention 2023, 32: 748-759. PMID: 36626383, DOI: 10.1158/1055-9965.epi-22-0607.Peer-Reviewed Original ResearchConceptsCOVID-19 outcomesCancer statusCancer diagnosisAssociated with higher ratesElectronic health record dataHealth record dataColorectal cancerIncreased riskAcademic medical centerKidney cancerCancer-free patientsIntensive care unit admissionCancer sitesAssociated with lower ratesChemotherapy receiptHigher ratesCOVID-19 precautionsRecord dataCOVID-19Logistic regressionMedical CenterUnit admissionRetrospective cohortVaccination statusLung cancer
2020
Fusobacterium nucleatum infection correlates with two types of microsatellite alterations in colorectal cancer and triggers DNA damage
Okita Y, Koi M, Takeda K, Ross R, Mukherjee B, Koeppe E, Stoffel E, Galanko J, McCoy A, Keku T, Okugawa Y, Kitajima T, Toiyama Y, Martens E, Carethers J. Fusobacterium nucleatum infection correlates with two types of microsatellite alterations in colorectal cancer and triggers DNA damage. Gut Pathogens 2020, 12: 46. PMID: 33005238, PMCID: PMC7526104, DOI: 10.1186/s13099-020-00384-3.Peer-Reviewed Original ResearchMicrosatellite instability-highCpG island hypermethylation phenotypeColorectal cancerMicrosatellite alterationsFusobacterium nucleatum infectionInflammatory tumor microenvironmentSubtypes of colorectal cancerDNA double strand breaksColorectal cancer cohortMicrosatellite instability-lowTumor microenvironmentFn infectionColorectal cancer tissuesHypermethylation phenotypeElevated levelsInfected cellsCancerInfectionAlterationsDouble strand breaksAssociated with microsatellite instability-highStrand breaks
2016
Decreased Anti-Tumor Cytotoxic Immunity among Microsatellite-Stable Colon Cancers from African Americans
Basa R, Davies V, Li X, Murali B, Shah J, Yang B, Li S, Khan M, Tian M, Tejada R, Hassan A, Washington A, Mukherjee B, Carethers J, McGuire K. Decreased Anti-Tumor Cytotoxic Immunity among Microsatellite-Stable Colon Cancers from African Americans. PLOS ONE 2016, 11: e0156660. PMID: 27310868, PMCID: PMC4911070, DOI: 10.1371/journal.pone.0156660.Peer-Reviewed Original ResearchConceptsGranzyme B+ cellsColorectal cancerCytotoxic immunityB+ cellsAnti-tumor cytotoxic T lymphocytesColon cancerMicrosatellite-stable colon cancerCytotoxic T lymphocytesIL-17 expressionWilcoxon rank sum testProtection to patientsAfrican American colorectal cancerRank sum testTwo-sample Wilcoxon rank-sum testCD57+CD8+Invasive borderCytotoxic markersNo significant differenceT lymphocytesColon tumorsDescriptive summary statisticsImmune biomarkersTumor samplesImmune cytotoxicitySu2003 Significance of EMAST/MSI-L and Chromosome 9p24.2 Loss of Heterozygosity (LOH) for Patient Survival With Stage II/III Colorectal Cancer (CRC)
Koi M, Garcia M, Choi C, Kim H, Koike J, Hemmi H, Nagasaka T, Okugawa Y, Toiyama Y, Kitajima T, Imaoka H, Kusunoki M, Chen Y, Mukherjee B, Boland C, Carethers J. Su2003 Significance of EMAST/MSI-L and Chromosome 9p24.2 Loss of Heterozygosity (LOH) for Patient Survival With Stage II/III Colorectal Cancer (CRC). Gastroenterology 2016, 150: s607. DOI: 10.1016/s0016-5085(16)32085-6.Peer-Reviewed Original ResearchMicrosatellite Alterations With Allelic Loss at 9p24.2 Signify Less-Aggressive Colorectal Cancer Metastasis
Koi M, Garcia M, Choi C, Kim H, Koike J, Hemmi H, Nagasaka T, Okugawa Y, Toiyama Y, Kitajima T, Imaoka H, Kusunoki M, Chen Y, Mukherjee B, Boland C, Carethers J. Microsatellite Alterations With Allelic Loss at 9p24.2 Signify Less-Aggressive Colorectal Cancer Metastasis. Gastroenterology 2016, 150: 944-955. PMID: 26752111, PMCID: PMC4808397, DOI: 10.1053/j.gastro.2015.12.032.Peer-Reviewed Original ResearchMeSH KeywordsBiomarkers, TumorChi-Square DistributionChromosome AberrationsChromosomes, Human, Pair 9Colorectal NeoplasmsDisease ProgressionDisease-Free SurvivalFemaleGenetic Predisposition to DiseaseHumansJapanKaplan-Meier EstimateLiver NeoplasmsLogistic ModelsLoss of HeterozygosityMaleMicrosatellite RepeatsMiddle AgedNeoplasm Recurrence, LocalNeoplasm StagingOdds RatioPhenotypeProportional Hazards ModelsProto-Oncogene Proteins B-rafProto-Oncogene Proteins p21(ras)Republic of KoreaRisk FactorsTime FactorsTreatment OutcomeConceptsPrimary colorectal tumorsLoss of heterozygosityLiver metastasesColorectal cancerColorectal tumorsElevated microsatellite alterationsMicrosatellite alterationsStage IICurative treatment of patientsStage III colorectal cancerOverall survival of patientsSurvival of patientsIII colorectal cancerTumor to liverColorectal cancer recurrenceTreatment of patientsMatched liver metastasesCancer cell nucleiMatched metastasesDisease recurrenceOverall survivalPrognostic factorsAllelic lossNo significant differenceCurative treatment
2015
Genome-wide association study of colorectal cancer identifies six new susceptibility loci
Schumacher FR, Schmit SL, Jiao S, Edlund CK, Wang H, Zhang B, Hsu L, Huang SC, Fischer CP, Harju JF, Idos GE, Lejbkowicz F, Manion FJ, McDonnell K, McNeil CE, Melas M, Rennert HS, Shi W, Thomas DC, Van Den Berg DJ, Hutter CM, Aragaki AK, Butterbach K, Caan BJ, Carlson CS, Chanock SJ, Curtis KR, Fuchs CS, Gala M, Giovannucci EL, Gogarten SM, Hayes RB, Henderson B, Hunter DJ, Jackson RD, Kolonel LN, Kooperberg C, Küry S, LaCroix A, Laurie CC, Laurie CA, Lemire M, Levine D, Ma J, Makar KW, Qu C, Taverna D, Ulrich CM, Wu K, Kono S, West DW, Berndt SI, Bezieau S, Brenner H, Campbell PT, Chan AT, Chang-Claude J, Coetzee GA, Conti DV, Duggan D, Figueiredo JC, Fortini BK, Gallinger SJ, Gauderman WJ, Giles G, Green R, Haile R, Harrison TA, Hoffmeister M, Hopper JL, Hudson TJ, Jacobs E, Iwasaki M, Jee SH, Jenkins M, Jia WH, Joshi A, Li L, Lindor NM, Matsuo K, Moreno V, Mukherjee B, Newcomb PA, Potter JD, Raskin L, Rennert G, Rosse S, Severi G, Schoen RE, Seminara D, Shu XO, Slattery ML, Tsugane S, White E, Xiang YB, Zanke BW, Zheng W, Le Marchand L, Casey G, Gruber SB, Peters U. Genome-wide association study of colorectal cancer identifies six new susceptibility loci. Nature Communications 2015, 6: 7138. PMID: 26151821, PMCID: PMC4967357, DOI: 10.1038/ncomms8138.Peer-Reviewed Original ResearchConceptsNew susceptibility lociAssociation studiesSusceptibility lociSignificant genetic lociGenome-wide association studiesGenome-wide thresholdCommon genetic variantsRare pathogenic mutationsTwo-stage association studyGenetic lociGenetic epidemiology studiesGenetic variantsLociUnderlying biological mechanismsPathogenic mutationsBiological mechanismsAsian ConsortiumGenetic susceptibilityMutationsAdditional insightColorectal cancerCancerVariants
2012
On the equivalence of posterior inference based on retrospective and prospective likelihoods: application to a case‐control study of colorectal cancer
Ghosh M, Song J, Forster J, Mitra R, Mukherjee B. On the equivalence of posterior inference based on retrospective and prospective likelihoods: application to a case‐control study of colorectal cancer. Statistics In Medicine 2012, 31: 2196-2208. PMID: 22495822, DOI: 10.1002/sim.5358.Peer-Reviewed Original ResearchConceptsPosterior inferenceCase-control study of colorectal cancerOdds ratio parametersCategorical response dataBayesian analysis of dataStudy of colorectal cancerCase-control studyGeneral classProspective likelihoodSimulation studyCategorical responsesBayesian analysisColorectal cancerMatched case-control studyInferenceAnalysis of dataResponse dataPriorsRetrospective designRetrospective modelEquivalenceLikelihood‐based methods for regression analysis with binary exposure status assessed by pooling
Lyles R, Tang L, Lin J, Zhang Z, Mukherjee B. Likelihood‐based methods for regression analysis with binary exposure status assessed by pooling. Statistics In Medicine 2012, 31: 2485-2497. PMID: 22415630, PMCID: PMC3528351, DOI: 10.1002/sim.4426.Peer-Reviewed Original ResearchConceptsPopulation-based case-control study of colorectal cancerCase-control study of colorectal cancerPopulation-based case-control studyStudy of colorectal cancerExposure statusBinary outcomesRegression modelsCase-control sampleLogistic regression modelsGene-disease associationsObserved binary outcomeStudy designEpidemiological studiesColorectal cancerAssess exposureMaximum likelihood analysisRegression analysisLikelihood-based methodsExposure assessmentMaximum likelihood approachLikelihood approachCross-sectionSimulation studyOutcomesLikelihood analysis
2011
Logistic regression analysis of biomarker data subject to pooling and dichotomization
Zhang Z, Liu A, Lyles R, Mukherjee B. Logistic regression analysis of biomarker data subject to pooling and dichotomization. Statistics In Medicine 2011, 31: 2473-2484. PMID: 21953741, DOI: 10.1002/sim.4367.Peer-Reviewed Original ResearchConceptsPopulation-based case-control study of colorectal cancerCase-control study of colorectal cancerProspective logistic regression modelPopulation-based case-control studyStudy of colorectal cancerEpidemiological studiesLogistic regression modelsAnalysis of epidemiological dataLogistic regression analysisBinary exposurePooled measureColorectal cancerRegression modelsEpidemiological dataRegression analysisAnalysis of biomarker dataDisease statusExposed subjectsBiomarker dataChoice of designSubjectsEstimated parametersStatusRecommendationsBayesian Modeling for Genetic Anticipation in Presence of Mutational Heterogeneity: A Case Study in Lynch Syndrome
Boonstra P, Mukherjee B, Taylor J, Nilbert M, Moreno V, Gruber S. Bayesian Modeling for Genetic Anticipation in Presence of Mutational Heterogeneity: A Case Study in Lynch Syndrome. Biometrics 2011, 67: 1627-1637. PMID: 21627626, PMCID: PMC3176998, DOI: 10.1111/j.1541-0420.2011.01607.x.Peer-Reviewed Original ResearchMeSH KeywordsAdolescentAdultAge of OnsetAgedAnticipation, GeneticBayes TheoremChildChild, PreschoolColorectal Neoplasms, Hereditary NonpolyposisComputer SimulationDenmarkFemaleHumansInfantInfant, NewbornMaleMiddle AgedModels, GeneticModels, StatisticalMutationPolymorphism, Single NucleotidePrevalenceRisk AssessmentRisk FactorsYoung AdultConceptsLynch syndromeBirth cohortGenetic anticipationHereditary nonpolyposis colorectal cancerCancer registry dataNonpolyposis colorectal cancerDanish Cancer RegisterGenetic counseling clinicAge-specific incidenceHigh-risk familiesRandom-effects modelCancer RegisterRegistry dataCounseling clinicMismatch repairRandom effectsSecular trendsMedical practiceColorectal cancerSurvival analysis methodsEffects modelConfounding effectsLynchFlexible random effects modelModel fit diagnosticsMRE11 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 lethalityHigh Risk of Colorectal and Endometrial Cancer in Ashkenazi Families With the MSH2 A636P Founder Mutation
Mukherjee B, Rennert G, Ahn J, Dishon S, Lejbkowicz F, Rennert H, Shiovitz S, Moreno V, Gruber S. High Risk of Colorectal and Endometrial Cancer in Ashkenazi Families With the MSH2 A636P Founder Mutation. Gastroenterology 2011, 140: 1919-1926. PMID: 21419771, PMCID: PMC4835182, DOI: 10.1053/j.gastro.2011.02.071.Peer-Reviewed Original ResearchMeSH KeywordsAdultAge FactorsAgedAged, 80 and overCase-Control StudiesColorectal Neoplasms, Hereditary NonpolyposisEndometrial NeoplasmsFemaleFounder EffectGene FrequencyGenetic Predisposition to DiseaseGenetic TestingHeredityHumansIsraelJewsLikelihood FunctionsMaleMass ScreeningMiddle AgedMutationMutS Homolog 2 ProteinPedigreePenetrancePhenotypeProportional Hazards ModelsRegistriesRisk AssessmentRisk FactorsSex FactorsYoung AdultConceptsRisk of colorectal cancerHazard ratioColorectal cancerCumulative riskPopulation-basedLifetime risk of colorectal cancerCumulative risk of colorectal cancerEstimates of colorectal cancerAge-specific cumulative riskHigh risk of colorectalCases of colorectal cancerModified segregation analysisRisk of colorectalClinical genetics servicesClinic-based sampleEndometrial cancerRisk of ECCase-control studyGenetic servicesLynch syndromeCancer screeningEC riskLifetime riskAshkenazi familiesEstimated penetrance
2010
Risk of colorectal cancer in self‐reported inflammatory bowel disease and modification of risk by statin and NSAID use
Samadder N, Mukherjee B, Huang S, Ahn J, Rennert H, Greenson J, Rennert G, Gruber S. Risk of colorectal cancer in self‐reported inflammatory bowel disease and modification of risk by statin and NSAID use. Cancer 2010, 117: 1640-1648. PMID: 21472711, PMCID: PMC3117060, DOI: 10.1002/cncr.25731.Peer-Reviewed Original ResearchConceptsRisk of colorectal cancerAssociated with reduced risk of colorectal cancerHistory of inflammatory bowel diseaseRisk of inflammatory bowel diseaseAssociated with reduced riskLong-term statin useColorectal cancerMolecular Epidemiology of Colorectal Cancer studyPersonal history of inflammatory bowel diseaseIncreased risk of CRCReduced risk of colorectal cancerRelative riskIBD-associated colorectal cancerIncident colorectal cancerNonsteroidal anti-inflammatory drugsUnconditional logistic regressionNonsteroidal anti-inflammatory drug useStatin useModification of riskReduced riskInflammatory bowel diseaseColorectal cancer studyIn-person interviewsNon-IBD colorectal cancersCase-control study
2009
Case–Control Studies of Gene–Environment Interaction: Bayesian Design and Analysis
Mukherjee B, Ahn J, Gruber S, Ghosh M, Chatterjee N. Case–Control Studies of Gene–Environment Interaction: Bayesian Design and Analysis. Biometrics 2009, 66: 934-948. PMID: 19930190, PMCID: PMC3103064, DOI: 10.1111/j.1541-0420.2009.01357.x.Peer-Reviewed Original ResearchConceptsGene-environment interactionsCase-control study of colorectal cancerStudy of gene-environment interactionsStudy of colorectal cancerGene-environment independenceRed meat consumptionBayesian designCase-control studyBayesian approachSample size determination criteriaCase-controlEpidemiological studiesColorectal cancerFrequentist counterpartsNatural wayMeat consumptionAnalyze current dataHypothesis testingDetermination criteriaSmokingEpidemiological exposureAnalysis strategyStudyCalculation of Risk of Colorectal and Endometrial Cancer Among Patients With Lynch Syndrome
Stoffel E, Mukherjee B, Raymond V, Tayob N, Kastrinos F, Sparr J, Wang F, Bandipalliam P, Syngal S, Gruber S. Calculation of Risk of Colorectal and Endometrial Cancer Among Patients With Lynch Syndrome. Gastroenterology 2009, 137: 1621-1627. PMID: 19622357, PMCID: PMC2767441, DOI: 10.1053/j.gastro.2009.07.039.Peer-Reviewed Original ResearchConceptsRisk of colorectal cancerCumulative risk of colorectal cancerHazard ratioColorectal cancerCumulative riskLifetime risk of colorectal cancerMismatch repair gene mutation carriersEstimates of colorectal cancerAge-specific cumulative riskMismatch repair gene mutationsEstimates of lifetime riskCancer genetics clinicsCases of colorectal cancerModified segregation analysisRisk of colorectalColorectal cancer riskHereditary colorectal cancerEndometrial cancerGene mutation carriersRepair gene mutationsRisk of ECOverestimation of penetrationFirst-degree relativesLynch syndromeCancer surveillancePreclinical 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 phenotypeM2006 Elevated Risk of Colorectal Cancer in Inflammatory Bowel Disease and Modification of Risk By Statin Use: A Population-Based Case-Control Study
Samadder N, Huang S, Mukherjee B, Rennert G, Gruber S. M2006 Elevated Risk of Colorectal Cancer in Inflammatory Bowel Disease and Modification of Risk By Statin Use: A Population-Based Case-Control Study. Gastroenterology 2009, 136: a-465. DOI: 10.1016/s0016-5085(09)62140-5.Peer-Reviewed Original ResearchGene 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
2008
Adenoma-infiltrating Lymphocytes (AILs) are a Potential Marker of Hereditary Nonpolyposis Colorectal Cancer
Polydorides A, Mukherjee B, Gruber S, McKenna B, Appelman H, Greenson J. Adenoma-infiltrating Lymphocytes (AILs) are a Potential Marker of Hereditary Nonpolyposis Colorectal Cancer. The American Journal Of Surgical Pathology 2008, 32: 1661-1666. PMID: 18753941, PMCID: PMC3500084, DOI: 10.1097/pas.0b013e31816ffa80.Peer-Reviewed Original ResearchConceptsHereditary nonpolyposis colorectal cancer syndromeColorectal adenomasControl adenomasHereditary nonpolyposis colorectal cancer patientsColorectal cancer syndromePresence of high-grade dysplasiaTumor-infiltrating lymphocytesHigh-grade dysplasiaPresence of necrosisNumbers of mitotic figuresColorectal cancer patientsHost immune responseVillous componentCancer syndromesLack of dirty necrosisSerrated architectureMicrosatellite-unstable colorectal cancersPatient ageGeneral populationPoor differentiationDirty necrosisInexpensive markerHistological featuresColorectal cancerAdenomas