2017
A germ-line deletion of APOBEC3B does not contribute to subtype-specific childhood acute lymphoblastic leukemia etiology
Wallace AD, Francis SS, Shao X, de Smith AJ, Walsh KM, Mckean-Cowdin R, Ma X, Dahl G, Barcellos LF, Wiemels JL, Metayer C. A germ-line deletion of APOBEC3B does not contribute to subtype-specific childhood acute lymphoblastic leukemia etiology. Haematologica 2017, 103: e29-e31. PMID: 29025908, PMCID: PMC5777211, DOI: 10.3324/haematol.2017.179317.Peer-Reviewed Original Research
2015
A Heritable Missense Polymorphism in CDKN2A Confers Strong Risk of Childhood Acute Lymphoblastic Leukemia and Is Preferentially Selected during Clonal Evolution
Walsh KM, de Smith AJ, Hansen HM, Smirnov IV, Gonseth S, Endicott AA, Xiao J, Rice T, Fu CH, McCoy LS, Lachance DH, Eckel-Passow JE, Wiencke JK, Jenkins RB, Wrensch MR, Ma X, Metayer C, Wiemels JL. A Heritable Missense Polymorphism in CDKN2A Confers Strong Risk of Childhood Acute Lymphoblastic Leukemia and Is Preferentially Selected during Clonal Evolution. Cancer Research 2015, 75: 4884-4894. PMID: 26527286, PMCID: PMC4651745, DOI: 10.1158/0008-5472.can-15-1105.Peer-Reviewed Original ResearchConceptsAcute lymphoblastic leukemiaChildhood acute lymphoblastic leukemiaLymphoblastic leukemiaCancer riskRisk allelesGeneral cancer riskPancreatic cancer riskGenome-wide association studiesCase-control populationCDKN2A variantsProtective allelesTumor growthClonal expansionChromosome 9p21.3Hispanic childrenMissense polymorphismStrong riskMissense variantsClonal evolutionRiskLeukemiaTumorsAllelic imbalanceEuropean ancestryPolymorphism
2012
HLA-DP genetic variation, proxies for early life immune modulation and childhood acute lymphoblastic leukemia risk
Urayama KY, Chokkalingam AP, Metayer C, Ma X, Selvin S, Barcellos LF, Wiemels JL, Wiencke JK, Taylor M, Brennan P, Dahl GV, Moonsamy P, Erlich HA, Trachtenberg E, Buffler PA. HLA-DP genetic variation, proxies for early life immune modulation and childhood acute lymphoblastic leukemia risk. Blood 2012, 120: 3039-3047. PMID: 22923493, PMCID: PMC3471514, DOI: 10.1182/blood-2012-01-404723.Peer-Reviewed Original ResearchMeSH KeywordsAdolescentAdultCase-Control StudiesChildChild, PreschoolFemaleGenetic Predisposition to DiseaseGenetic VariationGenotypeHispanic or LatinoHLA-DP alpha-ChainsHLA-DP beta-ChainsHumansImmunologic FactorsInfantMalePrecursor Cell Lymphoblastic Leukemia-LymphomaPrognosisRisk FactorsWhite PeopleYoung AdultConceptsAcute lymphoblastic leukemiaImmune modulationChildhood acute lymphoblastic leukemiaChildhood acute lymphoblastic leukemia riskAcute lymphoblastic leukemia riskEarly immune modulationHuman leukocyte antigen (HLA) genesLowest exposure categoryLogistic regression analysisEtiology of childhoodNon-Hispanic whitesHLA-DPB1 geneRace/ethnicityInfectious exposureLymphoblastic leukemiaImmune mechanismsExposure categoriesHispanic ethnicityLeukemia riskGenetic susceptibility lociHLA-DPA1Immune systemHispanic childrenRegression analysisEvidence of interaction
2011
Genetic variation in nucleotide excision repair pathway genes, pesticide exposure and prostate cancer risk
Barry KH, Koutros S, Andreotti G, Sandler DP, Burdette LA, Yeager M, Freeman L, Lubin JH, Ma X, Zheng T, Alavanja MC, Berndt SI. Genetic variation in nucleotide excision repair pathway genes, pesticide exposure and prostate cancer risk. Carcinogenesis 2011, 33: 331-337. PMID: 22102698, PMCID: PMC3271261, DOI: 10.1093/carcin/bgr258.Peer-Reviewed Original ResearchConceptsProstate cancer riskCancer riskSingle nucleotide polymorphismsPesticide exposurePesticide applicatorsPesticide manufacturing workersCase-control studyInteraction p valueProstate cancer casesNucleotide excision repair pathway genesWild-type TT genotypeLogistic regression modelsHuman biomonitoring studiesCancer casesLifetime daysTT genotypeERCC1 rs2298881Male controlsFalse discovery rate methodIntensity scoresSignificant associationNucleotide excision repair pathwayGenotype groupsManufacturing workersUnderlying mechanismGenetic Variation in Base Excision Repair Pathway Genes, Pesticide Exposure, and Prostate Cancer Risk
Barry KH, Koutros S, Berndt SI, Andreotti G, Hoppin JA, Sandler DP, Burdette LA, Yeager M, Freeman LE, Lubin JH, Ma X, Zheng T, Alavanja MC. Genetic Variation in Base Excision Repair Pathway Genes, Pesticide Exposure, and Prostate Cancer Risk. Environmental Health Perspectives 2011, 119: 1726-1732. PMID: 21810555, PMCID: PMC3261977, DOI: 10.1289/ehp.1103454.Peer-Reviewed Original ResearchConceptsProstate cancer riskCancer riskSingle nucleotide polymorphismsPesticide applicatorsCT/TT genotypesPesticide manufacturing workersCase-control studyProstate cancer casesLogistic regression modelsTag single nucleotide polymorphismsBase excision repair pathway genesProstate cancerCancer casesFamily historyOxidative DNA damageTT genotypeCC genotypeMale controlsExposure variablesPesticide exposureBase excision repairManufacturing workersUnderlying mechanismRiskBER genes
2010
Xenobiotic Metabolizing Genes, Meat-Related Exposures, and Risk of Advanced Colorectal Adenoma
Ferrucci LM, Cross AJ, Gunter MJ, Ahn J, Mayne ST, Ma X, Chanock SJ, Yeager M, Graubard BI, Berndt SI, Huang WY, Hayes RB, Sinha R. Xenobiotic Metabolizing Genes, Meat-Related Exposures, and Risk of Advanced Colorectal Adenoma. World Review Of Nutrition And Dietetics 2010, 101: 34-45. PMID: 20436251, PMCID: PMC3051350, DOI: 10.1159/000314509.Peer-Reviewed Original Research
2009
Xenobiotic Metabolizing Gene Variants, Dietary Heterocyclic Amine Intake, and Risk of Prostate Cancer
Koutros S, Berndt SI, Sinha R, Ma X, Chatterjee N, Alavanja MC, Zheng T, Huang WY, Hayes RB, Cross AJ. Xenobiotic Metabolizing Gene Variants, Dietary Heterocyclic Amine Intake, and Risk of Prostate Cancer. Cancer Research 2009, 69: 1877-1884. PMID: 19223546, PMCID: PMC2662592, DOI: 10.1158/0008-5472.can-08-2447.Peer-Reviewed Original ResearchConceptsProstate cancer riskProstate cancerOdds ratioCancer riskSingle nucleotide polymorphismsDietary Heterocyclic Amine IntakeOvarian Cancer Screening TrialHeterocyclic amine intakeCancer Screening TrialUnconditional logistic regressionCase-control studyDietary heterocyclic aminesProstate cancer casesHeterocyclic aminesHCA intakeCancer casesLow intakeScreening TrialHCA metabolismMalignant transformationLogistic regressionCancerIntakeGene variantsConfidence intervals