2016
Germline variation in inflammation-related pathways and risk of Barrett's oesophagus and oesophageal adenocarcinoma
Buas MF, He Q, Johnson LG, Onstad L, Levine DM, Thrift AP, Gharahkhani P, Palles C, Lagergren J, Fitzgerald RC, Ye W, Caldas C, Bird NC, Shaheen NJ, Bernstein L, Gammon MD, Wu AH, Hardie LJ, Pharoah PD, Liu G, Iyer P, Corley DA, Risch HA, Chow WH, Prenen H, Chegwidden L, Love S, Attwood S, Moayyedi P, MacDonald D, Harrison R, Watson P, Barr H, deCaestecker J, Tomlinson I, Jankowski J, Whiteman DC, MacGregor S, Vaughan TL, Madeleine MM. Germline variation in inflammation-related pathways and risk of Barrett's oesophagus and oesophageal adenocarcinoma. Gut 2016, 66: 1739. PMID: 27486097, PMCID: PMC5296402, DOI: 10.1136/gutjnl-2016-311622.Peer-Reviewed Original ResearchMeSH KeywordsAdenocarcinomaAgedBarrett EsophagusCytokinesEsophageal NeoplasmsFemaleGene-Environment InteractionGenetic Predisposition to DiseaseGenome-Wide Association StudyGerm-Line MutationGlutathione TransferaseHLA AntigensHumansInflammationMaleMiddle AgedNF-kappa BOxidative StressPolymorphism, Single NucleotidePrincipal Component AnalysisProstaglandin-Endoperoxide SynthasesRisk FactorsSignal TransductionConceptsBarrett's esophagusBE casesSingle nucleotide polymorphismsGermline variationOesophageal adenocarcinoma incidenceHuman leucocyte antigenInflammation-related pathwaysSymptomatic refluxSystemic inflammationAdenocarcinoma incidenceOesophageal adenocarcinomaOA pathogenesisInflammatory processLeucocyte antigenOA casesRisk factorsCOX pathwayBE riskOA riskDisease riskEsophagusStrong expression quantitative trait locusGenetic susceptibilityNuclear factorExpression quantitative trait loci
2007
GST, NAT1, CYP1A1 polymorphisms and risk of esophageal and gastric adenocarcinomas
Wideroff L, Vaughan TL, Farin FM, Gammon MD, Risch H, Stanford JL, Chow WH. GST, NAT1, CYP1A1 polymorphisms and risk of esophageal and gastric adenocarcinomas. Cancer Epidemiology 2007, 31: 233-236. PMID: 17646057, PMCID: PMC2268246, DOI: 10.1016/j.cdp.2007.03.004.Peer-Reviewed Original ResearchMeSH KeywordsAdenocarcinomaAdultAgedAllelesArylamine N-AcetyltransferaseCase-Control StudiesCytochrome P-450 CYP1A1Esophageal NeoplasmsFemaleGenetic Predisposition to DiseaseGlutathione S-Transferase piGlutathione TransferaseHumansIsoenzymesMaleMiddle AgedOdds RatioPolymerase Chain ReactionPolymorphism, GeneticRisk FactorsStomach NeoplasmsUnited StatesConceptsGastric adenocarcinomaOdds ratioGastric cardia adenocarcinomaEsophageal adenocarcinomaCardia adenocarcinomaElevated riskConfidence intervalsVal genotypePopulation-based case-control studyCYP1A1 Val/ValGSTP1 Val/Val genotypeNoncardia gastric adenocarcinomaEpidemiologic risk factorsRespective odds ratiosRisk of esophagealIle/Val genotypeVal/Val genotypeCase-control studyVal/ValN-acetyltransferase 1Same catchment areaHistologic subgroupsIncident casesRisk factorsGSTT1 genotype
2005
Glutathione S-transferase polymorphisms and ovarian cancer treatment and survival
Beeghly A, Katsaros D, Chen H, Fracchioli S, Zhang Y, Massobrio M, Risch H, Jones B, Yu H. Glutathione S-transferase polymorphisms and ovarian cancer treatment and survival. Gynecologic Oncology 2005, 100: 330-337. PMID: 16199080, DOI: 10.1016/j.ygyno.2005.08.035.Peer-Reviewed Original ResearchConceptsOvarian cancer treatmentDisease progressionGSTP1 genotypesGST polymorphismsPrimary epithelial ovarian cancerCox proportional hazards regressionFunctional polymorphismsGSTP1 Ile/IleCancer treatmentGSTP1 Ile/ValGlutathione S-transferase polymorphismsGSTM1 null patientsPost-operative chemotherapySubgroup of patientsProportional hazards regressionEpithelial ovarian cancerOvarian cancer survivalEffect of chemotherapyOvarian cancer prognosisOvarian cancer progressionVal/ValIle/IleIle/ValOverall survivalTumor characteristics