2011
Physical activity and breast cancer survival: an epigenetic link through reduced methylation of a tumor suppressor gene L3MBTL1
Zeng H, Irwin ML, Lu L, Risch H, Mayne S, Mu L, Deng Q, Scarampi L, Mitidieri M, Katsaros D, Yu H. Physical activity and breast cancer survival: an epigenetic link through reduced methylation of a tumor suppressor gene L3MBTL1. Breast Cancer Research And Treatment 2011, 133: 127-135. PMID: 21837478, DOI: 10.1007/s10549-011-1716-7.Peer-Reviewed Original ResearchMeSH KeywordsBreast NeoplasmsCarcinoma, Ductal, BreastCarcinoma, LobularChromosomal Proteins, Non-HistoneDNA MethylationEpigenesis, GeneticFemaleGene ExpressionGene Expression ProfilingGene Expression Regulation, NeoplasticGenes, Tumor SuppressorHumansKaplan-Meier EstimateMotor ActivityRepressor ProteinsTumor Suppressor ProteinsConceptsBreast cancer patientsBreast cancer survivalCancer patientsPhysical activityOverall survivalSurvival outcomesTumor suppressor geneCancer survivalHormone receptor-positive tumorsModerate-intensity aerobic exerciseHigh expressionBreast cancer deathsReceptor-positive tumorsRandomized clinical trialsExercise-related changesSuppressor genePeripheral blood leukocytesBreast cancer diagnosisGene expressionDisease recurrenceAerobic exerciseCancer deathClinical trialsTumor featuresBlood leukocytes
2003
Etiology of Pancreatic Cancer, With a Hypothesis Concerning the Role of N-Nitroso Compounds and Excess Gastric Acidity
Risch HA. Etiology of Pancreatic Cancer, With a Hypothesis Concerning the Role of N-Nitroso Compounds and Excess Gastric Acidity. Journal Of The National Cancer Institute 2003, 95: 948-960. PMID: 12837831, DOI: 10.1093/jnci/95.13.948.Peer-Reviewed Original ResearchConceptsPancreatic cancerGastric acidityRisk of nonsmokersConsumption of fruitsCurrent smokersDiabetes mellitusChronic pancreatitisCigarette smokingColorectal cancerCytokine mechanismsCancer deathDietary factorsDuodenal acidityRisk factorsEpidemiologic reviewFrequent causeHigh riskLower riskN-nitroso compoundsHelicobacter pyloriCancerGermline mutationsHost genetic variationRiskAnimal foods
2001
Etiologic Mechanisms in Epithelial Ovarian Cancer
Risch H. Etiologic Mechanisms in Epithelial Ovarian Cancer. 2001, 307-319. DOI: 10.1007/978-1-4612-2092-3_30.Peer-Reviewed Original ResearchOvarian cancerEpithelial ovarian cancerOvarian neoplasmsColorectal cancerIncessant ovulationCancer deathPrimary tumorRisk factorsCommon neoplasmInvasive tumorsFrequent causeEtiologic mechanismsOlder womenEpithelial subtypesSurface epitheliumEtiologic hypothesesAdult womenCancerEtiologic heterogeneityWomenNeoplasmsTumorsDisease occurrenceGerm cellsGonadotropin
1998
Hormonal Etiology of Epithelial Ovarian Cancer, With a Hypothesis Concerning the Role of Androgens and Progesterone
Risch HA. Hormonal Etiology of Epithelial Ovarian Cancer, With a Hypothesis Concerning the Role of Androgens and Progesterone. Journal Of The National Cancer Institute 1998, 90: 1774-1786. PMID: 9839517, DOI: 10.1093/jnci/90.23.1774.Peer-Reviewed Original ResearchConceptsEpithelial ovarian cancerOvarian cancerIncessant ovulationOvarian epithelial cellsOvarian inclusion cystsEpithelial cellsRole of androgensGonadotropin hypothesisGonadotropin secretionGonadotropin stimulationHormonal etiologyColorectal cancerCancer deathInclusion cystsAndrogenic stimulationFrequent causeCancerGermline mutationsProgesterone stimulationHormonal stimulationOvulationStimulationAdditional major factorAndrogensProgesterone