2012
Dietary Methyl Donor Depletion Protects Against Intestinal Tumorigenesis in ApcMin/+ Mice
Kadaveru K, Protiva P, Greenspan EJ, Kim YI, Rosenberg DW. Dietary Methyl Donor Depletion Protects Against Intestinal Tumorigenesis in ApcMin/+ Mice. Cancer Prevention Research 2012, 5: 911-920. PMID: 22677908, PMCID: PMC3397832, DOI: 10.1158/1940-6207.capr-11-0544.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBiomarkers, TumorCaloric RestrictionDietFolic AcidFolic Acid DeficiencyGene Expression ProfilingGenes, APCHumansIntestinal NeoplasmsMiceMice, Inbred C57BLOligonucleotide Array Sequence AnalysisReal-Time Polymerase Chain ReactionReverse Transcriptase Polymerase Chain ReactionRNA, MessengerSignal TransductionConceptsWeeks of ageIntestinal tumorigenesisCancer protectionNormal-appearing colonic mucosaMethyl donor statusSmall intestinal tumorsHigh-risk populationDietary folate supplementationVitamin B12 depletionColon cancer riskIntestinal tumor formationBody weight gainMD miceTumor numberTumor sizeMDS groupIntestinal tumorsColonic mucosaFolate supplementationProtective effectB12 depletionInflammatory signalingCancer riskDeficient dietFolate deficiency
2011
Altered Folate Availability Modifies the Molecular Environment of the Human Colorectum: Implications for Colorectal Carcinogenesis
Protiva P, Mason JB, Liu Z, Hopkins ME, Nelson C, Marshall JR, Lambrecht RW, Pendyala S, Kopelovich L, Kim M, Kleinstein SH, Laird PW, Lipkin M, Holt PR. Altered Folate Availability Modifies the Molecular Environment of the Human Colorectum: Implications for Colorectal Carcinogenesis. Cancer Prevention Research 2011, 4: 530-543. PMID: 21321062, PMCID: PMC3742550, DOI: 10.1158/1940-6207.capr-10-0143.Peer-Reviewed Original ResearchMeSH KeywordsAdultAgedBiological AvailabilityCell Transformation, NeoplasticColonColorectal NeoplasmsDietary SupplementsDNA BreaksDNA MethylationFemaleFolic AcidFolic Acid DeficiencyGene ExpressionGene Expression ProfilingHumansMaleMiddle AgedOligonucleotide Array Sequence AnalysisPromoter Regions, GeneticRectumReverse Transcriptase Polymerase Chain ReactionTumor Suppressor Protein p53ConceptsFolate supplementationFolate deliveryFolate depletionImmune responseColorectal carcinogenesisDNA strand breaksHuman colonColorectal cancer riskFolic acidSupplemental folic acidLow-folate dietLow folate statusImmune response pathwaysImmune-related pathwaysFirst studyRectosigmoid biopsiesRisk volunteersPrimary endpointGene array analysisPromoter-specific DNA methylationRepletion protocolFolate dietFolate levelsSecond studyFolate status
2009
Chemoprevention of Colorectal Neoplasia by Estrogen: Potential Role of Vitamin D Activity
Protiva P, Cross HS, Hopkins ME, Kállay E, Bises G, Dreyhaupt E, Augenlicht L, Lipkin M, Lesser M, Livote E, Holt PR. Chemoprevention of Colorectal Neoplasia by Estrogen: Potential Role of Vitamin D Activity. Cancer Prevention Research 2009, 2: 43-51. PMID: 19139017, DOI: 10.1158/1940-6207.capr-08-0103.Peer-Reviewed Original ResearchMeSH Keywords25-Hydroxyvitamin D3 1-alpha-HydroxylaseChemopreventionColorectal NeoplasmsEstradiolEstrogen Replacement TherapyEstrogensFemaleGene ExpressionGene Expression ProfilingHumansMiddle AgedReceptors, CalcitriolReverse Transcriptase Polymerase Chain ReactionSteroid HydroxylasesVitamin DVitamin D3 24-HydroxylaseConceptsHormone replacement therapyVitamin D activityReplacement therapyPostmenopausal hormone replacement therapyVitamin D receptor pathwayPrimary end pointRectal mucosal biopsiesVitamin D actionExpression of VDRColon cancer incidenceE-cadherinRegulation of VDREstrogen interventionEstrogen-responsive genesPostmenopausal womenPremenopausal levelsVDR pathwayMucosal biopsiesRectal biopsySerum estradiolVitamin DColorectal neoplasiaD activityRectal mucosaCancer incidence