2024
Asparagine synthetase and G‐protein coupled estrogen receptor are critical responders to nutrient supply in KRAS mutant colorectal cancer
Lu L, Zhang Q, Aladelokun O, Berardi D, Shen X, Marin A, Garcia‐Milian R, Roper J, Khan S, Johnson C. Asparagine synthetase and G‐protein coupled estrogen receptor are critical responders to nutrient supply in KRAS mutant colorectal cancer. International Journal Of Cancer 2024, 156: 52-68. PMID: 39039782, PMCID: PMC11537827, DOI: 10.1002/ijc.35104.Peer-Reviewed Original ResearchG protein-coupled estrogen receptor 1KRAS mutant colorectal cancerAsparagine synthetase expressionMutant colorectal cancerColorectal cancerAsparagine synthetaseG-protein coupled estrogen receptor 1 expressionG protein-coupled estrogen receptorWild-typeAssociated with poor overall survivalAdvanced stage tumorsKRAS wild-typeProtective effect of estradiolEffects of estradiolPoor overall survivalEstrogen receptor 1Expression of asparagine synthetasePresence of estradiolIncreased caspase-3 activityDepletion inhibited cell growthColon cancer cohortNutrient supplyAdvanced tumorsOverall survivalStage tumors
2021
Identification of Dose-Dependent DNA Damage and Repair Responses From Subchronic Exposure to 1,4-Dioxane in Mice Using a Systems Analysis Approach
Charkoftaki G, Golla JP, Santos-Neto A, Orlicky DJ, Garcia-Milian R, Chen Y, Rattray NJW, Cai Y, Wang Y, Shearn CT, Mironova V, Wang Y, Johnson CH, Thompson DC, Vasiliou V. Identification of Dose-Dependent DNA Damage and Repair Responses From Subchronic Exposure to 1,4-Dioxane in Mice Using a Systems Analysis Approach. Toxicological Sciences 2021, 183: 338-351. PMID: 33693819, PMCID: PMC8921626, DOI: 10.1093/toxsci/kfab030.Peer-Reviewed Original ResearchConceptsDX exposureBile acid quantificationRepair responseBDF-1 miceDNA damageDose-dependent DNA damageEffects of exposureHistopathological studySubchronic exposureImmunohistochemical analysisLiver carcinogenLiver carcinogenicityLiver transcriptomicsDrinking waterMetabolomic profilingMicePotential mechanismsLiverEnvironmental chemicalsState maximum contaminant levelToxic effectsCell deathExposureOxidative stress responsePresent study
2019
Molecular Pathway Analysis Indicates a Distinct Metabolic Phenotype in Women With Right-Sided Colon Cancer
Sun Y, Mironova V, Chen Y, Lundh EPF, Zhang Q, Cai Y, Vasiliou V, Zhang Y, Garcia-Milian R, Khan SA, Johnson CH. Molecular Pathway Analysis Indicates a Distinct Metabolic Phenotype in Women With Right-Sided Colon Cancer. Translational Oncology 2019, 13: 42-56. PMID: 31760268, PMCID: PMC6883319, DOI: 10.1016/j.tranon.2019.09.004.Peer-Reviewed Original ResearchRight-sided colon cancerLeft-sided colon cancerColon cancerAnatomical locationTumor tissueAnti-tumor immune responseGene Expression OmnibusImportant predictive markerPoor clinical outcomeTumor anatomical locationClinical outcomesPredictive markerPrimary tumorImmune phenotypeDistinct metabolic phenotypesImmune responseLower incidenceTreatment responseSex-specific differencesMolecular pathway analysisClinical importanceCancerProtein kinase alpha subunitBiotechnology Information Gene Expression OmnibusWomen
2018
Evaluation of potential carcinogenicity of organic chemicals in synthetic turf crumb rubber
Perkins AN, Inayat-Hussain SH, Deziel NC, Johnson CH, Ferguson SS, Garcia-Milian R, Thompson DC, Vasiliou V. Evaluation of potential carcinogenicity of organic chemicals in synthetic turf crumb rubber. Environmental Research 2018, 169: 163-172. PMID: 30458352, PMCID: PMC6396308, DOI: 10.1016/j.envres.2018.10.018.Peer-Reviewed Original ResearchConceptsSynthetic turf fieldsCrumb rubber infillEuropean Chemicals AgencyOrganic chemicalsUS EPAADMET PredictorRubber infillUnited States Environmental Protection AgencyFuture exposure studiesChemical constituentsStates Environmental Protection AgencyHazardous chemicalsComputational toxicologyChemical componentsVinyl chlorideChemicalsPriority carcinogensTurf fieldsToxicology assessmentEnvironmental Protection AgencyCarcinogenic chemicalsChemicals AgencyExposure studiesECHA databasePotential carcinogenicity
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