2024
Exploring a Novel Role of Glycerol Kinase 1 in Prostate Cancer PC-3 Cells
Park B, Kim S, Yu S, Kim K, Jeon H, Ahn S. Exploring a Novel Role of Glycerol Kinase 1 in Prostate Cancer PC-3 Cells. Biomolecules 2024, 14: 997. PMID: 39199385, PMCID: PMC11352368, DOI: 10.3390/biom14080997.Peer-Reviewed Original ResearchPC-3 cellsProstate cancer PC-3 cellsGK deficiencyCell deathProstate cancerAnti-cancer agentsKinase 1Apoptotic cell deathDNA microarray analysisHuman prostate cancer PC-3 cellsCancer cell deathModulating tumor microenvironmentProstate cancer cellsBiomarkers of cell deathX chromosomeReduced cell viabilityEpigenetic regulationExpression vectorInvestigated genesSynthesis of triglyceridesMicroarray analysisGenetic alterationsTumor microenvironmentNovel roleCancer cellsPre-treatment amino acids and risk of paclitaxel-induced peripheral neuropathy in SWOG S0221
Chen C, Zirpoli G, Budd G, Barlow W, Pusztai L, Hortobagyi G, Albain K, Godwin A, Thompson A, Henry N, Ambrosone C, Stringer K, Hertz D. Pre-treatment amino acids and risk of paclitaxel-induced peripheral neuropathy in SWOG S0221. Cancer Chemotherapy And Pharmacology 2024, 94: 311-321. PMID: 38814343, PMCID: PMC11878155, DOI: 10.1007/s00280-024-04680-6.Peer-Reviewed Original ResearchCIPN severityPeripheral neuropathyPaclitaxel-induced peripheral neuropathyEarly-stage breast cancerTrial of patientsBackgroundChemotherapy-induced peripheral neuropathyBody mass indexSerum amino acid concentrationsOver-Representation AnalysisDebilitating neurotoxicityPaclitaxel scheduleAnti-cancer agentsBreast cancerSelf-reported raceMass indexMetabolic pathways of amino acidsSerum concentrationsInverse associationAmino acid metabolic pathwaysPaclitaxelPrimary analysisBonferroni correctionTreatment limitationsS0221CIPN
2023
Evolution of systemic therapy from 2015 to 2019 for older patients in the United States with metastatic renal cell carcinoma.
Chow R, Long J, Hassan S, Wheeler S, Spees L, Leapman M, Hurwitz M, McManus H, Gross C, Dinan M. Evolution of systemic therapy from 2015 to 2019 for older patients in the United States with metastatic renal cell carcinoma. Journal Of Clinical Oncology 2023, 41: 610-610. DOI: 10.1200/jco.2023.41.6_suppl.610.Peer-Reviewed Original ResearchMetastatic renal cell carcinomaImmune checkpoint inhibitorsOral anti-cancer agentsNon-Hispanic white patientsSystemic therapyRenal cell carcinomaNHW patientsWhite patientsCell carcinomaMedicare beneficiariesService Medicare Parts ARetrospective cohort studyOverall treatment rateMedicare Part AIO therapyMRCC therapyAnti-cancer agentsCheckpoint inhibitorsCohort studyOlder patientsRandomized trialsSurvival improvementFirst therapyStudy criteriaTreatment receipt
2022
Neurospora crassa is a potential source of anti-cancer agents against breast cancer
Han R, Yang H, Ling C, Lu L. Neurospora crassa is a potential source of anti-cancer agents against breast cancer. Breast Cancer 2022, 29: 1032-1041. PMID: 35881300, DOI: 10.1007/s12282-022-01383-9.Peer-Reviewed Original ResearchConceptsBreast cancerT-47DBreast cancer stem cellsBreast cancer cell linesBreast cancer invasivenessCancer stem cell-related genesStem cell-related genesTumor cell proliferationCancer stem cellsMouse model resultsAnti-tumor agentsCell-related genesAnti-cancer agentsCancer cell linesTumor growthCancer invasivenessCancer stemCell proliferationMCF-10ACell linesCancerInhibition rateStem cellsSpheroid formationCASP3 activityFactors associated with the quality of end-of-life care for patients with metastatic renal cell carcinoma.
Dzimitrowicz H, Wilson L, Jackson B, Spees L, Baggett C, Greiner M, Kaye D, Zhang T, George D, Scales C, Pritchard J, Leapman M, Gross C, Dinan M, Wheeler S. Factors associated with the quality of end-of-life care for patients with metastatic renal cell carcinoma. Journal Of Clinical Oncology 2022, 40: 300-300. DOI: 10.1200/jco.2022.40.6_suppl.300.Peer-Reviewed Original ResearchMetastatic renal cell carcinomaOral anti-cancer agentsRenal cell carcinomaSEER-MedicareDays of lifeSystemic therapyICU admissionCell carcinomaOdds ratioLife careSEER-Medicare cohortSystemic therapy useMultivariable logistic regressionUse of hospiceQuality of endHigh-quality endMRCC diagnosisAnti-cancer agentsMost patientsOlder patientsHospital admissionMedian ageTherapy useImmunotherapy treatmentRetrospective study
2021
Patient- and provider-level predictors of mortality among patients with metastatic renal cell carcinoma receiving oral anticancer agents.
Spees L, Dinan M, Jackson B, Baggett C, Wilson L, Greiner M, Kaye D, Zhang T, George D, Scales C, Pritchard J, Leapman M, Gross C, Wheeler S. Patient- and provider-level predictors of mortality among patients with metastatic renal cell carcinoma receiving oral anticancer agents. Journal Of Clinical Oncology 2021, 39: 116-116. DOI: 10.1200/jco.2020.39.28_suppl.116.Peer-Reviewed Original ResearchMetastatic renal cell carcinomaOral anti-cancer agentsPatients' clinical characteristicsProvider-level factorsCause mortalityRenal cell carcinomaClinical characteristicsHazard ratioMetastatic diagnosisCell carcinomaState cancer registry dataCox proportional hazards modelProvider-level predictorsLower overall survivalOral anticancer agentsCancer registry dataReal-world populationProportional hazards modelSkilled nursing facilitiesProvider Enumeration SystemAnti-cancer agentsIndex dateOverall survivalPatient demographicsBlack patientsPatterns and predictors of oral anticancer agent utilization in diverse metastatic renal cell carcinoma patients.
Wheeler S, Spees L, Jackson B, Baggett C, Wilson L, Greiner M, George D, Scales C, Pritchard J, Dinan M. Patterns and predictors of oral anticancer agent utilization in diverse metastatic renal cell carcinoma patients. Journal Of Clinical Oncology 2021, 39: 279-279. DOI: 10.1200/jco.2021.39.6_suppl.279.Peer-Reviewed Original ResearchMetastatic renal cell carcinoma patientsRenal cell carcinoma patientsCell carcinoma patientsOral anti-cancer agentsCarcinoma patientsRisk ratioPatterns of useRisk differenceGreater comorbidity burdenMetastatic RCC patientsPopulation-based studyPatient-level characteristicsMonths of preAdjusted risk differencePoor quality careComorbidity burdenIndex dateAnti-cancer agentsMetastatic RCCPatient characteristicsContinuous enrollmentRCC patientsTreatment advancesType of insurancePatients
2020
Anti-Cancer Effects of RAW 264.7 Cells on Prostate Cancer PC-3 Cells.
Nam H, Bae J, Kim Y, An H, Kim S, Kim K, Yu S, Park B, Lee S, Ahn S. Anti-Cancer Effects of RAW 264.7 Cells on Prostate Cancer PC-3 Cells. Annals Of Clinical & Laboratory Science 2020, 50: 739-746. PMID: 33334788.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsApoptosisCell CommunicationCell Line, TumorCell MovementCoculture TechniquesCulture Media, ConditionedEpithelial-Mesenchymal TransitionHumansImmunotherapy, AdoptiveLipopolysaccharidesMacrophagesMaleMiceNeoplasm InvasivenessPC-3 CellsProstatic NeoplasmsRAW 264.7 CellsTumor MicroenvironmentConceptsPC-3 cellsAnti-cancer effectsProstate cancer PC-3 cellsCancer PC-3 cellsRAW 264.7 cellsTumor cellsHuman prostate cancer PC-3 cellsEMT-specific markersHigher anti-cancer effectEnzyme-linked immunosorbent assayQuantitative polymerase chain reactionAnti-cancer agentsPolymerase chain reactionImmune cellsInhibitor of metastasisTumor parametersTherapeutic targetingTGF-β2Snail-1Mesenchymal transitionTumor microenvironmentMigration markersWestern blotImmunosorbent assayAngiogenic ability
2019
Unlocking PARP inhibitor efficacy for HRD-negative cancers using the alphalex tumor targeting platform inhibitor efficacy for HRD-negative cancers using the alphalex tumor targeting platform.
Bindra R, Sundaram R, Aiello R, Marshall D, Bourassa P, Csengery J, Zhang Q, Robinson B, lopresti-Morrow L, Bechtold J, Tylaska L, Paradis T, Paralkar V, Hellsund P, Glazer P. Unlocking PARP inhibitor efficacy for HRD-negative cancers using the alphalex tumor targeting platform inhibitor efficacy for HRD-negative cancers using the alphalex tumor targeting platform. Journal Of Clinical Oncology 2019, 37: e14664-e14664. DOI: 10.1200/jco.2019.37.15_suppl.e14664.Peer-Reviewed Original ResearchHomologous recombination deficiencyHRD statusAnti-cancer agentsClinical trialsSignificant bone marrow toxicityTumor cellsInhibitor efficacyPhase I clinical trialIND-enabling studiesDose-limiting toxicityBone marrow toxicitySignificant tumor cell killingSmall molecule anti-cancer agentNormal tissue toxicityTumor cell killingTumor-targeting approachesPARP inhibitor efficacyRelevant chemotherapyVivo tumor modelsMarrow toxicityBRCA1/2 mutationsComplete sparingBone marrowSolid tumorsChemotherapyIncidence of Capillary Leak Syndrome as an Adverse Effect of Drugs in Cancer Patients: A Systematic Review and Meta-Analysis
Jeong G, Lee K, Lee I, Oh J, Kim D, Shin J, Kronbichler A, Eisenhut M, van der Vliet H, Abdel-Rahman O, Stubbs B, Solmi M, Veronese N, Dragioti E, Koyanagi A, Radua J, Shin J. Incidence of Capillary Leak Syndrome as an Adverse Effect of Drugs in Cancer Patients: A Systematic Review and Meta-Analysis. Journal Of Clinical Medicine 2019, 8: 143. PMID: 30691103, PMCID: PMC6406478, DOI: 10.3390/jcm8020143.Peer-Reviewed Original ResearchIncidence of capillary leak syndromeCapillary leak syndromeBone marrow transplantationInterleukin-2Meta-analysisEffects of anti-cancer agentsAnti-cluster of differentiationBetween-study heterogeneityAdverse effectsAdverse effects of drugsType of cancerEffects of drugsAnti-cancer agentsAnti-cancer drugsCausative drugsMarrow transplantationPooled incidenceVascular leakageAnti-CDCancer patientsClinical trialsRare diseaseSystematic reviewAnti-clusterCancer treatment
2018
Systemic Capillary Leak Syndrome (Clarkson Syndrome) in Cancer Patients: A Systematic Review
Shin J, Lee K, Lee I, Oh J, Kim D, Shin J, Eo T, Kronbichler A, Eisenhut M, van der Vliet H. Systemic Capillary Leak Syndrome (Clarkson Syndrome) in Cancer Patients: A Systematic Review. Journal Of Clinical Medicine 2018, 7: 418. PMID: 30404164, PMCID: PMC6262589, DOI: 10.3390/jcm7110418.Peer-Reviewed Original ResearchSystemic capillary leak syndromeGranulocyte-colony stimulating factorCapillary leak syndromeBone marrow transplantationCancer patientsAnti-cancer agentsIntravenous immunoglobulinMortality rate of patientsNon-Hodgkin's lymphomaTreated with steroidsInterleukin (IL)-2Rate of patientsEffective therapeutic strategyMarrow transplantationAssociated with cancerHematologic malignanciesMultiple myelomaPleural effusionCapillary hyperpermeabilityTreatment modalitiesB2 agonistsAdverse eventsClarkson syndromeFollow-upCommon symptomsSalinomycin ameliorates oxidative hepatic damage through AMP-activated protein kinase, facilitating autophagy
Kim K, Lee S, Baek S, Lee E, Jang E, Lee J, Ahn S, Chang J, Oh T, Kim S, Ma J, Kim S, Park K, Kim Y. Salinomycin ameliorates oxidative hepatic damage through AMP-activated protein kinase, facilitating autophagy. Toxicology And Applied Pharmacology 2018, 360: 141-149. PMID: 30290169, DOI: 10.1016/j.taap.2018.10.002.Peer-Reviewed Original ResearchConceptsImportance of AMPKMitochondrial dysfunctionAcidic vesicle organellesOxidative stressProtein kinase activationReactive oxygen species productionProtein kinaseAMPK inhibitionKinase activationSevere oxidative stressOxygen species productionLiver injuryMolecular mechanismsIron-induced apoptosisHepatic protectantStreptomyces albusHuman diseasesAMPKCellular mechanismsLC3-IISalinomycin's effectsArachidonic acidMitochondrial impairmentROS productionAnti-cancer agents
2017
A cell-penetrating antibody inhibits human RAD51 via direct binding
Turchick A, Hegan DC, Jensen RB, Glazer PM. A cell-penetrating antibody inhibits human RAD51 via direct binding. Nucleic Acids Research 2017, 45: 11782-11799. PMID: 29036688, PMCID: PMC5714174, DOI: 10.1093/nar/gkx871.Peer-Reviewed Original ResearchConceptsHomology-directed repairMolecular basisDirect bindingSynthetic lethal killingPre-clinical developmentBRCA2-deficient cancer cellsCell-penetrating antibodiesAnti-cancer agentsLupus autoantibodiesHuman Rad51DNA repairDNA bindingRAD51N-terminusCancer cellsSilico molecular modelingFunction mutationsCancer therapySpecific inhibitorDNANovel inhibitorsAttractive targetComplementarity-determining regionsMolecular modelingCell penetrationUnderstanding the Effectiveness of Natural Compound Mixtures in Cancer through Their Molecular Mode of Action
Aung TN, Qu Z, Kortschak RD, Adelson DL. Understanding the Effectiveness of Natural Compound Mixtures in Cancer through Their Molecular Mode of Action. International Journal Of Molecular Sciences 2017, 18: 656. PMID: 28304343, PMCID: PMC5372668, DOI: 10.3390/ijms18030656.Peer-Reviewed Original ResearchConceptsAnti-cancer agentsNatural compound mixturesTherapeutic benefitCancer progressionCancer cellsSynergistic therapeutic benefitsPotential molecular targetsPositive therapeutic benefitsAberrant apoptotic pathwaysClinical efficacyTreatment of cancerAdverse reactionsCancer managementMerit further investigationMultiple specific targetsDrug resistanceCancerGenetic abnormalitiesEffective dosageLimited evidenceMolecular targetsScientific evidenceApoptotic mechanismsFurther investigationProgression
2015
Metabolic disposition of the anti-cancer agent [14C]laromustine in male rats
Nassar AF, Wisnewski A, King I. Metabolic disposition of the anti-cancer agent [14C]laromustine in male rats. Xenobiotica 2015, 45: 711-721. PMID: 25798740, PMCID: PMC4681490, DOI: 10.3109/00498254.2015.1016475.Peer-Reviewed Original ResearchConceptsQuantitative whole-body autoradiographyBolus doseDrug-derived radioactivityPeak plasma concentrationWhole-body autoradiographyGroup 1 animalsUrinary bladder contentsLong-Evans ratsExcretion of drugsSmall intestine contentsRecovery of radioactivityNovel sulfonylhydrazineAnti-cancer agentsSpinal cordMale ratsPlasma concentrationsIntravenous administrationRenal cortexBladder contentsTotal bodyMetabolic dispositionOrgan exposureSmall intestineRatsMedical guidelines
2013
TBCRC 018: Phase II study of iniparib plus chemotherapy to treat triple-negative breast cancer (TNBC) central nervous system (CNS) metastases (mets).
Anders C, Deal A, Abramson V, Liu M, Storniolo A, Carpenter J, Puhalla S, Nanda R, Melhem-Bertrandt A, Lin N, Marcom P, Van Poznak C, Stearns V, Melisko M, Smith J, Karginova O, Winer E, Perou C, Wolff A, Carey L. TBCRC 018: Phase II study of iniparib plus chemotherapy to treat triple-negative breast cancer (TNBC) central nervous system (CNS) metastases (mets). Journal Of Clinical Oncology 2013, 31: 515-515. DOI: 10.1200/jco.2013.31.15_suppl.515.Peer-Reviewed Original ResearchQuality of lifeBlood-brain barrierResponse rateCommon grade 3/4 adverse eventsCentral nervous system metastasesGrade 3/4 adverse eventsClinical benefit rateNervous system metastasesPhase II studyTumor response rateKaplan-Meier methodWhole brain RTHalf of womenBetter response rateSmall molecule anti-cancer agentTopoisomerase I inhibitorAdvanced TNBCCorrelative endpointsEligible ptsGermline BRCA1/2Measurable lesionsMedian TTPRadiation-naïveAnti-cancer agentsPrimary endpoint
2011
OT3-01-03: Pre-Surgical Evaluation of the AKT Inhibitor MK-2206 in Patients with Operable Invasive Breast Cancer: New York Cancer Consortium Trial P8740.
Kalinsky K, Sparano J, Kim M, Crew K, Maurer M, Taback B, Feldman S, Hibshoosh H, Wiechmann L, Adelson K, Hershman D. OT3-01-03: Pre-Surgical Evaluation of the AKT Inhibitor MK-2206 in Patients with Operable Invasive Breast Cancer: New York Cancer Consortium Trial P8740. Cancer Research 2011, 71: ot3-01-03-ot3-01-03. DOI: 10.1158/0008-5472.sabcs11-ot3-01-03.Peer-Reviewed Original ResearchPre-surgical studyInvasive breast cancerBreast cancerPI3K/AktWeekly MKPost-treatment tissue samplesOperable invasive breast cancerPeripheral blood mononuclear cellsEarly phase clinical studiesDownstream PI3K/Akt pathwayClinical stage IClinical trial programBlood mononuclear cellsMain eligibility criteriaPre-surgical evaluationEarly clinical testingPI3K/Akt pathwayEffects of MKAKT inhibitor MKPost-treatment samplesAnti-cancer propertiesParaffin-embedded tissuesAccrue patientsAnti-cancer agentsNeoadjuvant chemotherapy
2009
Targeting the DNA damage response for cancer therapy
Powell SN, Bindra RS. Targeting the DNA damage response for cancer therapy. DNA Repair 2009, 8: 1153-1165. PMID: 19501553, DOI: 10.1016/j.dnarep.2009.04.011.Peer-Reviewed Original ResearchConceptsDNA damage responseCell cycle checkpointsDouble-strand breaksGenome integrityGenomic integrityHistone modificationsDamage responseCycle checkpointsDNA repairKey proteinsDNA damageAnti-cancer agentsHuman tumorsNew anti-cancer agentsPathwayCancer therapyTumor cellsCheckpointProteinTherapeutic interventionsRepairIntegrityDefectsCellsAppropriate responseAn ATP-competitive Mammalian Target of Rapamycin Inhibitor Reveals Rapamycin-resistant Functions of mTORC1*
Thoreen CC, Kang SA, Chang JW, Liu Q, Zhang J, Gao Y, Reichling LJ, Sim T, Sabatini DM, Gray NS. An ATP-competitive Mammalian Target of Rapamycin Inhibitor Reveals Rapamycin-resistant Functions of mTORC1*. Journal Of Biological Chemistry 2009, 284: 8023-8032. PMID: 19150980, PMCID: PMC2658096, DOI: 10.1074/jbc.m900301200.Peer-Reviewed Original ResearchMeSH KeywordsAdaptor Proteins, Signal TransducingAdenosine TriphosphateAnimalsAntibiotics, AntineoplasticAutophagyCarrier ProteinsCell Cycle ProteinsCell ProliferationCell SurvivalCells, CulturedDrug Resistance, NeoplasmEukaryotic Initiation FactorsImmunosuppressive AgentsMechanistic Target of Rapamycin Complex 1MiceMice, KnockoutMultienzyme ComplexesMultiprotein ComplexesPhosphoproteinsPhosphorylationPhosphotransferases (Alcohol Group Acceptor)Protein BiosynthesisProteinsRNA CapsSirolimusTOR Serine-Threonine KinasesTranscription FactorsConceptsRapamycin-resistant phosphorylationATP-competitive mammalian targetMammalian targetATP-competitive mTOR inhibitorsCell growthCap-dependent translationImpairs cell growthSuppression of autophagyDistinct complexesRapamycin kinaseCatalytic subunitKinase activityMTORC1 inhibitorMTORC2 inhibitionRapamycinAnti-cancer agentsDirect inhibitorMTOR inhibitorsInhibitorsProliferationMTORC2Torin1KinaseComplexesPhosphorylation
1999
Cellular pharmacology of polynuclear platinum anti-cancer agents
Roberts J, Peroutka J, Farrell N. Cellular pharmacology of polynuclear platinum anti-cancer agents. Journal Of Inorganic Biochemistry 1999, 77: 51-57. PMID: 10626354, DOI: 10.1016/s0162-0134(99)00147-6.Peer-Reviewed Original ResearchConceptsCisplatin-resistant cell linesCell linesCross-linking adductsWild-type cell linesDNA repair mechanismsL1210 murine leukemia cell lineCellular pharmacologyType cell linesGenomic accessMurine leukemia cell lineWild typeCytotoxic effectsLeukemia cell linesRepair mechanismsDNA interstrandAnti-cancer agentsDiminished accumulationDinuclear platinum complexesTrinuclear platinum complexBBR3464Enhanced activityPotential anticancer agentsPotent cytotoxic agentComplexesVivo activity
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