2019
Recurrence risk evaluation in T1N1M0/T2N0M0/T3N0M0 gastric cancer with TP53 codon 72 polymorphisms
Ohmori Y, Nomura T, Fukushima N, Takahashi F, Iwaya T, Koeda K, Nishizuka S, Consortium M. Recurrence risk evaluation in T1N1M0/T2N0M0/T3N0M0 gastric cancer with TP53 codon 72 polymorphisms. Journal Of Surgical Oncology 2019, 120: 1154-1161. PMID: 31578743, DOI: 10.1002/jso.25718.Peer-Reviewed Original ResearchMeSH KeywordsAdenocarcinomaAdultAgedAged, 80 and overCodonFemaleFollow-Up StudiesGastrectomyGenetic Predisposition to DiseaseGenotypeHumansIncidenceJapanMaleMiddle AgedNeoplasm Recurrence, LocalNeoplasm StagingPolymorphism, Single NucleotideRisk AssessmentStomach NeoplasmsSurvival RateTumor Suppressor Protein p53ConceptsRelapse-free survivalTP53 codon 72 polymorphismArg/ArgCodon 72 polymorphismGastric cancerOverall survivalHazard ratioHigh-risk patient groupsPostoperative adjuvant chemotherapyRecurrence risk evaluationArg/ProPro/Pro groupAdjuvant chemotherapyT3N0M0 patientsCurative intentStudy cohortPatient groupPro polymorphismEntire observation periodPolymorphism statusPRO groupPatientsArg/CancerPro/
2017
Inhibition of PI3K suppresses propagation of drug-tolerant cancer cell subpopulations enriched by 5-fluorouracil
Ishida K, Ito C, Ohmori Y, Kume K, Sato KA, Koizumi Y, Konta A, Iwaya T, Nukatsuka M, Kobunai T, Takechi T, Nishizuka SS. Inhibition of PI3K suppresses propagation of drug-tolerant cancer cell subpopulations enriched by 5-fluorouracil. Scientific Reports 2017, 7: 2262. PMID: 28536445, PMCID: PMC5442158, DOI: 10.1038/s41598-017-02548-9.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAntimetabolites, AntineoplasticCell Line, TumorCell ProliferationClass I Phosphatidylinositol 3-KinasesCodonDisease Models, AnimalDose-Response Relationship, DrugDrug Resistance, NeoplasmFluorouracilGenetic VariationHeterograftsHumansMiceNeoplasmsPhenotypePhosphatidylinositol 3-KinasesPhosphoinositide-3 Kinase InhibitorsPhosphorylationProteomeProteomicsRibosomal Protein S6 Kinases, 90-kDaSignal TransductionConceptsOrthotopic xenograftsCancer cell subpopulationsCell subpopulationsGastric cancer cell line MKN45Gastric cancer chemotherapyRibosomal S6 kinase phosphorylationPI3K inhibitorsDisease relapseSequential administrationS6 kinase phosphorylationNude miceTumor propagationCancer chemotherapyK inhibitorsXenograftsPI3KChemotherapyRelapseTolerant subpopulationSubpopulationsKinase phosphorylationAdministrationCellsPhosphorylated phosphatidylinositidesMice
2014
A Compensatory Role of NF-κB to p53 in Response to 5-FU–Based Chemotherapy for Gastric Cancer Cell Lines
Endo F, Nishizuka SS, Kume K, Ishida K, Katagiri H, Ishida K, Sato K, Iwaya T, Koeda K, Wakabayashi G. A Compensatory Role of NF-κB to p53 in Response to 5-FU–Based Chemotherapy for Gastric Cancer Cell Lines. PLOS ONE 2014, 9: e90155. PMID: 24587255, PMCID: PMC3937424, DOI: 10.1371/journal.pone.0090155.Peer-Reviewed Original ResearchMeSH KeywordsAntimetabolites, AntineoplasticCell Line, TumorCodonDrug Resistance, NeoplasmFluorouracilGene Expression ProfilingGene Expression Regulation, NeoplasticGene Knockdown TechniquesHumansNF-kappa BProtein BindingProtein TransportStomach NeoplasmsTranscription Factor RelATumor Suppressor Protein p53ConceptsGastric cancer cell linesCancer cell linesNF-κBAdjuvant chemotherapyPrediction markersCell linesNF-κB-dependent mannerGastric cancer patientsKnockdown of RelANF-κB bindingArg homozygosityCurative resectionRelapse rateCancer patientsGastric cancerPrediction biomarkersChemotherapyP65 subunitTP53 knockdownChemotherapeutic efficacyProtein levelsCompensatory roleP53Target protein levelsTreatment