2023
Discovery of decreased ferroptosis in male colorectal cancer patients with KRAS mutations
Yan H, Talty R, Jain A, Cai Y, Zheng J, Shen X, Muca E, Paty P, Bosenberg M, Khan S, Johnson C. Discovery of decreased ferroptosis in male colorectal cancer patients with KRAS mutations. Redox Biology 2023, 62: 102699. PMID: 37086630, PMCID: PMC10172914, DOI: 10.1016/j.redox.2023.102699.Peer-Reviewed Original ResearchMeSH KeywordsCell Line, TumorColorectal NeoplasmsFemaleFerroptosisHumansMaleMetabolomicsPrognosisProto-Oncogene Proteins p21(ras)Sex FactorsConceptsKRAS mutant tumorsMale CRC patientsCRC patientsMale patientsKRAS mutationsMutant tumorsOverall survivalMale colorectal cancer patientsKRAS wild-type tumorsAberrant tumor metabolismColorectal cancer patientsCRC patient cohortsColorectal cancer casesFerroptosis-related genesWild-type tumorsNovel potential avenuesNormal colon tissuesPoor OSKRAS statusAdverse outcomesCRC cellsPatient cohortCancer patientsType tumorsCancer casesFerroptosis in colorectal cancer: a future target?
Yan H, Talty R, Aladelokun O, Bosenberg M, Johnson C. Ferroptosis in colorectal cancer: a future target? British Journal Of Cancer 2023, 128: 1439-1451. PMID: 36703079, PMCID: PMC10070248, DOI: 10.1038/s41416-023-02149-6.Peer-Reviewed Original ResearchConceptsColorectal cancerRegulated cell deathCurrent treatment optionsForms of RCDCancer deathTreatment optionsCRC therapyCancer recurrenceTreatment strategiesRadiation therapyOvert toxicityTherapeutic targetDrug resistanceTherapyCancer cellsFerroptosisPotential roleCancerCell deathFuture targetsDeathRecent studiesBiological pathwaysChemotherapySurgery
2011
β-Catenin Signaling Controls Metastasis in Braf-Activated Pten-Deficient Melanomas
Damsky WE, Curley DP, Santhanakrishnan M, Rosenbaum LE, Platt JT, Rothberg BE, Taketo MM, Dankort D, Rimm DL, McMahon M, Bosenberg M. β-Catenin Signaling Controls Metastasis in Braf-Activated Pten-Deficient Melanomas. Cancer Cell 2011, 20: 741-754. PMID: 22172720, PMCID: PMC3241928, DOI: 10.1016/j.ccr.2011.10.030.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAntigens, DifferentiationBenzamidesBeta CateninCell Transformation, NeoplasticColorectal NeoplasmsEnzyme ActivationGene Knockdown TechniquesHumansImatinib MesylateKaplan-Meier EstimateLung NeoplasmsLymphatic MetastasisMelanocytesMelanoma, ExperimentalMiceMice, 129 StrainMice, Inbred C57BLMice, TransgenicPhosphorylationPiperazinesProtein StabilityProto-Oncogene Proteins B-rafProto-Oncogene Proteins c-aktPTEN PhosphohydrolasePyrimidinesSignal TransductionSkin NeoplasmsSplenic NeoplasmsTranscription, GeneticTumor Cells, CulturedConceptsΒ-catenin levelsPI3K/AktLymph nodesMetastatic tumorsFrequent metastasisTumor differentiationMalignant melanomaMAPK/ERKMelanoma metastasesMouse modelControl metastasisHuman melanomaMelanomaMetastasisΒ-catenin stabilizationPTEN lossCentral mediatorMetastasis regulatorsΒ-cateninSpecific changesFunctional implicationsWntLung
2001
Telomere dysfunction and evolution of intestinal carcinoma in mice and humans
Rudolph K, Millard M, Bosenberg M, DePinho R. Telomere dysfunction and evolution of intestinal carcinoma in mice and humans. Nature Genetics 2001, 28: 155-159. PMID: 11381263, DOI: 10.1038/88871.Peer-Reviewed Original ResearchConceptsHuman intestinal neoplasiaProgression of mouseTelomerase activationHuman colorectal carcinogenesisTelomere dysfunctionInitiated lesionsIntestinal carcinomaColorectal carcinogenesisIntestinal neoplasiaHuman colorectalDysfunctionAdvanced stageMalignant transformationTumor progressionChromosomal instabilityColon carcinomaCarcinoma transitionMacroscopic adenomasTransient telomere dysfunctionEarly carcinogenesisCancer initiationHuman cancersTelomerase activityCarcinomaDifferential effects