2010
Defending the end zone: Studying the players involved in protecting chromosome ends
Chan SS, Chang S. Defending the end zone: Studying the players involved in protecting chromosome ends. FEBS Letters 2010, 584: 3773-3778. PMID: 20579983, PMCID: PMC3657741, DOI: 10.1016/j.febslet.2010.06.016.Peer-Reviewed Original Research
2004
Tumor-Specific Low Molecular Weight Forms of Cyclin E Induce Genomic Instability and Resistance to p21, p27, and Antiestrogens in Breast Cancer
Akli S, Zheng PJ, Multani AS, Wingate HF, Pathak S, Zhang N, Tucker SL, Chang S, Keyomarsi K. Tumor-Specific Low Molecular Weight Forms of Cyclin E Induce Genomic Instability and Resistance to p21, p27, and Antiestrogens in Breast Cancer. Cancer Research 2004, 64: 3198-3208. PMID: 15126360, DOI: 10.1158/0008-5472.can-03-3672.Peer-Reviewed Original ResearchMeSH KeywordsAdultAgedAged, 80 and overAnimalsBreast NeoplasmsCDC2-CDC28 KinasesCell Cycle ProteinsCell DivisionCell Line, TumorCyclin ECyclin-Dependent Kinase 2Cyclin-Dependent Kinase Inhibitor p21Cyclin-Dependent Kinase Inhibitor p27CyclinsEstradiolEstrogen Receptor ModulatorsFemaleFulvestrantG1 PhaseGenomic InstabilityHumansMiddle AgedMolecular WeightPolyploidyProtein IsoformsTransfectionTumor Suppressor ProteinsConceptsBreast cancer patientsPoor outcomeCancer patientsBreast cancerCyclin ELMW formsPoor clinical outcomeEffects of antiestrogensPotential therapeutic targetLow molecular weight isoformsCyclin-dependent kinase inhibitor p21Clinical outcomesAggressive diseaseSurrogate markerDisease progressionPathobiological mechanismsTherapeutic targetMolecular weight isoformsPatientsTumor cellsLMW isoformsTumorsPowerful predictorLow molecular weight formWeight isoformsEndogenous oncogenic K-rasG12D stimulates proliferation and widespread neoplastic and developmental defects
Tuveson D, Shaw A, Willis N, Silver D, Jackson E, Chang S, Mercer K, Grochow R, Hock H, Crowley D, Hingorani S, Zaks T, King C, Jacobetz M, Wang L, Bronson R, Orkin S, DePinho R, Jacks T. Endogenous oncogenic K-rasG12D stimulates proliferation and widespread neoplastic and developmental defects. Cancer Cell 2004, 5: 375-387. PMID: 15093544, DOI: 10.1016/s1535-6108(04)00085-6.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCell CycleCell DivisionCell Transformation, NeoplasticCellular SenescenceCongenital AbnormalitiesCrosses, GeneticCyclin-Dependent Kinase Inhibitor p16Embryo, MammalianFemaleFibroblastsGene Expression Regulation, DevelopmentalGenes, rasIntegrasesMaleMiceMice, Inbred C57BLMice, TransgenicMutationNeoplasmsStem CellsTumor Suppressor Protein p14ARFTumor Suppressor Protein p53Viral ProteinsConceptsCanonical Ras effectorRas effectorsOncogenic RasEmbryonic developmentAbnormal cellular proliferationDevelopmental defectsRas oncogeneGenetic lesionsConditional expressionWidespread expressionK-RasG12DCellular proliferationFurther genetic abnormalitiesEnhanced proliferationOncogeneProliferationExpressionGenetic abnormalitiesEffectorsMutationsAllelesRegulationPathwayFibroblastsFrank malignancy
2002
Telomerase extracurricular activities
Chang S, DePinho R. Telomerase extracurricular activities. Proceedings Of The National Academy Of Sciences Of The United States Of America 2002, 99: 12520-12522. PMID: 12271146, PMCID: PMC130491, DOI: 10.1073/pnas.212514699.Peer-Reviewed Original Research