2009
Replicative Senescence as an Intrinsic Tumor-Suppressor Mechanism
Chang S. Replicative Senescence as an Intrinsic Tumor-Suppressor Mechanism. 2009, 201-217. DOI: 10.1007/978-1-4419-1075-2_8.Peer-Reviewed Original ResearchDysfunctional telomeresGenomic instabilityIntrinsic tumor suppressor mechanismsDNA damage response pathwayProtein-DNA complexesDamage response pathwayTumor suppressor mechanismEukaryotic chromosomal endsEnds of chromosomesP53-dependent senescenceAbsence of p53Complex cytogenetic profileTriggers senescenceDDR pathwaysResponse pathwaysChromosomal endsReplicative senescenceTelomere dysfunctionCellular senescenceOnset of cancerTelomeresSenescenceCancer progressionEpithelial tissuesHuman carcinomas
2001
Modeling chromosomal instability and epithelial carcinogenesis in the telomerase-deficient mouse
Chang S, Khoo C, DePinho R. Modeling chromosomal instability and epithelial carcinogenesis in the telomerase-deficient mouse. Seminars In Cancer Biology 2001, 11: 227-238. PMID: 11407947, DOI: 10.1006/scbi.2000.0374.Peer-Reviewed Original ResearchConceptsComplex cytogenetic profileHuman carcinomasChromosomal structural aberrationsTelomerase-deficient miceEukaryotic chromosomesNucleoprotein complexesGenomic instabilitySpecies distinctionP53 mutant miceChromosomal instabilityTumor suppressor gene mutationsShort telomeresSuppressor gene mutationsMutant miceStructural aberrationsEpithelial carcinogenesisGene mutationsCytogenetic profileChromosomesTelomeresMiceMutationsRegulationHumansAneuploidy