2015
Monitoring the DNA Damage Response at Dysfunctional Telomeres
Rai R, Chang S. Monitoring the DNA Damage Response at Dysfunctional Telomeres. Methods In Molecular Biology 2015, 1343: 175-180. PMID: 26420717, DOI: 10.1007/978-1-4939-2963-4_14.Peer-Reviewed Original ResearchConceptsDysfunctional telomeresDNA damage sensorDNA damage responseDNA damage fociSitu hybridization approachEukaryotic chromosomesShelterin componentsDNA repeatsGenomic stabilityDDR proteinsDamage responseTelomeric DNADDR pathwaysDamage fociChromosomal endsTelomere dysfunctionDamage sensorTelomeresDNA damageHybridization approachCellular viabilityPathwayProper maintenanceChromosomesRepeats
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
2008
Dual roles of telomere dysfunction in initiation and suppression of tumorigenesis
Cosme-Blanco W, Chang S. Dual roles of telomere dysfunction in initiation and suppression of tumorigenesis. Experimental Cell Research 2008, 314: 1973-1979. PMID: 18448098, PMCID: PMC3690559, DOI: 10.1016/j.yexcr.2008.03.011.Peer-Reviewed Original ResearchConceptsDNA double-strand breaksDysfunctional telomeresGenomic instabilityPotent tumor suppressor mechanismTumorigenic potentialSimple repeat sequencesTumor suppressor mechanismDouble-strand breaksCell tumorigenic potentialSuppression of tumorigenesisCancer cellsChromosomal endsTelomere dysfunctionCellular senescenceRepeat sequencesGenetic changesTelomeresGenetic lesionsP53 pathwayTumor initiationDicentric chromosomesSuppressor mechanismIntact p53 pathwayHuman carcinomasRare cells