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
2007
Role of telomeres and telomerase in genomic instability, senescence and cancer
Deng Y, Chang S. Role of telomeres and telomerase in genomic instability, senescence and cancer. Laboratory Investigation 2007, 87: 1071-1076. PMID: 17767195, DOI: 10.1038/labinvest.3700673.Peer-Reviewed Original ResearchConceptsHuman cancersAnti-telomerase therapyAttractive therapeutic targetClinical trialsTherapeutic targetDNA damage responseRole of telomeresAbsence of p53Progressive lossHuman carcinomasSuppress tumorigenesisCancerLinear chromosomesCellular senescenceDamage responseTelomeric repeatsDysfunctional telomeresGenomic instabilityTelomeric structureChromosomal instabilityTelomeresP53TelomeraseImportant mechanismFunction results