2008
Evidence that senescent human prostate epithelial cells enhance tumorigenicity: Cell fusion as a potential mechanism and inhibition by p16INK4a and hTERT
Bhatia B, Multani AS, Patrawala L, Chen X, Calhoun‐Davis T, Zhou J, Schroeder L, Schneider‐Broussard R, Shen J, Pathak S, Chang S, Tang DG. Evidence that senescent human prostate epithelial cells enhance tumorigenicity: Cell fusion as a potential mechanism and inhibition by p16INK4a and hTERT. International Journal Of Cancer 2008, 122: 1483-1495. PMID: 18059027, DOI: 10.1002/ijc.23222.Peer-Reviewed Original ResearchConceptsHuman prostate epithelial cellsNHP cellsProstate epithelial cellsCell fusionVivo tumorigenicityTumor cellsTumor developmentNormal human prostate epithelial cellsEpithelial cellsAR mRNA expressionCell-cell fusionProstate cancer cell linesPotential mechanismsGene expression analysisP16INK4a protein expressionModel cell systemGenomic stabilityLNCaP prostate cancerCancer cell linesExogenous p16Expression analysisProstate cancerSenescent fibroblastsProgenitor markersProstate tumorigenesis
2000
Telomere dysfunction promotes non-reciprocal translocations and epithelial cancers in mice
Artandi S, Chang S, Lee S, Alson S, Gottlieb G, Chin L, DePinho R. Telomere dysfunction promotes non-reciprocal translocations and epithelial cancers in mice. Nature 2000, 406: 641-645. PMID: 10949306, DOI: 10.1038/35020592.Peer-Reviewed Original ResearchConceptsEpithelial cancersSoft tissue sarcomasTelomere lengthP53 mutant miceTumor suppressor gene mutationsSuppressor gene mutationsNon-reciprocal translocationsTissue sarcomasTelomere dysfunctionAged humansMutant miceCytogenetic featuresCancerMiceHuman carcinomasGene mutationsEpithelial renewalTelomerase expressionCritical reductionCarcinomaDysfunctionHigh rateReverse transcriptaseEukaryotic chromosomesNucleoprotein complexes