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
1996
Establishment of an in vitro cell model system to study human prostate carcinogenesis.
Ozen M, Multani A, Chang S, Voneschenbach A, Chung L, Pathak S. Establishment of an in vitro cell model system to study human prostate carcinogenesis. International Journal Of Oncology 1996, 8: 883-8. PMID: 21544441, DOI: 10.3892/ijo.8.5.883.Peer-Reviewed Original ResearchChromosome 5Tumor suppressorPassage cellsMolecular cytogenetic methodsHuman prostate carcinogenesisCell strainsLate passagesCell linesCell model systemNear-diploid cellsLate passage cellsSame chromosomeProstate carcinogenesisCertain genesEarly passage cellsHigh passage cellsQ armProstate cancer cell linesMetastatic phenotypeChromosome constitutionNormal copyCancer cell linesCytogenetic methodsLong armGenetic alterations