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Exposure to chlorambucil, fludarabine, and Nutlin\u20103 induced p53 accumulation and variably affected cell cycle progression in SKW6.4 lymphoblastoid cells. In particular, chlorambucil induced cell cycle accumulation at the G2\/M checkpoint; Nutlin\u20103 induced early cell cycle arrest at the G1\/S checkpoint, while fludarabine showed an intermediate behavior. On the other hand, recombinant TRAIL alone did not affect cell cycle progression but induced a rapid increase of apoptosis. Analysis of the gene expression profile of the p53\u2010transcriptional targets showed distinct features between chlorambucil, Nutlin\u20103 and fludarabine, which likely account for their differential effect on cell cycle in SKW6.4 cells. In particular, chlorambucil upregulated the steady\u2010state mRNA expression of SFN\/14\u20103\u20103\u03c3, a gene involved in G2\/M cell cycle arrest. Of note, all agonists upregulated TRAIL\u2010R2 expression in SKW6.4 cells both at the mRNA and protein levels. Consistently, pretreatment with chlorambucil, fludarabine and Nutlin\u20103 enhanced SKW6.4 sensitivity to TRAIL\u2010mediated apoptosis. J. Cell. Biochem. 104: 595\u2013605, 2008. \u00a9 2007 Wiley\u2010Liss, Inc.<\/jats:p>","DOI":"10.1002\/jcb.21649","type":"journal-article","created":{"date-parts":[[2007,12,18]],"date-time":"2007-12-18T18:51:29Z","timestamp":1198003889000},"page":"595-605","source":"Crossref","is-referenced-by-count":6,"title":["Differential effects of chemotherapeutic drugs versus the MDM\u20102 antagonist nutlin\u20103 on cell cycle progression and induction of apoptosis in SKW6.4 lymphoblastoid 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