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[Cancer Research 57, 1013-1019, March 15, 1997]
© 1997 American Association for Cancer Research
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DNA Rereplication in the Presence of Mitotic Spindle Inhibitors in Human and Mouse Fibroblasts Lacking either p53 or pRb Function1

Aldo Di Leonardo2,3,, Shireen Hussain Khan3, Steven P. Linke, Valentina Greco, Gregorio Seidita4 and Geoffrey M. Wahl

Department of Cell and Developmental Biology "A. Monroy," University of Palermo, viale delle Scienze 90128, Palermo, Italy [A.D.L., V.G., G.S.]; Gene Expression Lab, The Salk Institute, La Jolla California 92037 [S.H.K., S.P.L., G.M.W.]; and Department of Biology, University of California, San Diego, La Jolla, California 92037 [S.H.K., S.P.L.]

Cell cycle checkpoints are biochemical signal transduction pathways that prevent downstream events from being initiated until upstream processes are completed. We analyzed whether the p53 or pRb tumor suppressors are involved in a checkpoint(s) that prevents DNA rereplication in the presence of drugs that interfere with spindle assembly. Normal mouse and human fibroblasts arrested with a 4N DNA content when treated with nocodazole and Colcemid, whereas isogeneic p53-deficient or pRb-deficient derivatives became polyploid. Flow cytometric and cytogenetic analyses demonstrated that the polyploidy resulted from genomewide rereplication without an intervening mitosis. Thus, p53 and pRb help maintain normal cell ploidy by preventing DNA rereplication prior to mitotic division.

1 This work was supported by grants from Associazione Italiana per la Ricerca sul Cancro and the National Cancer Institute.

2 To whom requests for reprints should be addressed.

3 These authors contributed equally to this work.

4 Recipient of a University of Palermo Postdoctoral Fellowship.

Received 11/19/96. Accepted 1/31/97.




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Cancer Epidemiology Biomarkers & Prevention Molecular Cancer Therapeutics
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Cancer Prevention Journals Portal Cancer Reviews Online
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Copyright © 1997 by the American Association for Cancer Research.