Cancer Research Infection and Cancer: Biology, Therapeutics, and Prevention Translational Medicine Conference in Israel
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Cancer Research Clinical Cancer Research
Cancer Epidemiology Biomarkers & Prevention Molecular Cancer Therapeutics
Molecular Cancer Research Cancer Prevention Research
Cancer Prevention Journals Portal Cancer Reviews Online
Annual Meeting Education Book Meeting Abstracts Online
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by van Vugt, M. A.T.M.
Right arrow Articles by Medema, R. H.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by van Vugt, M. A.T.M.
Right arrow Articles by Medema, R. H.
Related Collections
Right arrow Cellular Pathobiology
Right arrow Cellular Pathobiology: DNA Damage and Stress Responses
[Cancer Research 65, 7037-7040, August 15, 2005]
© 2005 American Association for Cancer Research

Review Articles

Restarting the Cell Cycle When the Checkpoint Comes to a Halt

Marcel A.T.M. van Vugt, Alexandra Bràs and René H. Medema

Department of Medical Oncology, University Medical Center Utrecht, Utrecht, the Netherlands

Requests for reprints: René H. Medema, Laboratory of Experimental Oncology, University Medical Center Utrecht, Stratenum 2.118, Universiteitsweg 100, 3584 CG Utrecht, The Netherlands. Phone: 31-30-2539689; Fax: 31-30-2538479; E-mail: r.h.medema{at}med.uu.nl.

The DNA damage checkpoint coordinates a block in cell proliferation with the DNA repair process that follows when lesions are inflicted on the genome. However, we do not know exactly how cell division can recommence following a DNA damage–induced arrest. Recent work from our lab has identified Polo-like kinase-1 and Cdc25B as two essential components of the machinery that sets the cell division process back in motion when the checkpoint response is abrogated. Here, we discuss these novel insights and discuss their possible implications for the treatment of cancer.




This article has been cited by other articles:


Home page
 Cancer Res.Home page
P. Bansal and J. S. Lazo
Induction of Cdc25B Regulates Cell Cycle Resumption after Genotoxic Stress
Cancer Res., April 1, 2007; 67(7): 3356 - 3363.
[Abstract] [Full Text] [PDF]

Home page
 Molecular Cancer TherapeuticsHome page
M. Gu, R. P. Singh, S. Dhanalakshmi, S. Mohan, and R. Agarwal
Differential effect of silibinin on E2F transcription factors and associated biological events in chronically UVB-exposed skin versus tumors in SKH-1 hairless mice.
Mol. Cancer Ther., August 1, 2006; 5(8): 2121 - 2129.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Cancer Research Clinical Cancer Research
Cancer Epidemiology Biomarkers & Prevention Molecular Cancer Therapeutics
Molecular Cancer Research Cancer Prevention Research
Cancer Prevention Journals Portal Cancer Reviews Online
Annual Meeting Education Book Meeting Abstracts Online
Copyright © 2005 by the American Association for Cancer Research.