Cancer Research Annual Meeting 2010  Protein Translation and Cancer
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[Cancer Research 65, 10635, November 15, 2005]
© 2005 American Association for Cancer Research


Corrections

Apoptosis of Prostate Cancer Cells by CKIs

In the article on apoptosis of prostate cancer cells by CKIs in the September 1, 2005 issue of Cancer Research (1), the heading in panel D of Figure 5 should have read "Roscovitine." The corrected figure appears below.



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Figure 5. Requirement for p53 for efficient apoptosis of CKI-treated prostate cancer cells. A, LNCaP cells received no addition (NA) or 30 µmol/L pifithrin-{alpha} (PTF{alpha}) for 24 hours. Cells subsequently received DMSO (control, C) or 25 µmol/L roscovitine (ROS) for 16 hours. Amounts of p53 and cleaved PARP were determined by Western blotting of cell extracts. B, LNCaP and PC3 cells received the indicated concentrations of roscovitine for 20 hours. Amounts of cytosolic, histone-associated DNA fragments were determined by a cell death detection ELISA. Bars, SD. bgd, background (buffer only). C, LNCaP and PC3 cells received the indicated concentrations of CGP74514A for 20 hours. Amounts of cleaved PARP and XIAP were determined by Western blotting of cell extracts. D, LNCaP and DU145 cells received the indicated concentrations of roscovitine for 20 hours. Amounts of cleaved PARP and XIAP were determined by Western blotting of cell extracts.

 
References

  1. Mohapatra S, Chu B, Zhao X, Pledger WJ. Accumulation of p53 and reductions in XIAP abundance promote the apoptosis of prostate cancer cells. Cancer Res2005;65:7717–23.[Abstract/Free Full Text]




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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