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Volume 16, Issue 11, pp. 2543-2551
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History
- Received February 1, 2017
- Revision received May 24, 2017
- Accepted July 27, 2017
- Published first August 11, 2017.
Article Versions
- Previous version (August 11, 2017 - 09:25).
- You are viewing the most recent version of this article.
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©2017 American Association for Cancer Research.
Author Information
- Muthana Al Abo1,
- Hiroyuki Sasanuma2,
- Xiaojun Liu3,
- Vinodh N. Rajapakse1,
- Shar-yin Huang1,
- Evgeny Kiselev1,
- Shunichi Takeda2,
- William Plunkett3, and
- Yves Pommier1,*
- 1Developmental Therapeutics Branch and Laboratory of Molecular Pharmacology, Center for Cancer Research, NCI, NIH, Bethesda, Maryland.
- 2Department of Radiation Genetics, Kyoto University, Graduate School of Medicine, Yoshida Konoe, Sakyo-ku, Kyoto, Japan.
- 3Department of Experimental Therapeutics, University of Texas M.D. Anderson Cancer Center, Houston, Texas.
- ↵*Corresponding Author:
Yves Pommier, National Cancer Institute, Building 37, Room 5068, MD 20892-4255. Phone: 240-760-6142; Fax: 240-541-4475; E-mail: pommier{at}nih.gov
November 2017
Volume 16, Issue 11
Volume 16, Issue 11
TDP1 is Critical for the Repair of DNA Breaks Induced by Sapacitabine, a Nucleoside also Targeting ATM- and BRCA-Deficient Tumors
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