Editorial
Copyright ©2011 Baishideng Publishing Group Co., Limited. All rights reserved.
World J Clin Oncol. Sep 10, 2011; 2(9): 329-338
Published online Sep 10, 2011. doi: 10.5306/wjco.v2.i9.329
DNA damage and breast cancer
Jennifer D Davis, Shiaw-Yih Lin
Jennifer D Davis, Shiaw-Yih Lin, Department of Systems Biology, Unit 950, The University of Texas MD Anderson Cancer Center, Houston, TX 77030, United States
Author contributions: Davis JD made substantial contribution to the conception, writing and revision of the editorial for important intellectual content; Lin SY provided critical evaluation, writing and revision for important intellectual content; All authors approved the version to be published.
Supported by (in part) Grants from the National Institutes of Health (to Lin SY)
Correspondence to: Shiaw-Yih Lin, Dr, Associate Professor, Department of Systems Biology, Unit 950, The University of Texas MD Anderson Cancer Center, South Campus Research Building II, 7435 Fannin Street, Houston, TX 77054, United States. sylin@mdanderson.org
Telephone: +1-713-5634217 Fax: +1-713-5634235
Received: July 1, 2011
Revised: August 8, 2011
Accepted: August 15, 2011
Published online: September 10, 2011
Abstract

Cancer is intimately related to the accumulation of DNA damage, and repair failures (including mutation prone repair and hyperactive repair systems). This article relates current clinical categories for breast cancer and their common DNA damage repair defects. Information is included on the potential for accumulation of DNA damage in the breast tissue of a woman during her lifetime and the role of DNA damage in breast cancer development. We then cover endogenous and exogenous sources of DNA damage, types of DNA damage repair and basic signal transduction pathways for three gene products involved in the DNA damage response system; namely BRCA1, BRIT1 and PARP-1. These genes are often considered tumor suppressors because of their roles in DNA damage response and some are under clinical investigation as likely sources for effective new drugs to treat breast cancers. Finally we discuss some of the problems of DNA damage repair systems in cancer and the conundrum of hyper-active repair systems which can introduce mutations and confer a survival advantage to certain types of cancer cells.

Keywords: BRCA1; BRIT1; Classification of breast cancer; DNA damage; PARP-1; Triple-negative breast cancer; Tumor-initiating cells