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Cancers 2014, 6(2), 771-795; doi:10.3390/cancers6020771

BRCA1 and Oxidative Stress

Received: 19 December 2013 / Revised: 20 March 2014 / Accepted: 24 March 2014 / Published: 3 April 2014
(This article belongs to the Special Issue Role of Oxidatively-Induced DNA Damage in Carcinogenesis)
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The breast cancer susceptibility gene 1 (BRCA1) has been well established as a tumor suppressor and functions primarily by maintaining genome integrity. Genome stability is compromised when cells are exposed to oxidative stress. Increasing evidence suggests that BRCA1 regulates oxidative stress and this may be another mechanism in preventing carcinogenesis in normal cells. Oxidative stress caused by reactive oxygen species (ROS) is implicated in carcinogenesis and is used strategically to treat human cancer. Thus, it is essential to understand the function of BRCA1 in oxidative stress regulation. In this review, we briefly summarize BRCA1’s many binding partners and mechanisms, and discuss data supporting the function of BRCA1 in oxidative stress regulation. Finally, we consider its significance in prevention and/or treatment of BRCA1-related cancers.
Keywords: BRCA; oxidative stress; reactive oxygen species (ROS); carcinogenesis; detoxification BRCA; oxidative stress; reactive oxygen species (ROS); carcinogenesis; detoxification
This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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Yi, Y.W.; Kang, H.J.; Bae, I. BRCA1 and Oxidative Stress. Cancers 2014, 6, 771-795.

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