Double Strand Break

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There are an estimated 1.6 million new cancer cases anticipated in the United States in 2014, with breast cancer in women accounting for approximately 232,000 of those cases (5). More than half a million people in the United States alone will die this year from cancer (6). To date there are more than 100 known cancers from most every tissue in the body. The development of cancer within the body stems from a cellular malfunction that leads to disruption of cell cycle control. This lack of control may originate from an alteration of mitosis leading to rapid cell division or from prevention of senescence or apoptosis. Regardless of the final fate, the initial perturbation is introduced at the molecular level through genetic alterations. …show more content…
In this case, the process of homologous recombination is necessary to utilize the other gene copy as a template to fill the gap created by the break. There are a significant number of proteins utilized in the repair of a double stranded break as illustrated in Figure 1 (1). This pathway is ultimately regulated by Ataxia telangiectasia mutated (ATM) a serine/threonine protein kinase. Following the identification of a DNA double strand break, ATM is recruited and activated to begin phosphorylation of a number of other proteins involved in damage repair. The effects on cell cycle regulation as a result of the inability to repair DNA double stranded breaks have been shown to be involved in cancers such as breast cancer. The genes breast cancer 1, early onset (BRCA1) and breast cancer 2, early onset (BRCA2) are known to be part of the cell cycle check point regulation in response to DNA double strand breaks.

The BRCA1 and BRCA2 genes encode for the BRCA1 and BRCA2 tumor suppressor proteins, respectively. These proteins play roles cell cycle control and DNA double strand repair through the completion of homologous recombination. As illustrated in Figure 2, BRCA1 and BRCA2 proteins are expressed from the G1 through M phases of the cell cycle. The levels of protein are gradually increased to allow for proper regulation of DNA breaks and other cell cycle checkpoints. With improper interactions …show more content…
In the case of a trauma resulting in a DNA double strand break, ATM phosphorylates ataxia telangiectasia and Rad3-related protein (ATR). ATR is a serine/threonine protein kinase that phosphorylates the hydroxyl group on serines and threonines and in the case of double strand breaks, is responsible for phosphorylation of BRCA1. The phosphorylated BRCA1 is then responsible for recruiting a variety of other tumor suppressor proteins to the site of the double stranded break. BRCA1 will bind to the DNA holding the other proteins in place to repair the break. This action also causes a cascading effect that allows for cell cycle check point regulation to prevent the cell from progressing through the cycle until the DNA is
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