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The Center for Law, Brain & Behavior puts the most accurate and actionable neuroscience in the hands of judges, lawyers, policymakers and journalists—people who shape the standards and practices of our legal system and affect its impact on people’s lives. We work to make the legal system more effective and more just for all those affected by the law.

Mammary Stem Cells and Tumor-Initiating Cells Are More Resistant to Apoptosis and Exhibit Increased DNA Repair Activity in Response to DNA Damage

By Chi-Hsuan Chang, Mei Zhang, Kimal Rajapakshe, Cristian Coarfa, Dean Edwards, Shixia Huang, and Jeffrey M. Rosen | Stem Cell Reports | August 20, 2015

Summary:

Adult stem cells and tumor-initiating cells (TICs) often employ different mechanisms of DNA damage response (DDR) as compared to other tissue cell types. However, little is known about how mammary stem cells (MaSCs) and mammary TICs respond to DNA damage. Using the mouse mammary gland and syngeneic p53-null tumors as models, we investigated the molecular and physiological consequences of DNA damage in wild-type MaSCs, p53-null MaSCs, and p53-null TICs. We showed that wild-type MaSCs and basal cells are more resistant to apoptosis and exhibit increased non-homologous end joining (NHEJ) activity. Loss of p53 in mammary epithelium affected both cell-cycle regulation and DNA repair efficiency. In p53-null tumors, we showed that TICs are more resistant to ionizing radiation (IR) due to decreased apoptosis, elevated NHEJ activity, and more-rapid DNA repair. These results have important implications for understanding DDR mechanisms involved in both tumorigenesis and therapy resistance.

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