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. Author manuscript; available in PMC: 2014 Nov 27.
Published in final edited form as: Oncogene. 2014 Jan 13;33(48):5483–5490. doi: 10.1038/onc.2013.554

Figure 2.

Figure 2

Inactivation of p38 signaling and aberrant regulation of PERK foster early breast cancer progression. In the tumorigenic setting, migratory and less differentiated cells abrogate p38 signaling and co-opt PERK signaling to maximize survival capacity via continuous autophagy induction and an antioxidant response. As a result, transformed cells are simultaneously refractory to apoptosis and more tolerant to oxidative stress in scenarios where adhesion signaling is lacking. Together, this deregulated stress response may give rise to the lumen-filled structures seen in DCIS and could explain how cancer stem cells (CSCs) are selected and expanded.