期刊
SEMINARS IN RADIATION ONCOLOGY
卷 23, 期 4, 页码 252-261出版社
W B SAUNDERS CO-ELSEVIER INC
DOI: 10.1016/j.semradonc.2013.05.006
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资金
- Ontario Ministry of Health and Long Term Care (OMOHLTC)
- Terry Fox Foundation/Research Institute [PPG09-020005]
- Ontario Institute for Cancer Research
- Government of Ontario
- Canadian Institute for Health Research (CIHR) [201592]
- EU (METOXIA project) [222741]
- Dutch Science Foundation [NWO VENI 916.56.015]
- Dutch Cancer Society [KWF UM-2008-4068]
- Princess Margaret Hospital Foundation
Tumor hypoxia (low oxygenation) causes treatment resistance and poor patient outcome. A substantial fraction of tumor cells experience cycling hypoxia, characterized by transient episodes of hypoxia and reoxygenation. These cells are under a unique burden of stress, mediated by excessive production of reactive oxygen species (ROS). Cellular components damaged by ROS can be cleared by autophagy, rendering cycling hypoxic tumor cells particularly vulnerable to inhibition of autophagy and its upstream regulatory pathways. Activation of the PERK-mediated signaling arm of the unfolded protein response during hypoxia plays a critical role in the defense against ROS, both by stimulating glutathione synthesis pathways and through promoting autophagy. Semin Radiat Oncol 23:252-261 (C) 2013 Published by Elsevier Inc.
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