Our current studies suggest mitochondrial dysfunction causes oxygen-associated genomic DNA damage. Because oxygen serves as an essential factor for oxidative stress, a cause of genomic instability, we have been examining the effect of modulating ambient oxygen on de novo tumorigenesis in different cancer models. As oxidative stress is also involved in inflammation, we have been examining its effect on atherosclerosis. The goal of these lines of investigation is to provide basic experimental evidence for the importance of ambient oxygen on disease pathogenesis and to obtain insights useful for developing new preventive strategies against the two major causes of human diseases.

Project Start
Project End
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Budget End
Support Year
1
Fiscal Year
2010
Total Cost
$489,440
Indirect Cost
Name
National Heart, Lung, and Blood Institute
Department
Type
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Chen, Jichun; Kang, Ju-Gyeong; Keyvanfar, Keyvan et al. (2016) Long-term adaptation to hypoxia preserves hematopoietic stem cell function. Exp Hematol :
Park, Ji-Hoon; Zhuang, Jie; Li, Jie et al. (2016) p53 as guardian of the mitochondrial genome. FEBS Lett 590:924-34
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Lago, Cory U; Sung, Ho Joong; Ma, Wenzhe et al. (2011) p53, aerobic metabolism, and cancer. Antioxid Redox Signal 15:1739-48
Sung, Ho Joong; Ma, Wenzhe; Starost, Matthew F et al. (2011) Ambient oxygen promotes tumorigenesis. PLoS One 6:e19785

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