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 (e.g., lymphoma or colon polyp formation) in different cancer models. As oxidative stress is also involved in inflammation, we have been examining its effect on atherosclerosis. The goals of these investigations are 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
Budget Start
Budget End
Support Year
2
Fiscal Year
2011
Total Cost
$488,875
Indirect Cost
Name
National Heart, Lung, and Blood Institute
Department
Type
DUNS #
City
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Zip Code
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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Sung, Ho Joong; Ma, Wenzhe; Starost, Matthew F et al. (2011) Ambient oxygen promotes tumorigenesis. PLoS One 6:e19785

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