國家衛生研究院 NHRI:Item 3990099045/9688
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    Please use this identifier to cite or link to this item: http://ir.nhri.org.tw/handle/3990099045/9688


    Title: Role of mitochondria, ROS, and DNA damage in arsenic induced carcinogenesis
    Authors: Lee, CH;Yu, HS
    Contributors: National Institute of Environmental Health Sciences
    Abstract: The International Agency for Research on Cancer (IARC) declared arsenic a class I carcinogen. Arsenic exposure induces several forms of human cancers, including cancers of skin, lung, liver, and urinary bladder. The majority of the arsenic-induced cancers occur in skin. Among these, the most common is Bowen's disease, characterized by epidermal hyperplasia, full layer epidermal dysplasia, leading to intraepidermal carcinoma as well as apoptosis, and moderate dermal infiltrates, which require the participation of mitochondria. The exact mechanism underlying arsenic induced carcinogenesis remains unclear, although increased reactive oxidative stresses, leading to chromosome abnormalities and uncontrolled growth, and aberrant immune regulations might be involved. Here, we highlight how increased mitochondrial biogenesis and oxidative stress lead to mitochondrial DNA damage and mutation in arsenic induced cancers. We also provide therapeutic rationale for targeting mitochondria in the treatment of arsenic induced cancers.
    Date: 2016-06
    Relation: Frontiers in Bioscience. 2016 Jun;8(2):312-320.
    Link to: http://dx.doi.org/10.2741/465
    Cited Times(Scopus): https://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=85016161591
    Appears in Collections:[Hsin-Su Yu] Periodical Articles

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