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논문 기본 정보

자료유형
학술저널
저자정보
Bai, Jing (Department of Radiotherapy, Bao Tou Tumor Hospital) Guo, Xiao-Guang (Department of Head and Neck Surgical Oncology, Bao Tou Tumor Hospital) Bai, Xiao-Ping (Department of Radiotherapy, Bao Tou Tumor Hospital)
저널정보
아시아태평양암예방학회 Asian Pacific journal of cancer prevention : APJCP Asian Pacific journal of cancer prevention : APJCP 제13권 제10호
발행연도
2012.1
수록면
4,879 - 4,881 (3page)

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Epidermal growth factor receptor (EGFR) overexpression is associated with resistance to chemotherapy and radiotherapy. The EGFR modulates DNA repair after radiation-induced damage through an association with the catalytic subunit of DNA protein kinase. DNA double-strand breaks (DSBs) are the most lethal type of DNA damage induced by ionizing radiation, and non-homologous end joining is the predominant pathway for repair of radiation-induced DSBs. Some cell signaling pathways that respond to normal growth factors are abnormally activated in human cancer. These pathways also invoke the cell survival mechanisms that lead to resistance to radiation. The molecular connection between the EGFR and its control over DNA repair capacity appears to be mediated by one or more signaling pathways downstream of this receptor. The purpose of this mini-review was not only to highlight the relation of the EGFR signal as a regulatory mechanism to DNA repair and radiation resistance, but also to provide clues to improving existing radiation resistance through novel therapies based on the above-mentioned mechanism.

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