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BioMed Research International - Volume20142014, Article ID153867, 18 pages -

Review Article

Department of Pathology, Kaohsiung Municipal Ta-Tung Hospital, Kaohsiung City 801, Taiwan

Department of Pathology, Faculty of Medicine, College of Medicine, Kaohsiung Medical University, Kaohsiung City 807, Taiwan

Department of Medical Laboratory Sciences and Biotechnology, Fooyin University, Kaohsiung City 831, Taiwan

Cancer Center and Division of General & Gastroenterological Surgery, Department of Surgery, Kaohsiung Medical University Hospital, Kaohsiung City, Taiwan

Department of Pathology, Kaohsiung Armed Forces General Hospital, Kaohsiung City 802, Taiwan

Department of Biological Sciences, National Sun Yat-sen University, Kaohsiung City 804, Taiwan

Department of Surgery, Faculty of Medicine, College of Medicine, Kaohsiung Medical University, Kaohsiung City 807, Taiwan

Division of Hepato-Pancreatico-Biliary Surgery, Kaohsiung Medical University Hospital, Kaohsiung City 807, Taiwan

Received 8 November 2013; Revised 23 January 2014; Accepted 25 March 2014; Published 28 April 2014

Academic Editor: Wei MikeLiu

Copyright 2014 Sheau-Fang Yang et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Hepatocellular carcinoma HCC has been known as one of the most lethal human malignancies, due to the difficulty of early detection, chemoresistance, and radioresistance, and is characterized by active angiogenesis and metastasis, which account for rapid recurrence and poor survival. Its development has been closely associated with multiple risk factors, including hepatitis B and C virus infection, alcohol consumption, obesity, and diet contamination. Genetic alterations and genomic instability, probably resulted from unrepaired DNA lesions, are increasingly recognized as a common feature of human HCC. Dysregulation of DNA damage repair and signaling to cell cycle checkpoints, known as the DNA damage response DDR, is associated with a predisposition to cancer and affects responses to DNA-damaging anticancer therapy. It has been demonstrated that various HCC-associated risk factors are able to promote DNA damages, formation of DNA adducts, and chromosomal aberrations. Hence, alterations in the DDR pathways may accumulate these lesions to trigger hepatocarcinogenesis and also to facilitate advanced HCC progression. This review collects some of the most known information about the link between HCC-associated risk factors and DDR pathways in HCC. Hopefully, the review will remind the researchers and clinicians of further characterizing and validating the roles of these DDR pathways in HCC.

Autor: Sheau-Fang Yang,Chien-Wei Chang,Ren-Jie Wei,Yow-Ling Shiue,Shen-Nien Wang,and Yao-Tsung Yeh



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