Skip Navigation

JNCI Journal of the National Cancer Institute 2001 93(21):1652-1655; doi:10.1093/jnci/93.21.1652
© 2001 by Oxford University Press
This Article
Right arrow Full Text Freely available
Right arrow FREE Full Text (PDF) Freely available
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrow Request Permissions
Google Scholar
Right arrow Articles by Marrogi, A. J.
Right arrow Articles by Harris, C. C.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Marrogi, A. J.
Right arrow Articles by Harris, C. C.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Journal of the National Cancer Institute, Vol. 93, No. 21, 1652-1655, November 7, 2001
© 2001 Oxford University Press

BRIEF COMMUNICATION

Oxidative Stress and p53 Mutations in the Carcinogenesis of Iron Overload-Associated Hepatocellular Carcinoma

Aizen J. Marrogi, Mohammed A. Khan, Hilda E. van Gijssel, Judith A. Welsh, Haress Rahim, Anthony J. Demetris, Kris V. Kowdley, S. Perwez Hussain, Jagdish Nair, Helmut Bartsch, Nadir Okby, Miriam C. Poirier, Kumal G. Ishak, Curtis C. Harris

Affiliations of authors: A. J. Marrogi, M. A. Khan, J. A. Welsh, H. Rahim, S. P. Hussain, C. C. Harris (Laboratory of Human Carcinogenesis, Center for Cancer Research), H. E. van Gijssel, M. C. Poirier (Laboratory of Cellular Carcinogenesis and Tumor Promotion, Center for Cancer Research), National Cancer Institute, Bethesda, MD; A. J. Demetris, Department of Pathology and Laboratory Medicine, University of Pittsburgh, PA; K. W. Kowdley, Department of Surgery, University of Washington, Seattle; J. Nair, H. Bartsch, German Cancer Center, Heidelberg, Germany; N. Okby, K. G. Ishak, Department of Hepatic and Gastrointestinal Pathology, The Armed Forces Institute of Pathology, Washington, DC.

Correspondence to: Curtis C. Harris, M.D., National Institutes of Health, Bldg. 37, Rm. 2C05, MSC 4255, Bethesda, MD 20892–4255 (e-mail: Curtis_Harris@nih.gov).

The incidence of hepatocellular carcinoma (HCC) in individuals with hereditary hemochromatosis is 200 times greater than in the general population (1). This increased risk of HCC may be the result of deregulation of oxidation reduction and generation of reactive oxygen species from free iron, directly through the Fenton reaction and indirectly through the acceleration of lipid peroxidation [reviewed in (2)]. In an iron–nitrilotriacetic acid rat model of hemochromatosis, renal samples showed an increase in the levels of several reactive intermediates, including 4-hydroxy-2-nonenal and malondialdehyde (3,4), both of which are known to be cytotoxic and genotoxic (5,6). These increases were accompanied by decreased availability of systems that protect against oxidation by iron, such as vitamin E levels, the glutathione system, thiol-specific antioxidants, and superoxide dismutase (7,8). In addition, excess iron provides a strong growth-promotion advantage . . . [Full Text of this Article]

REFERENCES


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
 CarcinogenesisHome page
K. Arab, M. Pedersen, J. Nair, M. Meerang, L. E. Knudsen, and H. Bartsch
Typical signature of DNA damage in white blood cells: a pilot study on etheno adducts in Danish mother-newborn child pairs
Carcinogenesis, February 1, 2009; 30(2): 282 - 285.
[Abstract] [Full Text] [PDF]

Home page
 CarcinogenesisHome page
S. S. Wang, S. Davis, J. R. Cerhan, P. Hartge, R. K. Severson, W. Cozen, Q. Lan, R. Welch, S. J. Chanock, and N. Rothman
Polymorphisms in oxidative stress genes and risk for non-Hodgkin lymphoma
Carcinogenesis, September 1, 2006; 27(9): 1828 - 1834.
[Abstract] [Full Text] [PDF]

Home page
 Cancer Res.Home page
P. A. Farazi, J. Glickman, J. Horner, and R. A. DePinho
Cooperative Interactions of p53 Mutation, Telomere Dysfunction, and Chronic Liver Damage in Hepatocellular Carcinoma Progression.
Cancer Res., May 1, 2006; 66(9): 4766 - 4773.
[Abstract] [Full Text] [PDF]

Home page
 CarcinogenesisHome page
L. E. Mechanic, A. J. Marrogi, J. A. Welsh, E. D. Bowman, M. A. Khan, L. Enewold, Y.-L. Zheng, S. Chanock, P. G. Shields, and C. C. Harris
Polymorphisms in XPD and TP53 and mutation in human lung cancer
Carcinogenesis, March 1, 2005; 26(3): 597 - 604.
[Abstract] [Full Text] [PDF]