|
Sign In to gain access to subscriptions and/or personal tools.
|
Toxicologic Pathology, Vol. 32, No. 2 suppl,
6-11 (2004)
DOI: 10.1080/01926230490451680
Peroxisome Proliferators and Receptor-Mediated Hepatic Carcinogenesis
Russell C. Cattley
Department of Pathology, Amgen Inc., Thousand Oaks, California 91320, USA, rcattley@ amgen.com
The peroxisome proliferators represent an important group of hepatic carcinogens in rodents that act via the nuclear receptor PPAR . The primary role of PPAR in mediating this response had led to the further characterization of potential events downstream that likely enable the carcinogenic response, including increased peroxisomal fatty acid beta oxidation and the modulation of hepatocellular replication and death, either generally or in preneoplastic lesions. A cooperative role of Kupffer cell activation has been proposed to function in the modulation of hepatocellular proliferation in rodent liver by peroxisome proliferators, but data that confirm or refute this proposal are mixed. Presently there is no evidence that links the Kupffer cell activation by peroxisome proliferators directly to the development of liver tumors. There are marked species differences in susceptibility to peroxisomal proliferation, and active investigation concerning the molecular basis of these differences continues.
Key Words: Peroxisome liver cancer.

CiteULike Connotea Del.icio.us Digg Reddit Technorati What's this?
This article has been cited by other articles:

|
 |

|
 |
 
Q. Yang, T. Nagano, Y. Shah, C. Cheung, S. Ito, and F. J. Gonzalez
The PPAR{alpha}-Humanized Mouse: A Model to Investigate Species Differences in Liver Toxicity Mediated by PPAR{alpha}
Toxicol. Sci.,
January 1, 2008;
101(1):
132 - 139.
[Abstract]
[Full Text]
[PDF]
|
 |
|

|
 |

|
 |
 
Q. Yang, S. Ito, and F. J. Gonzalez
Hepatocyte-restricted constitutive activation of PPAR{alpha} induces hepatoproliferation but not hepatocarcinogenesis
Carcinogenesis,
June 1, 2007;
28(6):
1171 - 1177.
[Abstract]
[Full Text]
[PDF]
|
 |
|
|