Peroxisome proliferation and its role in carcinogenesis
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Peroxisome proliferation and its role in carcinogenesis views and expert opinions of an IARC working group, Lyon, 7-11 December 1994. by

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Published by International Agency for Research on Cancer, World Health Organization in Geneva .
Written in English


  • Carcinogenesis -- Congresses.,
  • Peroxisomes -- Congresses.

Book details:

Edition Notes

SeriesIARC technical report -- no. 24
ContributionsIARC Working Group on Peroxisome Proliferation. Meeting
LC ClassificationsQH603.P474 P47 1995
The Physical Object
Paginationv, 85 p. :
Number of Pages85
ID Numbers
Open LibraryOL20489855M
ISBN 109283214390

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Marsman DS, Cattley RC, Conway JG, Popp JA () Relationship of hepatic peroxisome proliferation and replicative DNA synthesis to the hepatocarcinogenicity of the peroxisome proliferators di(2-ethylhexyl)phthalate and [4-chloro(2, 3-xylidino)pyrimidinylthiolacetic acid (Wy,) in rats. Cancer Res – Google ScholarAuthor: B. G. Lake. Gonzalez F.J. () The Role of Peroxisome Proliferator Activated Receptor α in Peroxisome Proliferation, Physiological Homeostasis, and Chemical Carcinogenesis. In: American Institute for Cancer Research (eds) Dietary Fat and Cancer. Advances in Experimental Medicine and Biology, vol Springer, Boston, MACited by: In rodents, peroxisome proliferators induce liver cancer via a mode of action that includes activation of the peroxisome proliferator-activated receptor α (PPARα) transcription factor, increased cell proliferation, decreased apoptosis, and secondary oxidative stress leading to DNA damage. Peroxisome proliferator-activated receptors (PPARs) are nuclear hormone receptors, initially described as molecular targets for synthetic compounds inducing peroxisome proliferation. PPAR, the best characterized of the PPARs, plays a crucial role in adipogenesis and insulin sensitization. Furthermore, PPARhas been reported to affect cell proliferation/ differentiation pathways in various.

Overview of Peroxisome Proliferation and PPAR"Agonism Events leading to carcinogenic response following exposure to an environmental agent are varied and may range from mutations of the genome to the activation/deactivation of genes and/or receptors. An example of .   Mitogenic chemical such as phenobarbital, oxazepam, and the peroxisome proliferating agents exert a short-term cell proliferative response that may exert its primary effect in carcinogenesis at the promotion stages. The peroxisome proliferator class of non‐genotoxic carcinogens includes hypolipidemic drugs, such as ciprofibrate, Wy 14, and nafenopin; as well as pthalate plasticisers, such as diethylhexylphthalate. Peroxisome proliferators have been demonstrated to cause cancer in . IARC () Peroxisome Proliferation and its Role in Carcinogenesis (IARC Technical Report No. 24), Lyon, IARCPress. Keyhanfar F., Caldwell J. Factors affecting the metabolism of cinnamyl anthranilate in the rat and mouse.

The peroxisome proliferator-activated receptor γ (PPARγ) is the most extensively studied subtype of the PPARs. Over the last decade, research on PPARγ unveiled its role in important biological processes, including lipid biosynthesis, glucose metabolism, anti-inflammatory response and atheroscle-rosis. The results suggest that the selective induction of peroxisomal fatty acid oxidation is consistent with the hypothesis that imbalance between H 2 O 2 overproduction and its destruction could play a role in the modulation of hepatocarcinogenesis by peroxisome proliferators.   Youssef J, Badr M. Enhanced hepatocarcinogenicity due to agonists of peroxisome proliferator-activated receptors in senescent rats: role of peroxisome proliferation, cell proliferation, and apoptosis. Sci World J Youssef JA, Bouziane M, Badr MZ. If peroxisome proliferation and acyl-CoA oxidase induction, which generates H2O2, are required for carcinogenesis, there should be a direct relationship between potency of the chemical for peroxisome proliferation and potency for hepatocarcinogenesis.