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Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the daughter...
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Related Experiment Video

Updated: Jun 18, 2026

A Murine Pancreatic Islet Cell-based Screening for Diabetogenic Environmental Chemicals
07:39

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Published on: June 25, 2018

PPARalpha- and DEHP-Induced Cancers.

Yuki Ito1, Tamie Nakajima

  • 1Department of Occupational and Environmental Health, Nagoya University Graduate School of Medicine, 65 Tsurumai-cho, Showa-ku, Nagoya 466-8550, Japan.

PPAR Research
|September 5, 2008
PubMed
Summary

Di(2-ethylhexyl)phthalate (DEHP) is a potential carcinogen. Extrapolating rodent cancer data to humans is challenging due to species differences in DEHP metabolism and PPARalpha pathways, necessitating further research.

Area of Science:

  • Toxicology
  • Carcinogenesis
  • Metabolism

Background:

  • Di(2-ethylhexyl)phthalate (DEHP) is a common plasticizer with potential non-genotoxic carcinogenic effects.
  • The peroxisome proliferator-activated receptor alpha (PPARalpha) pathway was initially implicated in DEHP-induced carcinogenesis.
  • Emerging evidence suggests non-PPARalpha pathways also contribute to DEHP's carcinogenic mechanisms.

Purpose of the Study:

  • To investigate the complexities of DEHP-induced carcinogenesis.
  • To address the challenges in extrapolating rodent carcinogenicity data to humans.
  • To highlight the importance of species-specific differences in DEHP metabolism and PPARalpha function.

Main Methods:

  • Review of existing literature on DEHP carcinogenicity mechanisms.

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  • Analysis of species-specific differences in PPARalpha expression and function.
  • Consideration of variations in lipase activity crucial for DEHP metabolism.

    • Main Results:

    • DEHP carcinogenicity involves both PPARalpha-dependent and independent pathways.
    • Significant species differences exist in PPARalpha activity and DEHP metabolism (e.g., lipase activity).
    • These variations complicate direct extrapolation of rodent DEHP carcinogenicity findings to humans.

    Conclusions:

    • Direct extrapolation of DEHP carcinogenicity from rodents to humans is difficult.
    • Development of PPARalpha-null mice and humanized PPARalpha mice offers potential tools for improved extrapolation.
    • Further mechanistic studies using these specialized mouse models are essential to elucidate DEHP's carcinogenic effects across species.