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FasL deficiency enhances the development of tumors in p53+/- mice

Michelle Embree-Ku1, Kim Boekelheide

  • 1Department of Pathology and Laboratory Medicine, Brown University, Providence, Rhode Island 02912, USA.

Toxicologic Pathology
|January 7, 2003
PubMed

Insights

Fas ligand deficiency did not affect tumor development in p53-deficient mice but shortened lifespan and increased lymphoma incidence in p53-mutated mice, suggesting utility in carcinogenicity testing.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Tumorigenesis involves multiple genetic events transforming normal cells into malignant ones.
  • The tumor suppressor gene p53 is frequently mutated in various cancers.
  • Interactions between p53 and other genes, like the Fas system, in tumor progression are under investigation.

Purpose of the Study:

  • To investigate the impact of the Fas system's interaction with p53 on tumor development and progression.
  • To assess the role of Fas ligand (FasL) deficiency in mice with disrupted p53 tumor suppressor genes.

Main Methods:

  • Generation of mice with targeted disruption of the p53 gene and mutations in Fas ligand (FasL).
  • Assessment of organ weights, life expectancy, and tumor and tissue histology in the generated mouse models.
  • Comparative analysis of tumor spectrum and survival rates between FasL-deficient and FasL-sufficient p53-mutated mice.

Main Results:

  • FasL deficiency did not alter life expectancy or tumor spectrum in homozygous p53-deficient mice.
  • In p53-mutated mice (p53+/-), FasL deficiency reduced median survival from 12.1 to 9.6 months.
  • FasL deficiency shifted the tumor spectrum in p53-mutated mice from predominantly sarcomas to lymphomas.

Conclusions:

  • FasL deficiency significantly impacts tumor progression and survival in the context of p53 mutations, promoting lymphoma development.
  • The FasL-deficient, p53-mutated mouse model shows potential utility in carcinogenicity testing, especially for nongenotoxic compounds.
  • Further research is warranted to elucidate the specific mechanisms underlying the Fas system's interplay with p53 in cancer.

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