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Related Experiment Videos

Cutting edge: TRAIL deficiency accelerates hematological malignancies.

Nadeen Zerafa1, Jennifer A Westwood, Erika Cretney

  • 1Cancer Immunology Program, Trescowthick Laboratories, Peter MacCallum Cancer Centre, Melbourne, Victoria, Australia.

Journal of Immunology (Baltimore, Md. : 1950)
|October 21, 2005
PubMed
Summary

Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) deficiency leads to lymphoid malignancies in mice. TRAIL suppresses tumor initiation and development, particularly in p53-deficient contexts, but its role in epithelial cancers requires further study.

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Area of Science:

  • Immunology
  • Oncology
  • Molecular Biology

Background:

  • Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) is investigated as a tumor suppressor.
  • Previous studies show conflicting results on the significance of the TRAIL pathway in cancer.
  • The role of TRAIL in spontaneous tumor formation has not been previously evaluated.

Purpose of the Study:

  • To assess the role of TRAIL in spontaneous tumor formation throughout the lifespan of TRAIL-deficient mice.
  • To investigate TRAIL's function in tumor suppression, particularly in conjunction with p53 deficiency.
  • To determine TRAIL's involvement in Her2/neu oncogene-driven mammary epithelial cancer.

Main Methods:

  • Lifelong monitoring of spontaneous tumor formation in TRAIL-deficient mice.

Related Experiment Videos

  • Evaluation of tumor initiation and development in mice with TRAIL deficiency and p53 allelic loss.
  • Analysis of TRAIL's role in Her2/neu-driven mammary cancer models.

    • Main Results:

    • Over 25% of TRAIL-deficient mice developed lymphoid malignancies by 500 days of age.
    • TRAIL deficiency accelerated tumor development in mice with at least one p53 allele loss.
    • TRAIL did not play a critical role in Her2/neu-driven mammary epithelial cancers, despite their TRAIL sensitivity.

    Conclusions:

    • TRAIL plays a significant role in controlling carcinogenesis, particularly in lymphoid and stromal tumors.
    • The function of TRAIL in epithelial malignancies warrants further investigation.
    • TRAIL's tumor suppressive activity is context-dependent, influenced by genetic background and tumor type.