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Related Experiment Videos

TNF blockade: an inflammatory issue.

B B Aggarwal1, S Shishodia, Y Takada

  • 1Cytokine Research Laboratory, Department of Experimental Therapeutics, University of Texas, M.D. Anderson Cancer Hospital 77030, USA. aggarwal@mdanderson.org

Ernst Schering Research Foundation Workshop
|December 8, 2005
PubMed
Summary
This summary is machine-generated.

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Tumor necrosis factor (TNF) plays a dual role in cancer and inflammation. New safe and effective TNF-targeting therapies are needed, potentially from natural sources, to balance its beneficial immune functions with its harmful effects.

Area of Science:

  • Immunology
  • Oncology
  • Pharmacology

Background:

  • Tumor necrosis factor (TNF) has a complex role, mediating tumor progression and various inflammatory diseases.
  • TNF is crucial for immune surveillance and the function of immune cells like NK, T, B cells, macrophages, and dendritic cells.
  • Current TNF inhibitors (e.g., Remicade, Humira, Enbrel) alleviate inflammatory symptoms but increase risks of infections, cancers, and cardiotoxicity.

Purpose of the Study:

  • To address the urgent need for safe and effective TNF-targeting therapeutics.
  • To explore the differential roles of transmembrane versus soluble TNF.
  • To identify agents that can selectively modulate TNF expression or signaling pathways.

Main Methods:

  • Review of existing literature on TNF's role in disease and immunity.

Related Experiment Videos

  • Analysis of TNF signaling pathways (caspases, NF-kappaB, AP-1, MAPKs).
  • Identification of natural product-derived agents with potential to regulate TNF.

    • Main Results:

    • TNF is implicated in tumor initiation, promotion, and metastasis.
    • Dysregulated TNF is linked to numerous inflammatory and autoimmune diseases.
    • Evidence suggests transmembrane TNF may be beneficial, while soluble TNF mediates toxicity.
    • TNF blockade carries significant risks, highlighting the need for safer alternatives.
    • Natural agents have been identified that may differentially regulate TNF.

    Conclusions:

    • Developing therapeutics that selectively target TNF pathways is critical for managing inflammatory diseases and cancer.
    • Future therapies should aim to harness beneficial TNF functions while mitigating toxic effects.
    • Natural product-derived agents represent a promising avenue for discovering novel, safer TNF modulators.