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Interference of glucocorticoids with apoptosis signaling and host-tumor interactions

Hans Peter Rutz1, Ingrid Herr

  • 1Division of Radiation Medicine, Paul Scherrer Institute (PSI), Villigen, Switzerland. hanspeter.rutz@psi.ch

Cancer Biology & Therapy
|June 16, 2004
PubMed

Insights

Glucocorticoids can worsen cancer treatment outcomes by inducing resistance, interfering with apoptosis, and impacting immune response and glucose metabolism. This review examines these iatrogenic effects in clinical cancer therapy.

Area of Science:

  • Oncology
  • Pharmacology
  • Cancer Biology

Background:

  • Cancer treatment efficacy is hindered by factors like tumor origin, drug resistance, and poor drug delivery.
  • Treatment resistance can be intrinsic, acquired, or induced, affecting radiation or chemotherapy.
  • Corticosteroid-induced cancer treatment resistance is a growing concern, yet inadequately studied clinically.

Purpose of the Study:

  • To review the mechanisms by which glucocorticoids influence the effectiveness of cytotoxic cancer therapy.
  • To highlight the clinical implications of iatrogenic resistance induced by corticosteroids.

Main Methods:

  • Literature review of existing studies on glucocorticoid effects in cancer treatment.
  • Analysis of mechanisms including apoptosis interference, immune response modulation, and glucose metabolism impact.

Main Results:

  • Glucocorticoids can induce resistance to cancer therapies through various pathways.
  • Mechanisms include interference with apoptosis signaling, suppression of anti-tumor immune responses, and alterations in cancer cell glucose metabolism.

Conclusions:

  • Glucocorticoids present a significant challenge to successful cancer treatment by inducing resistance.
  • Further clinical examination is needed to understand and mitigate these iatrogenic effects on cancer therapy outcomes.

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