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Thermal stress and the disruption of redox-sensitive signalling and transcription factor activation: possible role in

D Gius1, D Mattson, C M Bradbury

  • 1Molecular Radiation Oncology Section, Radiation Oncology Branch, Radiation Oncology Sciences Program, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA. giusd@mail.nih.gov

International Journal of Hyperthermia : the Official Journal of European Society for Hyperthermic Oncology, North American Hyperthermia Group
|June 16, 2004
PubMed

Insights

Heat shock may alter cancer therapy outcomes by disrupting cellular redox balance, affecting immediate early response genes. This review explores the link between heat shock, oxidative stress, and radiosensitization.

Area of Science:

  • Cellular Biology
  • Radiation Oncology
  • Molecular Mechanisms

Background:

  • The precise mechanisms of heat-induced alterations in cellular response to ionizing radiation (IR) are not fully understood.
  • Immediate early response genes are implicated in both cytotoxic and cytoprotective roles in cancer therapy.
  • Cellular redox status is a key regulator of immediate early response gene activity.

Purpose of the Study:

  • To summarize evidence linking heat shock to oxidative stress.
  • To discuss the hypothesis that heat shock disrupts redox-sensitive signaling factors.
  • To explore how this disruption may alter cellular responses to anticancer agents, including hyperthermic radiosensitization.

Main Methods:

  • Review of recent scientific literature.
  • Analysis of mechanistic links between heat shock, oxidative stress, and gene expression.
  • Discussion of redox-sensitive signaling pathways.

Main Results:

  • Heat shock and oxidative stress share common alterations in immediate early response genes.
  • Heat shock may induce oxidative stress, similar to other environmental antagonists.
  • Evidence supports a mechanistic link between heat shock and oxidative stress.

Conclusions:

  • Heat shock may alter cellular responses to ionizing radiation and other anticancer agents.
  • Disruption of redox-sensitive signaling factors by heat shock is a proposed mechanism for hyperthermic radiosensitization.
  • Understanding these mechanisms could optimize cancer therapy strategies.

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