High LET Heavy Ion Radiation Induces p53-Independent Apoptosis

  • MORI Eiichiro
    Departments of Biology, School of Medicine, Nara Medical University
  • TAKAHASHI Akihisa
    Departments of Biology, School of Medicine, Nara Medical University
  • YAMAKAWA Nobuhiro
    Departments of Oral and Maxillofacial Surgery, School of Medicine, Nara Medical University
  • KIRITA Tadaaki
    Departments of Oral and Maxillofacial Surgery, School of Medicine, Nara Medical University
  • OHNISHI Takeo
    Departments of Biology, School of Medicine, Nara Medical University

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Abstract

Conventional clinical treatments with X-rays provide an effective modality for widely various human cancers, however, therapeutic results are sometimes poor. Many mutations have been reported to be in the p53 gene in advanced human cancers. The p53 plays a pivotal role in the pathway which controls apoptosis, cell growth and cell proliferation, and mutations or deletions in the p53 gene lead to resistance to cancer therapy. The involvement of the p53 gene in determining the sensitivity of many cell types toward low linear energy transfer (LET) radiation is now well established. In contrast to low LET radiation, high LET radiation has several potential advantages over X-rays, one of which is the fact that its effects may be independent of cellular p53 gene status. It is conceivable that effective future therapeutic strategies may be designed on the basis of genetic and biochemical events involved in cell death. Therefore, the accurate characterization and quantification of the mode of cell death, such as apoptosis and necrosis, has become increasingly important for the further understanding of the biological effectiveness of high LET radiation. This review discusses the mechanisms of p53-independent apoptosis by high LET radiation.

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