Recent Advances in the Biology of Heavy-Ion Cancer Therapy

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  • HAMADA Nobuyuki
    Radiation Safety Research Center, Nuclear Technology Research Laboratory, Central Research Institute of Electric Power Industry
  • IMAOKA Tatsuhiko
    Experimental Radiobiology for Children's Health Research Group, Research Center for Radiation Protection, National Institute of Radiological Sciences
  • MASUNAGA Shin-ichiro
    Particle Radiation Oncology Research Center, Research Reactor Institute, Kyoto University
  • OGATA Toshiyuki
    Department of Radiation Oncology, Osaka University Graduate School of Medicine
  • OKAYASU Ryuichi
    Heavy-ion Radiobiology Research Group, Research Center for Charged Particle Therapy, National Institute of Radiological Sciences
  • TAKAHASHI Akihisa
    Department of Biology, School of Medicine, Nara Medical University
  • KATO Takamitsu A.
    Heavy-ion Radiobiology Research Group, Research Center for Charged Particle Therapy, National Institute of Radiological Sciences
  • KOBAYASHI Yasuhiko
    Microbeam Radiation Biology Group, Japan Atomic Energy Agency
  • OHNISHI Takeo
    Department of Biology, School of Medicine, Nara Medical University
  • ONO Koji
    Particle Radiation Oncology Research Center, Research Reactor Institute, Kyoto University
  • SHIMADA Yoshiya
    Experimental Radiobiology for Children's Health Research Group, Research Center for Radiation Protection, National Institute of Radiological Sciences
  • TESHIMA Teruki
    Department of Radiation Oncology, Osaka University Graduate School of Medicine

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Abstract

Superb biological effectiveness and dose conformity represent a rationale for heavy-ion therapy, which has thus far achieved good cancer controllability while sparing critical normal organs. Immediately after irradiation, heavy ions produce dense ionization along their trajectories, cause irreparable clustered DNA damage, and alter cellular ultrastructure. These ions, as a consequence, inactivate cells more effectively with less cell-cycle and oxygen dependence than conventional photons. The modes of heavy ion–induced cell death/inactivation include apoptosis, necrosis, autophagy, premature senescence, accelerated differentiation, delayed reproductive death of progeny cells, and bystander cell death. This paper briefly reviews the current knowledge of the biological aspects of heavy-ion therapy, with emphasis on the authors' recent findings. The topics include (i) repair mechanisms of heavy ion–induced DNA damage, (ii) superior effects of heavy ions on radioresistant tumor cells (intratumor quiescent cell population, TP53-mutated and BCL2-overexpressing tumors), (iii) novel capacity of heavy ions in suppressing cancer metastasis and neoangiogenesis, and (iv) potential of heavy ions to induce secondary (especially breast) cancer.

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