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High-precision radiation therapy has been developed through the integration of technologies and knowledge in engineering, physics, biology, chemistry, and medicine. It enables radiation oncologists to decrease an excessive dose of radiation delivered to normal tissues and also administer a high and booster dose of radiation, particularly to small target fractions in a malignant tumour. However, even the most innovative strategies have sometimes failed to achieve a complete remission, and patients often suffer from tumour recurrence and/or distant metastasis after treatments. To overcome these problems, it is critical to elucidate biological mechanisms by which cancer cells acquire radioresistance, and consequently, survive, recur, and metasta after radiation therapy.
Hypoxic tumour cells have been attracting increasing attention in the fields of radiation biology and oncology since Thomlinson and Gray demonstrated the presence of hypoxic regions in malignant solid tumours and showed that they exert a negative impact on the outcome of radiation therapy. My laboratory has contributed to elucidate molecular mechanisms, wherein radioresistance of hypoxic cancer cells is induced by a hypoxia-inducible transcription factor, HIF-1. In this talk, I would like to present direct in vivo evidence that hypoxic cancer cells are the major source of recurrence after radiation therapy. I would like to provide a rational basis for targeting hypoxic tumour cells to enhance the effect of radiation therapy.