Abstract

In parallel with boron neutron capture therapy (BNCT), fast neutron radiotherapy began shortly after the discovery of the neutron by Chadwick. The earliest clinical studies showed considerable toxicity and little efficacy1, and the field languished until the 1950’s when mammalian cell culture techniques allowed a better understanding of the different radiobiological properties of conventional photon radiation and fast neutrons. Clinical trials were resumed at Hammersmith Hospital, London, England in the 1960’s, and since that time approximately 20,000 patients have received fast neutron radiation as all or a part of their cancer therapy. Compared to conventional radiotherapy, fast neutrons offer a therapeutic advantage for salivary gland tumors2, locally-advanced prostate cancer3’4, and sarcomas5. For other tumor systems, the results have been less encouraging. It is not possible to increase tumor control by simply increasing the fast neutron dose because of treatment related toxicity due to normal tissue side effects. For fast neutrons, the dose response curves for both tumor control and normal tissue damage are quite steep, and often located close together, resulting in a narrow therapeutic window. An adjuvant BNCT boost to fast neutron radiotherapy has the potential of selectively increasing tumor dose relative to normal tissue dose, and thus widening the therapeutic window for selected tumor systems. While the physical dose augmentation is relatively small, it is multiplied both by its increased biological effectiveness and the steepness of the dose response curve resulting in a clinically-significant effect.

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