Current clinical experience in radiation therapy is based upon dose computations that report the absorbed dose to water, even though the patient is not made of water but of many different types of tissue. While Monte Carlo dose calculation algorithms have the potential for higher dose accuracy, they usually transport particles in and compute the absorbed dose to the patient media such as soft tissue, lung or bone. Therefore, for dose calculation algorithm comparisons, or to report dose to water or tissue contained within a bone matrix for example, a method to convert dose to the medium to dose to water is required. This conversion has been developed here by applying Bragg-Gray cavity theory. The dose ratio for 6 and 18 MV photon beams was determined by computing the average stopping power ratio for the primary electron spectrum in the transport media. For soft tissue, the difference between dose to medium and dose to water is approximately 1.0%, while for cortical bone the dose difference exceeds 10%. The variation in the dose ratio as a function of depth and position in the field indicates that for photon beams a single correction factor can be used for each particular material throughout the field for a given photon beam energy. The only exception to this would be for the clinically non-relevant dose to air. Pre-computed energy spectra for 60Co to 24 MV are used to compute the dose ratios for these photon beams and to determine an effective energy for evaluation of the dose ratio.

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Most calculations of the biological effect of radiation on tumours assume that the clonogenic cell density is uniform even if account is taken of non-uniform dose distribution. In practice tumours will almost certainly have a non-uniform clonogenic cell density. This paper extends one particular model of tumour control probability (TCP) to incorporate a variable clonogenic cell density while at the same time assuming a constant 2 Gy fraction size and a uniform radiosensitivity throughout the treatment. Since there are virtually no in vivo data on the variation of density we consider some model situations. One clear conclusion is that a large reduction in clonogenic cell density at the edges of a tumour would permit only a very modest decrease in dose if the TCP is not to be reduced. In general the effect on TCP is a complicated function of the variation in both dose and clonogenic cell density. We give the equations which enable both to be included.