The tumour microenvironment is considered to be responsible for the outcome of cancer treatment and therefore it is extremely important to characterize and quantify it. Unfortunately, most of the experimental techniques available now are invasive and generally it is not known how this influences the results. Non-invasive methods on the other hand have a geometrical resolution that is not always suited for the modelling of the tumour response. Theoretical simulation of the microenvironment may be an alternative method that can provide quantitative data for accurately describing tumour tissues. This paper presents a computerized model that allows the simulation of the tumour oxygenation. The model simulates numerically the fundamental physical processes of oxygen diffusion and consumption in a two-dimensional geometry in order to study the influence of the different parameters describing the tissue geometry. The paper also presents a novel method to simulate the effects of diffusion-limited (chronic) hypoxia and perfusion-limited (acute) hypoxia. The results show that all the parameters describing tissue vasculature are important for describing tissue oxygenation. Assuming that vascular structure is described by a distribution of inter-vessel distances, both the average and the width of the distribution are needed in order to fully characterize the tissue oxygenation. Incomplete data, such as distributions measured in a non-representative region of the tissue, may not give relevant tissue oxygenation. Theoretical modelling of tumour oxygenation also allows the separation between acutely and chronically hypoxic cells, a distinction that cannot always be seen with other methods. It was observed that the fraction of acutely hypoxic cells depends not only on the fraction of collapsed blood vessels at any particular moment, but also on the distribution of vessels in space as well. All these suggest that theoretical modelling of tissue oxygenation starting from the basic principles is a robust method that can be used to quantify the tissue oxygenation and to provide input parameters for other simulations.
Purpose. To determine the dose response parameters and the fractionation sensitivity of prostate tumours from clinical results of patients treated with external beam radiotherapy. Material and methods. The study was based on five-year biochemical results from 14 168 patients treated with external beam radiotherapy. Treatment data from 11 330 patients treated with conventional fractionation have been corrected for overall treatment time and fitted with a logit equation. The results have been used to determine the optimum a/b values that minimise differences in predictions from 2838 patients treated with hypofractionated schedules. Results. Conventional fractionation data yielded logit dose response parameters for all risk groups and for all definitions of biochemical failures. The analysis of hypofractionation data led to very low a/b values (1-1.7 Gy) in all mentioned cases. neglecting the correction for overall treatment time has little impact on the derivation of a/b values for prostate cancers. Conclusions. These results indicate that the high fractionation sensitivity is an intrinsic property of prostate carcinomas and they support the use of hypofractionation to increase the therapeutic gain for these tumours.The interest in the radiobiology of prostate cancers has increased considerably since the publication of the initial report of Brenner and Hall [1] of a rather low a/b 1.5 Gy for these tumours. Indeed, according to standard clinical knowledge, a higher fractionation sensitivity than that of normal tissues at risk would suggest that a departure from the conventionally fractionated schedules and the use of higher doses per fraction for these tumours could widen the therapeutic window, leading either to the same tumour control with less complications or to better tumour response for the same level of complications [2]. The original report of a low a/b value for prostate had been based on a comparison of results from low dose rate brachytherapy with those from high dose rate external beam radiotherapy. not unexpectedly, its results have been disputed on various grounds, such as the relative biological effectiveness of brachytherapy radiation, tumour proliferation, heterogeneity of dose distributions or of tumour cell radiosensitivity, as reviewed by Dasu [3]. nevertheless, the initial report of a low a/b value for prostates had been followed by an increasing number of publications suggesting that prostate carcinomas might indeed have a high fractionation sensitivity that would favour therapeutic hypofractionation [3][4][5][6][7][8][9][10]. Consequently, several clinical studies exploring the feasibility and effectiveness of hypofractionated schemes have been initiated in recent years [2]. Enough results have now matured to warrant a new evaluation of the clinically relevant a/b value for prostates and this is the aim of the present study. Material and methodsClinical studies reporting the outcome of prostate radiotherapy have been identified in the literature using standardised queries or trackin...
Disregarding RBE variations might lead to suboptimal proton plans giving lower effect in the tumor and higher effect in normal tissues than expected. For cases where the target is situated close to structures sensitive to hot spot doses, this trend may lead to bias in favor of proton plans in treatment plan comparisons.
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