Hypoxia, low glucose and acidosis influence radiation-induced apoptosis and thus may be detrimental to radiotherapy.

Background:The effects of radiotherapy treatment delays vary considerably depending on several factors, including tumour type, tumour characteristics, extent of delay and the radiation schedule. Both delays during treatment and delays in starting treatment may have an impact on tumour outcomes. In developing countries, particularly, budget constraints and overwhelming patient numbers may contribute to long waiting lists that may affect treatment efficacy. Empirical evidence on which to base treatment decisions and to motivate for additional resources is important. Aim:The aim of this study was to review the evidence that radiotherapy treatment delays may affect tumour response in several common tumour types and to determine, where reported, estimates of specific, commonly applied parameters to incorporate time and proliferation.Setting: Clinical radiotherapy of solid tumours.Methods: A review of the literature from an online database and search engine using terms associated with treatment delays or interruptions for a range of common tumour types was conducted.Results: There is evidence in several of the tumour types reviewed, including those of the head and neck, breast, cervix, prostate, lung, colorectal, anus, brain and bladder, that delays in radiotherapy can affect treatment outcomes. While, in most cases, delays in treatment are detrimental, there are certain examples cited where delays between other modalities and radiotherapy may be beneficial. Conclusion:While levels of evidence vary, failure to take note of proliferative effects of tumours because of extensions in treatment may in many cases result in avoidable treatment failures. It is thus prudent for radiation oncology departments to have clear policies for avoiding and dealing with treatment delays.

Both 2DG and azide can influence radiation-induced apoptosis possibly through their effects on glycolysis and ATP levels. We suggest that modulation of energy metabolism provides mechanistic insight into radiation-induced apoptotic pathways.