Split-course accelerated therapy in head and neck cancer: An analysis of toxicity

Delaney, Geoff P.; Fisher, Richard; Smee, Robert; Hook, Carolyn; Bartoň, Michael

doi:10.1016/0360-3016(95)00093-e

Cited by 26 publications

(7 citation statements)

References 17 publications

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“…13,14 Late dysphagia can persist for many years 13,15 and is associated with injury to the pharyngeal constrictors and larynx. 15,16 The Radiation Therapy Oncology Group 0615 guidelines recommend that the mean dose to these OAR should not exceed 45 Gy. Rancati et al 17 recommended that minimizing the volume of the pharyngeal constrictors and larynx receiv-ing 60 Gy, and, when possible, reducing the volume receiving 50 Gy, was associated with reduced dysphagia/aspiration.…”

Section: Discussionmentioning

confidence: 99%

Reduction of clinical target volume in patients with lateralized cancer of the nasopharynx and without contralateral lymph node metastasis receiving intensity‐modulated radiotherapy

Sun

Zhang

et al. 2015

Head & Neck

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Section: Discussionmentioning

confidence: 99%

Reduction of clinical target volume in patients with lateralized cancer of the nasopharynx and without contralateral lymph node metastasis receiving intensity‐modulated radiotherapy

Sun

Zhang

et al. 2015

Head & Neck

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“…Delaney et al noted that pharyngeal fibrosis after an accelerated radiotherapy regimen predisposed patients to overt aspiration. [9] Abitbol et al…”

Section: Discussionmentioning

confidence: 99%

Competing risk: An illustration with aspiration pneumonia in head and neck cancer patients undergoing radical radiotherapy: A biostatistician′s perspective

Bhattacharyya

Bhattacharjee

2014

Indian J Cancer

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Interest in survival analysis is to look and capture the information about the occurrence of events, i.e., death. In human life different types of events may happen at the same time. Sometimes, few events completely interrupt or make subtle changes on the occurrence of an event of interest. The method to capture information about the specific event of interest along with other events is known as competing risk modeling. This paper is dedicated to explore the application of competing risk model in oncology practice. It is aimed in near future that more and more survival analysis will be performed through application of competing risk modeling instead of traditional survival analysis to generate robust statistical inference.

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“…The delay differential model's advantage, however, is that it can naturally be used to study issues that the simple model does not address-the likely effects of schedules that increase or decrease the dose-perday over time 55,56 or that split the radiation course into relatively intense segments separated by gaps. 57,58 These issues will be explored in the next phase of this work, in which the current model will be fitted to clinical data 2,23 ͑mindful of the difficulties possibly presented by schedules delivered without weekend breaks or using multiple fractions per day͒ and the model fit used to assess the likely impact of schedule changes. In the future it is also intended to factor chemotherapy into the modeling, opening up an exploration of the effectiveness of chemoirradiation strategies, an approach that seems promising as the mathematical biology community is currently using delay differential equations to model the tumorcidal effects of chemotherapy.…”

Section: Discussionmentioning

confidence: 99%

Delay differential equations and the dose-time dependence of early radiotherapy reactions

Fenwick

2006

Med. Phys.

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The dose-time dependence of early radiotherapy reactions impacts on the design of accelerated fractionation schedules--oral mucositis, for example, can be dose limiting for short treatments designed to avoid tumor repopulation. In this paper a framework for modeling early reaction dose-time dependence is developed. Variation of stem cell number with time after the start of a radiation schedule is modeled using a first-order delay differential equation (DDE), motivated by experimental observations linking the speed of compensatory proliferation in early reacting tissues to the degree of tissue damage. The modeling suggests that two types of early reaction radiation response are possible, stem cell numbers either monotonically approaching equilibrium plateau levels or overshooting before returning to equilibrium. Several formulas have been derived from the delay differential equation, predicting changes in isoeffective total radiation dose with schedule duration for different types of fractionation scheme. The formulas have been fitted to a wide range of published animal early reaction data, the fits all implying a degree of overshoot. Results are presented illustrating the scope of the delay differential model: most of the data are fitted well, although the model struggles with a few datasets measured for schedules with distinctive dose-time patterns. Ways of extending the current model to cope with these particular dose-time patterns are briefly discussed. The DDE approach is conceptually more complex than earlier descriptive dose-time models but potentially more powerful. It can be used to study issues not addressed by simpler models, such as the likely effects of increasing or decreasing the dose-per-day over time, or of splitting radiation courses into intense segments separated by gaps. It may also prove useful for modeling the effects of chemoirradiation.

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Split-course accelerated therapy in head and neck cancer: An analysis of toxicity

Cited by 26 publications

References 17 publications

Reduction of clinical target volume in patients with lateralized cancer of the nasopharynx and without contralateral lymph node metastasis receiving intensity‐modulated radiotherapy

Reduction of clinical target volume in patients with lateralized cancer of the nasopharynx and without contralateral lymph node metastasis receiving intensity‐modulated radiotherapy

Competing risk: An illustration with aspiration pneumonia in head and neck cancer patients undergoing radical radiotherapy: A biostatistician′s perspective

Delay differential equations and the dose-time dependence of early radiotherapy reactions

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