A New Incomplete-repair Model Based on a 'Reciprocal-time' Pattern of Sublethal Damage Repair

Rg, Dale; Jf, Fowler; Jones, Bleddyn

doi:10.1080/028418699432608

Cited by 48 publications

(26 citation statements)

References 34 publications

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“…In Fig. 5 the BED values are shown for the external beam dose (dashed curves) which is isoeffective for 5-year biochemical control with permanent I-125 implants prescribed to 145 Gy (full curves for three different values of T There is only slight evidence that this might be a real problem for tissues other than spinal cord or brain (34)(35)(36).…”

Section: Results For Slowly Proliferating Tumorsmentioning

confidence: 99%

Biological Factors Influencing Optimum Fractionation in Radiation Therapy

Fowler

2001

Acta Oncologica

124

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Section: Results For Slowly Proliferating Tumorsmentioning

confidence: 99%

Biological Factors Influencing Optimum Fractionation in Radiation Therapy

Fowler

2001

Acta Oncologica

124

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“…The knowledge of this proportion would allow, on the one hand, a more precise calculation of the interfractional time required for full repair of the repairable DNA damage in high-LET radiotherapy, and, on the other, the possibility to establish a correlation between unrepairable DNA damage and the RBE of different particles for cell inactivation. In this paper an extended version of the models proposed by Fowler [13,14] and Dale et al [15] is presented. The extended model is capable of differentiating between unrepairable and repairable damage and can be used to determine the final proportion of the former and the repair half-time of the latter at any given LET and particle type.…”

mentioning

confidence: 99%

Repair kinetic considerations in particle beam radiotherapy

Carabe‐Fernandez

Dale²,

Paganetti³

2011

BJR

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Objectives: A second-order repair kinetics model is developed to predict damage repair rates following low or high linear energy transfer (LET) irradiations and to assess the amount of unrepairable damage produced by such radiations. The model is a further development of an earlier version designed to test if low-LET radiation repair processes could be quantified in terms of second-order kinetics. The newer version allows calculation of both the repair rate of the proportion of DNA damages that repair according to secondorder kinetics and the proportion of DNA damages that do not repair. Methods: The original and present models are intercompared in terms of their goodness-of-fit to a number of data sets obtained from different ion beams. The analysis demonstrates that the present model provides a better fit to the data in all cases studied. Results: The proportions of unrepairable damage created by radiations of different LET predicted by the new model correspond well with previous studies on the increased effectiveness of high-LET radiations in inducing reproductive cell death. The results show that the original model may underestimate the proportion of unrepaired damage at any given time after its creation as well as failing to predict very slow or unrepairable damage components, which may result from high-LET irradiation. Conclusion: It is suggested that the second-order model presented here offers a more realistic view of the patterns of repair in cell lines or tissues exposed to high-LET radiation. investigations provide evidence that radiations of different linear energy transfer (LET) produce different types of DNA damage and that a larger proportion of complex damage is being created by higher LET. There is also evidence that different types of DNA damage are associated with different repair rates, with more complex damage taking longer to repair (if at all) [3,4]. It has been reported [5,6] that highly complex DNA breaks imply in some cases such a massive loss of DNA coding that the chances of correct repair are very low.For a given particle type, the relative biological effectiveness (RBE) increases with LET until reaching a maximum and then decreases. Belli et al [7] have recently studied the repair characteristics of double-strand breaks (DSBs) produced by radiations of different LET, arriving at the conclusion that the increase in RBE for cell inactivation with LET might be related to the increasing proportion of unrepaired DSB rather than the proportion of induced DSB. A similar conclusion was reached by Barendsen [1,8,9], who studied the LET dependency of different types of DNA strand breaks and suggested different candidates of DNA damage to explain cell inactivation. Other authors also have found a correspondence between unrepaired DNA strand breaks and cell lethality (e.g. Ritter et al [10], Goodhead et al [11] and more recently Eguchi-Kasai et al [12]), but none of them provided information on the specific nature of the unrepairable DNA strand breaks.In practical terms, DNA DSBs with very slow...

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“…Since an increasing number of experiments indicate a change of the half-time of repair, biexponential or binary repair (including two components of mono-exponential repair) is taken into account by several authors [8]. The observation of a fast repair shortly after irradiation and a following slower repair rate compared to exponential repair may also be explained by a second order process [6]. This implies, that the  -dependent…”

Section: Methodsmentioning

confidence: 99%

“…Tobias [3] Curtis [4] and Carlone et al [5] and Dale [6]). However, the extension to tissue interaction is difficult, since these models are based on the number of DNAlesions.…”

Section: Introductionmentioning

confidence: 99%

Kinetic Model for Dose Equivalent - an Efficient Way to Predict Systems Response of Irradiated Cells

Scheidegger¹,

Füchslin²

2011

SNE

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The response of tumours onto ionizing radiation cannot be fully understood by commonly used radiobiological models. The reason may lie in the complex structure of the cellular systems which show a high degree of compartmentalisation and which is characterised by a network of interacting processes at different time scales. To access the dynamic response of cells onto radiation, compartmental models based on a biological dose equivalent can be used. Two different models (-LQ-and -IRmodel) are used to fit experimental data of the clonogenic survival of irradiated cells at very high dose rates. The models reveal the correct dose rate dependence over a wide range of the parameter space when adapting the kinetic constants to the dose rate. This adaption could be an indication for the multi-scale structure of the system.

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A New Incomplete-repair Model Based on a 'Reciprocal-time' Pattern of Sublethal Damage Repair

Cited by 48 publications

References 34 publications

Biological Factors Influencing Optimum Fractionation in Radiation Therapy

Biological Factors Influencing Optimum Fractionation in Radiation Therapy

Repair kinetic considerations in particle beam radiotherapy

Kinetic Model for Dose Equivalent - an Efficient Way to Predict Systems Response of Irradiated Cells

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