A Microdosimetric-Kinetic Model for Cell Killing by Protracted Continuous Irradiation II: Brachytherapy and Biologic Effective Dose

Hawkins, Roland B.; Inaniwa, Taku

doi:10.1667/rr13558.1

Cited by 11 publications

(10 citation statements)

References 31 publications

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“…Let z be a dose to one of the domains at a specific energy in Gy, and the PLLs are created in proportion to the specific energy and the DNA amount in the domain. If the mass of DNA per domain is denoted by g that varies from domain to domain according to the cell phase, the number of PLLs in the domain as a function of time after irradiation, x d ( t ), is described by

\begin{matrix} right \frac{d}{normald t} x_{d} (t) & left = - (a + c) x_{d} (t) - 2 b_{d} x_{d} {false(t false)}^{2} \\ left ≅ - (a + c) x_{d} (t) . ∵ (a + c) x_{d} (t) > > 2 b_{d} x_{d} {false(t false)}^{2} \end{matrix} .

…”

Section: Methodsmentioning

confidence: 99%

Markov chain Monte Carlo analysis for the selection of a cell‐killing model under high‐dose‐rate irradiation

2017

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\begin{matrix} right \frac{d}{normald t} x_{d} (t) & left = - (a + c) x_{d} (t) - 2 b_{d} x_{d} {false(t false)}^{2} \\ left ≅ - (a + c) x_{d} (t) . ∵ (a + c) x_{d} (t) > > 2 b_{d} x_{d} {false(t false)}^{2} \end{matrix} .

…”

Section: Methodsmentioning

confidence: 99%

Markov chain Monte Carlo analysis for the selection of a cell‐killing model under high‐dose‐rate irradiation

2017

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“…Different approaches to investigate and to model the dose-rate time effects have been carried out using the MKM as a theoretical base. Some examples of these approaches can be found in [23,39,67,[101][102][103][104]. In these studies, the kinetic Eq.…”

Section: The Dependence Of the Biological Effect On The Dose-rate Time Structurementioning

confidence: 99%

Linking Microdosimetric Measurements to Biological Effectiveness in Ion Beam Therapy: A Review of Theoretical Aspects of MKM and Other Models

et al. 2021

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Different qualities of radiation are known to cause different biological effects at the same absorbed dose. Enhancements of the biological effectiveness are a direct consequence of the energy deposition clustering at the scales of DNA molecule and cell nucleus whilst absorbed dose is a macroscopic averaged quantity which does not take into account heterogeneities at the nanometer and micrometer scales. Microdosimetry aims to measure radiation quality at cellular or sub-cellular levels trying to increase the understanding of radiation damage mechanisms and effects. Existing microdosimeters rely on the well-established gas-based detectors or the more recent solid-state devices. They provide specific energy z spectra and other derived quantities as lineal energy (y) spectra assessed at the micrometer level. The interpretation of the radio-biological experimental data in the framework of different models has raised interest and various investigations have been performed to link in vitro and in vivo radiobiological outcomes with the observed microdosimetric data. A review of the major models based on experimental microdosimetry, with a particular focus on ion beam therapy applications and an emphasis on the microdosimetric kinetic model (MKM), will be presented in this work, enlightening the advantages of each one in terms of accuracy, initial assumptions, and agreement with experimental data. The MKM has been used to predict different kinds of radiobiological quantities such as the relative biological effects for cell inactivation or the oxygen enhancement ratio. Recent developments of the MKM will be also presented, including new non-Poissonian correction approaches for high linear energy transfer radiation, the inclusion of partial repair effects for fractionation studies, and the extension of the model to account for non-targeted effects. We will also explore developments for improving the models by including track structure and the spatial damage correlation information, by using the full fluence spectrum and by better accounting for the energy-deposition fluctuations at the intra- and inter-cellular level.

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“…Contrary to this, the cell survival curves for the dose rates with 1.00 and 1.50 Gy/h can be favorably reproduced by incorporating the amount of DNA modulated by the accumulation of cells in G 2 . Under protracted irradiation such as 0.186 Gy/h, there is a possibility that other factors such as cell proliferation [21, 40, 41] and adaptive response [42, 43] affect the surviving fraction. Further investigations are necessary on this point with regard to lower-dose-rate exposure.…”

Section: Resultsmentioning

confidence: 99%

“…For simplicity, the domain is generally defined as a sphere with diameter from 1.0 to 2.0 μm [18–21]. When ionizing radiation transfers its energy into a cell domain, PLLs may be induced.…”

Section: Methodsmentioning

confidence: 99%

Modeling cell survival and change in amount of DNA during protracted irradiation

Matsuya

Tsutsumi

Yoshii

et al. 2016

Journal of Radiation Research

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Hyper-radiosensitivity (HRS) is a well-known bioresponse under low-dose or low-dose-rate exposures. Although disorder of the DNA repair function, non-targeted effects and accumulation of cells in G2 have been experimentally observed, the mechanism for inducing HRS by long-term irradiation is still unclear. On the basis of biological experiments and a theoretical study, we have shown that change in the amount of DNA associated with accumulation of cells in G2 enhances radiosensitivity. To demonstrate continuous irradiation with 250 kVp X-rays, we adopted a fractionated regimen of 0.186 or 1.00 Gy per fraction at intervals of 1 h (i.e. 0.186 Gy/h, 1.00 Gy/h on average) to Chinese Hamster Ovary (CHO)-K1 cells. The change in the amount of DNA during irradiation was quantified by flow cytometric analysis with propidium iodide (PI). Concurrently, we attempted a theoretical evaluation of the DNA damage by using a microdosimetric-kinetic (MK) model that was modified to incorporate the change in the amount of DNA. Our experimental results showed that the fraction of the cells in G2/M phase increased by 6.7% with 0.186 Gy/h and by 22.1% with 1.00 Gy/h after the 12th irradiation. The MK model considering the change in amount of DNA during the irradiation exhibited a higher radiosensitivity at a high dose range, which could account for the experimental clonogenic survival. The theoretical results suggest that HRS in the high dose range is associated with an increase in the total amount of DNA during irradiation.

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A Microdosimetric-Kinetic Model for Cell Killing by Protracted Continuous Irradiation II: Brachytherapy and Biologic Effective Dose

Cited by 11 publications

References 31 publications

Markov chain Monte Carlo analysis for the selection of a cell‐killing model under high‐dose‐rate irradiation

Markov chain Monte Carlo analysis for the selection of a cell‐killing model under high‐dose‐rate irradiation

Linking Microdosimetric Measurements to Biological Effectiveness in Ion Beam Therapy: A Review of Theoretical Aspects of MKM and Other Models

Modeling cell survival and change in amount of DNA during protracted irradiation

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