DNA double strand break (DSB) induction and cell survival in iodine-enhanced computed tomography (CT)

Streitmatter, Seth; Stewart, Robert D.; Jenkins, Peter; Jevremović, Tatjana

doi:10.1088/1361-6560/aa772d

Cited by 14 publications

(34 citation statements)

References 73 publications

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“…For the special case when

2 {\overset{z}{true}}_{F} R B E_{DSB} / {(α / β)}_{R} ≪ 1

, the low‐dose and high‐dose RBE are equal to the RBE DSB (i.e., RBE LD = RBE HD = RBE DSB ). Streitmatter et al . provides evidence in support of the hypothesis that RBE LD ≅ RBE HD ≅ RBE DSB in representative mammalian cells irradiated by electrons and photons with a wide range of kinetic energies.…”

Section: Rbe Models and Mechanisms Of Actionmentioning

confidence: 80%

“…To minimize the number of ad hoc adjustable parameters, RBE DSB is typically computed as a function of particle type, kinetic energy and oxygen concentration using the independently developed and tested MCDS software . Other Monte Carlo models or measurements could also potentially be used to estimate RBE DSB .…”

Section: Rbe Models and Mechanisms Of Actionmentioning

confidence: 99%

“…For most mammalian cell lines, the effective diameter d of the cell nucleus that gives the best fits to cell survival data usually falls within the range from about 2 to 5 μm; however, a representative value of d = 4 μm often suffices. It is important to note that estimates of α for low‐LET radiations are insensitive to the value of d because

2 {\overset{z}{true}}_{F} R B E_{DSB} / {(α / β)}_{R}

is usually small compared to unity. For a 200 MeV proton (LET = 0.451 keV/μm) and (α/β) R = 1 Gy, RBE DSB = 1.0 and

{\overset{z}{true}}_{F} = 4 \times 10^{- 3}

( d = 5 μm); therefore,

2 {\overset{z}{true}}_{F} R B E_{DSB} / {(α / β)}_{R} = 0.007 ≪ 1

.…”

Section: Rbe Models and Mechanisms Of Actionmentioning

confidence: 99%

“…The three mechanism‐inspired RBE models considered here are the local effect model (LEM), the microdosimetric‐kinetic (MK) model, and the repair‐misrepair‐fixation (RMF) model . The original version of LEM, referred to as LEM I, as well as the MK model are in routine clinical use for carbon ion treatment planning and have been implemented in commercially available treatment planning systems (LEM: Syngo RT, Siemens, Erlangen, Germany, and LEM + MK: RayStation, RaySearch Laboratories AB, Stockholm, Sweden).…”

Section: Introductionmentioning

confidence: 99%

“…The original version of LEM, referred to as LEM I, as well as the MK model are in routine clinical use for carbon ion treatment planning and have been implemented in commercially available treatment planning systems (LEM: Syngo RT, Siemens, Erlangen, Germany, and LEM + MK: RayStation, RaySearch Laboratories AB, Stockholm, Sweden). The RMF and an improved version of LEM, referred to as LEM IV, have also been implemented into research‐oriented treatment planning systems and other RBE modeling platforms …”

Section: Introductionmentioning

confidence: 99%

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A comparison of mechanism‐inspired models for particle relative biological effectiveness (RBE)

et al. 2018

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Background and Significance The application of heavy ion beams in cancer therapy must account for the increasing relative biological effectiveness (RBE) with increasing penetration depth when determining dose prescriptions and organ at risk (OAR) constraints in treatment planning. Because RBE depends in a complex manner on factors such as the ion type, energy, cell and tissue radiosensitivity, physical dose, biological endpoint, and position within and outside treatment fields, biophysical models reflecting these dependencies are required for the personalization and optimization of treatment plans. Aim To review and compare three mechanism‐inspired models which predict the complexities of particle RBE for various ion types, energies, linear energy transfer (LET) values and tissue radiation sensitivities. Methods The review of models and mechanisms focuses on the Local Effect Model (LEM), the Microdosimetric‐Kinetic (MK) model, and the Repair‐Misrepair‐Fixation (RMF) model in combination with the Monte Carlo Damage Simulation (MCDS). These models relate the induction of potentially lethal double strand breaks (DSBs) to the subsequent interactions and biological processing of DSB into more lethal forms of damage. A key element to explain the increased biological effectiveness of high LET ions compared to MV x rays is the characterization of the number and local complexity (clustering) of the initial DSB produced within a cell. For high LET ions, the spatial density of DSB induction along an ion's trajectory is much greater than along the path of a low LET electron, such as the secondary electrons produced by the megavoltage (MV) x rays used in conventional radiation therapy. The main aspects of the three models are introduced and the conceptual similarities and differences are critiqued and highlighted. Model predictions are compared in terms of the RBE for DSB induction and for reproductive cell survival. Results and Conclusions Comparisons of the RBE for DSB induction and for cell survival are presented for proton (1H), helium (4He), and carbon (12C) ions for the therapeutically most relevant range of ion beam energies. The reviewed models embody mechanisms of action acting over the spatial scales underlying the biological processing of potentially lethal DSB into more lethal forms of damage. Differences among the number and types of input parameters, relevant biological targets, and the computational approaches among the LEM, MK and RMF models are summarized and critiqued. Potential experiments to test some of the seemingly contradictory aspects of the models are discussed.

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“…For the special case when