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Modeling the risk of secondary malignancies after radiotherapy.

Schneider U - Genes (Basel) (2011)

Bottom Line: Better semi-empirical models include the effect of dose fractionation and represent the dose-response relationships more accurately.Most uncertainties are related to the time patterns of cancer induction, the population specific dependencies and to the organ specific cancer induction rates.If a treatment plan is compared relative to another one only the shape of the dose-response curve (the so called risk-equivalent dose) is of importance and errors can be minimized.

View Article: PubMed Central - PubMed

Affiliation: Vetsuisse Faculty, University of Zürich, Zürich 8057, Switzerland. uwe.schneider@uzh.ch.

ABSTRACT
In developed countries, more than half of all cancer patients receive radiotherapy at some stage in the management of their disease. However, a radiation-induced secondary malignancy can be the price of success if the primary cancer is cured or at least controlled. Therefore, there is increasing concern regarding radiation-related second cancer risks in long-term radiotherapy survivors and a corresponding need to be able to predict cancer risks at high radiation doses. Of particular interest are second cancer risk estimates for new radiation treatment modalities such as intensity modulated radiotherapy, intensity modulated arc-therapy, proton and heavy ion radiotherapy. The long term risks from such modern radiotherapy treatment techniques have not yet been determined and are unlikely to become apparent for many years, due to the long latency time for solid tumor induction. Most information on the dose-response of radiation-induced cancer is derived from data on the A-bomb survivors who were exposed to γ-rays and neutrons. Since, for radiation protection purposes, the dose span of main interest is between zero and one Gy, the analysis of the A-bomb survivors is usually focused on this range. With increasing cure rates, estimates of cancer risk for doses larger than one Gy are becoming more important for radiotherapy patients. Therefore in this review, emphasis was placed on doses relevant for radiotherapy with respect to radiation induced solid cancer. Simple radiation protection models should be used only with extreme care for risk estimates in radiotherapy, since they are developed exclusively for low dose. When applied to scatter radiation, such models can predict only a fraction of observed second malignancies. Better semi-empirical models include the effect of dose fractionation and represent the dose-response relationships more accurately. The involved uncertainties are still huge for most of the organs and tissues. A major reason for this is that the underlying processes of the induction of carcinoma and sarcoma are not well known. Most uncertainties are related to the time patterns of cancer induction, the population specific dependencies and to the organ specific cancer induction rates. For radiotherapy treatment plan optimization these factors are irrelevant, as a treatment plan comparison is performed for a patient of specific age, sex, etc. If a treatment plan is compared relative to another one only the shape of the dose-response curve (the so called risk-equivalent dose) is of importance and errors can be minimized.

No MeSH data available.


Related in: MedlinePlus

Comparison of neutron dose equivalent given in mSv per treatment Gy for two proton therapy beam lines for a prostate treatment. The red curve shows the results of measurements at the passive (scatter) beam line at Loma Linda [29,30] and the blue curve results from measurements at the active beam line at Paul Scherrer Institute (PSI) [28]. All measurements were performed perpendicular to the beam direction.
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f3-genes-02-01033: Comparison of neutron dose equivalent given in mSv per treatment Gy for two proton therapy beam lines for a prostate treatment. The red curve shows the results of measurements at the passive (scatter) beam line at Loma Linda [29,30] and the blue curve results from measurements at the active beam line at Paul Scherrer Institute (PSI) [28]. All measurements were performed perpendicular to the beam direction.

Mentions: When proton or ion therapy is used to treat a patient, the integral dose is lower per se when compared to an equivalent photon treatment. The reason for this is that the dose deposited by protons rises sharply near the end of their range, giving rise to the so-called Bragg peak (Figure 2). This differs significantly from the dose deposition by photons, which is quasi exponential. As a result the integral dose from proton or ion therapy is a factor of 2–3 lower than a comparable photon treatment [27]. This integral dose advantage is somewhat balanced by the additional neutron dose. The nuclear interactions of protons create a halo of neutrons and are responsible for a low dose everywhere in the patient. Two possible beam delivery systems for proton and ion therapy have to be distinguished regarding neutron dose. Active scanning sweeps a fine pencil beam through the target. Since scanning is mainly accomplished by magnetic means, neutrons are mainly produced in the patient itself [28]. In contrast, passively scattered beams are produced by interposing scattering material into a pencil beam to produce a broad beam which covers the whole target volume. Therefore, more neutrons are produced and the neutron dose from scattered beams is much larger than from pencil beam scanning, which is depicted in Figure 3 [29,30]. Close to the target protons offer a distinct advantage due to the lower integral dose. Out-of-field, but within approximately 25 cm from the field edge, the scattered photon dose in intensity modulation turned out to be roughly a factor of 2 lower than the neutron equivalent dose from scattered proton therapy. At larger distances to the field (beyond approximately 25 cm), protons offer an advantage, resulting in doses that are roughly a factor of 2–3 lower [31].


Modeling the risk of secondary malignancies after radiotherapy.

Schneider U - Genes (Basel) (2011)

Comparison of neutron dose equivalent given in mSv per treatment Gy for two proton therapy beam lines for a prostate treatment. The red curve shows the results of measurements at the passive (scatter) beam line at Loma Linda [29,30] and the blue curve results from measurements at the active beam line at Paul Scherrer Institute (PSI) [28]. All measurements were performed perpendicular to the beam direction.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC3927608&req=5

f3-genes-02-01033: Comparison of neutron dose equivalent given in mSv per treatment Gy for two proton therapy beam lines for a prostate treatment. The red curve shows the results of measurements at the passive (scatter) beam line at Loma Linda [29,30] and the blue curve results from measurements at the active beam line at Paul Scherrer Institute (PSI) [28]. All measurements were performed perpendicular to the beam direction.
Mentions: When proton or ion therapy is used to treat a patient, the integral dose is lower per se when compared to an equivalent photon treatment. The reason for this is that the dose deposited by protons rises sharply near the end of their range, giving rise to the so-called Bragg peak (Figure 2). This differs significantly from the dose deposition by photons, which is quasi exponential. As a result the integral dose from proton or ion therapy is a factor of 2–3 lower than a comparable photon treatment [27]. This integral dose advantage is somewhat balanced by the additional neutron dose. The nuclear interactions of protons create a halo of neutrons and are responsible for a low dose everywhere in the patient. Two possible beam delivery systems for proton and ion therapy have to be distinguished regarding neutron dose. Active scanning sweeps a fine pencil beam through the target. Since scanning is mainly accomplished by magnetic means, neutrons are mainly produced in the patient itself [28]. In contrast, passively scattered beams are produced by interposing scattering material into a pencil beam to produce a broad beam which covers the whole target volume. Therefore, more neutrons are produced and the neutron dose from scattered beams is much larger than from pencil beam scanning, which is depicted in Figure 3 [29,30]. Close to the target protons offer a distinct advantage due to the lower integral dose. Out-of-field, but within approximately 25 cm from the field edge, the scattered photon dose in intensity modulation turned out to be roughly a factor of 2 lower than the neutron equivalent dose from scattered proton therapy. At larger distances to the field (beyond approximately 25 cm), protons offer an advantage, resulting in doses that are roughly a factor of 2–3 lower [31].

Bottom Line: Better semi-empirical models include the effect of dose fractionation and represent the dose-response relationships more accurately.Most uncertainties are related to the time patterns of cancer induction, the population specific dependencies and to the organ specific cancer induction rates.If a treatment plan is compared relative to another one only the shape of the dose-response curve (the so called risk-equivalent dose) is of importance and errors can be minimized.

View Article: PubMed Central - PubMed

Affiliation: Vetsuisse Faculty, University of Zürich, Zürich 8057, Switzerland. uwe.schneider@uzh.ch.

ABSTRACT
In developed countries, more than half of all cancer patients receive radiotherapy at some stage in the management of their disease. However, a radiation-induced secondary malignancy can be the price of success if the primary cancer is cured or at least controlled. Therefore, there is increasing concern regarding radiation-related second cancer risks in long-term radiotherapy survivors and a corresponding need to be able to predict cancer risks at high radiation doses. Of particular interest are second cancer risk estimates for new radiation treatment modalities such as intensity modulated radiotherapy, intensity modulated arc-therapy, proton and heavy ion radiotherapy. The long term risks from such modern radiotherapy treatment techniques have not yet been determined and are unlikely to become apparent for many years, due to the long latency time for solid tumor induction. Most information on the dose-response of radiation-induced cancer is derived from data on the A-bomb survivors who were exposed to γ-rays and neutrons. Since, for radiation protection purposes, the dose span of main interest is between zero and one Gy, the analysis of the A-bomb survivors is usually focused on this range. With increasing cure rates, estimates of cancer risk for doses larger than one Gy are becoming more important for radiotherapy patients. Therefore in this review, emphasis was placed on doses relevant for radiotherapy with respect to radiation induced solid cancer. Simple radiation protection models should be used only with extreme care for risk estimates in radiotherapy, since they are developed exclusively for low dose. When applied to scatter radiation, such models can predict only a fraction of observed second malignancies. Better semi-empirical models include the effect of dose fractionation and represent the dose-response relationships more accurately. The involved uncertainties are still huge for most of the organs and tissues. A major reason for this is that the underlying processes of the induction of carcinoma and sarcoma are not well known. Most uncertainties are related to the time patterns of cancer induction, the population specific dependencies and to the organ specific cancer induction rates. For radiotherapy treatment plan optimization these factors are irrelevant, as a treatment plan comparison is performed for a patient of specific age, sex, etc. If a treatment plan is compared relative to another one only the shape of the dose-response curve (the so called risk-equivalent dose) is of importance and errors can be minimized.

No MeSH data available.


Related in: MedlinePlus