Site-specific dose-response relationships for cancer induction from the combined Japanese A-bomb and Hodgkin cohorts for doses relevant to radiotherapy

<p>Abstract</p> <p>Background and Purpose</p> <p>Most information on the dose-response of radiation-induced cancer is derived from data on the A-bomb survivors. 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. However, estimates of cancer risk for doses larger than one Gy are becoming more important for radiotherapy patients. Therefore in this work, emphasis is placed on doses relevant for radiotherapy with respect to radiation induced solid cancer.</p> <p>Materials and methods</p> <p>For various organs and tissues the analysis of cancer induction was extended by an attempted combination of the linear-no-threshold model from the A-bomb survivors in the low dose range and the cancer risk data of patients receiving radiotherapy for Hodgkin's disease in the high dose range. The data were fitted using organ equivalent dose (OED) calculated for a group of different dose-response models including a linear model, a model including fractionation, a bell-shaped model and a plateau-dose-response relationship.</p> <p>Results</p> <p>The quality of the applied fits shows that the linear model fits best colon, cervix and skin. All other organs are best fitted by the model including fractionation indicating that the repopulation/repair ability of tissue is neither 0 nor 100% but somewhere in between. Bone and soft tissue sarcoma were fitted well by all the models. In the low dose range beyond 1 Gy sarcoma risk is negligible. For increasing dose, sarcoma risk increases rapidly and reaches a plateau at around 30 Gy.</p> <p>Conclusions</p> <p>In this work OED for various organs was calculated for a linear, a bell-shaped, a plateau and a mixture between a bell-shaped and plateau dose-response relationship for typical treatment plans of Hodgkin's disease patients. The model parameters (α and R) were obtained by a fit of the dose-response relationships to these OED data and to the A-bomb survivors. For any three-dimensional inhomogenous dose distribution, cancer risk can be compared by computing OED using the coefficients obtained in this work.</p

Radiation-induced second malignancies after involved-node radiotherapy with deep-inspiration breath-hold technique for early stage Hodgkin Lymphoma: a dosimetric study

BACKGROUND: To estimate the risk of radiation induced second cancers after radiotherapy using deep-inspiration breath-hold (DI) technique with three-dimensional conformal (3DCRT) and volumetric arc therapy (VMAT) for patients with Hodgkin’s lymphoma (HL). METHODS: Early-stage HL with mediastinal and supraclavicular involvement was studied using an Alderson phantom. A whole body CT was performed and all tissues were delineated. The clinical target volumes and planning target volumes (PTV) were determined according to the German Hodgkin study group guidelines. Free-breathing (FB) technique and DI technique were simulated by different safety margins for the PTV definition. In both cases, 30 Gy in 15 fractions was prescribed. Second cancer risk was estimated for various tissues with a second cancer model including fractionation. RESULTS: When compared with FB-3DCRT, estimated relative life time attributable risk (LAR) of cancer induction after DI-3DCRT was 0.86, 0.76, 0.94 and 0.92 for breast, lung, esophagus and stomach, respectively. With DI-VMAT, the corresponding values were 2.05, 1.29, 1.01, 0.93, respectively. For breast cancer, the LAR observed with DI-VMAT was not substantially distinguishable from the LAR computed for mantle RT with an administered dose of 40 Gy. CONCLUSIONS: This study suggests that DI may reduce the LAR of secondary cancers of all OARs and may be a valuable technique when using 3DCRT. Conversely, VMAT may increase substantially the LAR and should be cautiously implemented in clinical practice

Dose-response relationship for breast cancer induction at radiotherapy dose

<p>Abstract</p> <p>Purpose</p> <p>Cancer induction after radiation therapy is known as a severe side effect. It is therefore of interest to predict the probability of second cancer appearance for the patient to be treated including breast cancer.</p> <p>Materials and methods</p> <p>In this work a dose-response relationship for breast cancer is derived based on</p> <p>(i) the analysis of breast cancer induction after Hodgkin's disease,</p> <p>(ii) a cancer risk model developed for high doses including fractionation based on the linear quadratic model, and</p> <p>(iii) the reconstruction of treatment plans for Hodgkin's patients treated with radiotherapy,</p> <p>(iv) the breast cancer induction of the A-bomb survivor data.</p> <p>Results</p> <p>The fitted model parameters for an <it>α/β = 3 </it>Gy were <it>α = 0.067Gy</it>^{<it>-1 </it>}and <it>R = 0.62</it>. The risk for breast cancer is according to this model for small doses consistent with the finding of the A-bomb survivors, has a maximum at doses of around 20 Gy and drops off only slightly at larger doses. The predicted <it>EAR </it>for breast cancer after radiotherapy of Hodgkin's disease is 11.7/10000PY which can be compared to the findings of several epidemiological studies where EAR for breast cancer varies between 10.5 and 29.4/10000PY. The model was used to predict the impact of the reduction of radiation volume on breast cancer risk. It was estimated that mantle field irradiation is associated with a 3.2-fold increased risk compared with mediastinal irradiation alone, which is in agreement with a published value of 2.7. It was also shown that the modelled age dependency of breast cancer risk is in satisfying agreement with published data.</p> <p>Conclusions</p> <p>The dose-response relationship obtained in this report can be used for the prediction of radiation induced secondary breast cancer of radiotherapy patients.</p