Risk of secondary cancers from scattered radiation during intensity-modulated radiotherapies for hepatocellular carcinoma

Abstract

PurposeTo evaluate and compare the risks of secondary cancers from therapeutic doses received by patients with hepatocellular carcinoma (HCC) during intensity-modulated radiotherapy (IMRT), volumetric arc therapy (VMAT), and tomotherapy (TOMO).MethodsTreatments for five patients with hepatocellular carcinoma (HCC) were planned using IMRT, VMAT, and TOMO. Based on the Biological Effects of Ionizing Radiation VII method, the excess relative risk (ERR), excess absolute risk (EAR), and lifetime attributable risk (LAR) were evaluated from therapeutic doses, which were measured using radiophotoluminescence glass dosimeters (RPLGDs) for each organ inside a humanoid phantom.ResultsThe average organ equivalent doses (OEDs) of 5 patients were measured as 0.23, 1.18, 0.91, 0.95, 0.97, 0.24, and 0.20 Gy for the thyroid, lung, stomach, liver, small intestine, prostate (or ovary), and rectum, respectively. From the OED measurements, LAR incidence were calculated as 83, 46, 22, 30, 2 and 6 per 104 person for the lung, stomach, normal liver, small intestine, prostate (or ovary), and rectum.ConclusionsWe estimated the secondary cancer risks at various organs for patients with HCC who received different treatment modalities. We found that HCC treatment is associated with a high secondary cancer risk in the lung and stomach.

Risk of second cancer following radiotherapy for prostate cancer: a population-based analysis

“…Apparently this is due to low-dose radiation from internally scattered X-rays, leakage of X-rays from the machine and/or neutron production, especially observed after doses ≥10 MV photons [38]. Apart from skin cancer Zelefsky et al could not find any excessive risk of SC [21].…”

Disease drivers of aging

“…This hypothesis is supported by data collected from cancer survivors who report poorer physical function, 120,136,137 poorer quality of life, 138,139 and increased number of comorbidities, 140,141 as well as risk for cognitive decline. 142,143 The underlying cancer treatment may affect telomere length, [144][145][146][147] increase p16 expression, 123 increase proinflammatory cytokines, 148,149 and increase resting energy expenditure. 150,151 There are several unanswered questions.…”

IL-17 induces radiation resistance of B lymphoma cells by suppressing p53 expression and thereby inhibiting irradiation-triggered apoptosis

“…Radioresistance may be induced by repeated exposures to small doses of ionizing radiation; 6 the latter is a common procedure in cancer treatment with ionizing radiation. 7 Thus, radioresistance is also a common phenomenon in cancer patients receiving ionizing radiation. 8 The mechanism of radioresistance will be further investigated.…”