Objective To figure out the optimal parameters of a volumetric modulated arc therapy ( VMAT) plan for cervical and upper esophageal cancer by quality evaluation of VMAT plans with different parameters, and to provide a reference for the design of clinical VMAT treatment plan. Methods Ten patients with cervical esophageal cancer and ten patients with upper esophageal cancer were enrolled as subjects. The Nucletron Oncentra 4. 3 treatment planning system was used to generate plans for Elekta Synergy VMAT accelerator. Six VMAT plans were made with variation in the gantry angle ( 2°, 3°, and 4°), the maximum delivery time (80 s, 110 s, and 150 s), and the collimator angle (0° and 45°). The doses to the planning target volume and organs at risk were analyzed by paired t test. Results For cervical and upper esophageal cancer, the quality of VMAT plans with a collimator angle of 45° was better than those with a collimator angle of 0°(P=0. 003?0. 007). For cervical esophageal cancer, there was no significant difference in quality between VMAT plans with a maximum delivery time of 110 s or 150 s and those with a maximum delivery time of 80 s ( P>0. 05 );for upper esophageal cancer, there was also no significant difference in quality between VMAT plans with three different maximum delivery times ( P>0. 05 ) . For cervical esophageal cancer, the VMAT plans with a gantry angle of 3° had a better quality than those with a gantry angle of 2° or 4°(P=0. 010?0. 048). For upper esophageal cancer, the VMAT plans with a gantry angle of 3° had a better quality than those with a gantry angle of 4° ( P=0. 010?0. 048) . Compared with those with a gantry angle of 2° , the VMAT plans with a gantry angle of 3° had a slightly better dose distribution in the target volume ( P=0. 046 ) , but a slightly higher dose to lung tissue ( V25 and V30 , P=0. 007 and 0. 026) . Conclusions The optimal initial parameters of a VMAT plan for cervical and upper esophageal cancer are a collimator angle of 45°, a maximum delivery time of 80 s, and a gantry angle of 3°.

Objective Because of statistical noise in Monte Carlo dose calculations,the effective point doses may not be accurately calculated.A user-defined sphere volume was adopted to substitute the effective point to take sphere sampling around the effective point,which minimize the random errors and improve the accuracy of statistical dose.Methods Direct dose measurements were performed at 0°and 90° using a 0.125 cm3 Semiflex ionization chamber (IC) 31010 isocentrically placed in the center of a homogeneous Cylindric sliced RW3 phantom (PTW,Germany).In the scanned CT phantom series,the sensitive volume length of the IC (6.5 mm) was delineated and the isocenter was defined as the simulated effective point.All beams were simulated in the treatment planning system (TPS) in accordance to the measured model.The grid spacing was calculated by 2 mm voxels and the relative standard deviation should be ≤ 0.5％.The statistical and measured doses were statistically compared among three IC models with different electron densities (ED;esophageal lumen ED =0.210 g/cm3 for model A,air ED =0.001 g/cm3 for model B and the default CT scanned ED for model C) at different sampling sphere radius (2.5,2.0,1.5 and 1.0 mm) to evaluate the effect of Monte Carlo.calculation uncertainty upon the dose accuracy.Results In the Monaco TPS,the statistical value was in the highest accordance with the measured value with an absolute average deviation of 0.49％ when the IC was set as esophageal lumen ED =0.210 g/cm3 and the sampling sphere radius was 1.5 mm.When the IC was set as air ED=0.001 g/cm3 and default CT scanned ED,and,the recommended statistical sampling sphere radius was 2.5 mm,the absolute average deviations were 0.61％ and 0.70％.Conclusion In the Monaco TPS,the calculation model with an ED of 0.210 g/cm3 and a sampling radius of 1.5 mm is recommended for the ionization chamber 31010 to substitute the effective point dose measurement to decrease the random stochastic errors of Monte Carlo.

Objective To investigate the effects of nimotuzumab on radiosensitivity of ECA?109 and TE?13 esophageal carcinoma cell lines and explore its possible mechanism. Methods The ECA?109 and TE?13 cells were divided into control group, irradiation group, medicine group, and combined group ( irradiation + medicine) . In the combined group, ECA?109 and TE?13 cells were treated with nimotuzumab for 24 h before irradiation, and the cells were collected 2 h after irradiation. The radiosensitizing effects of nimotuzumab on ECA?109 and TE?13 cells were evaluated by clone formation assay. Cell apoptosis was detected by flow cytometry. Western blotting was used to evaluate the expression of EGFR, p?EGFR, DNA?PKcs, p?DNA?PKcs and γH2AX. Results The values of Dq( quasithreshold dose) , D0( mean lethal dose) and SF2(surviving fraction at 2 Gy) of ECA?109 and TE?13 cells in the combined group were significantly lower than those of the radiation group ( for ECA?109 cells, 1. 11 vs. 1. 72, 1. 40 vs. 2. 14, 0. 42 vs. 0. 66, respectively;for TE?13 cells, 0.41 vs. 0.46, 0.43 vs. 0.65, 0.40 vs. 0.71, respectively ( all P<0.05) . The sensitivity enhancement ratio (SER) of ECA?109 and TE?13 cells were 1.35 and 1.43, respectively. Flow cytometry showed that the apoptosis rate of ECA?109 and TE?13 cells in the combined group were significantly higher than those of the radiation group [ for ECA?109 cells, ( 41. 31 ± 1. 52)% vs. ( 9. 54 ± 0.52)%;for TE?13 cells, (46.28±0.28)% vs. (11.32±0.31)%, both P<0.01]. Western blotting showed that the expression levels of EGFR and DNA?PKcs were not significantly different in all groups ( all P>0.05) . Compared with those of the control group, p?EGFR and p?DNA?PKcs of the radiation group were significantly higher in both cell lines ( P<0.05) , and theγH2AX levels in the radiation group and medicine group were significantly higher than that of the control group ( P<0.05) . Compared with those of the radiation group and medicine group, p?EGFR and p?DNA?PKcs protein expression in the combined group were decreased significantly (P<0.05), while γH2AX protein expression was significantly increased (P<0.05). Conclusions Nimotuzumab can enhance the radiosensitivity of esophageal cancer ECA?109 and TE?13 cells. The potential mechanism may be related to the inhibition of EGFR phosphorylation and down?regulation of DNA damage repair proteins. The radiosensitizing effect of nimotuzumab is greater on poorly differentiated esophageal cancer cells.

Objective To investigate the effects of nimotuzumab on radiosensitivity of ECA?109 and TE?13 esophageal carcinoma cell lines and explore its possible mechanism. Methods The ECA?109 and TE?13 cells were divided into control group, irradiation group, medicine group, and combined group ( irradiation + medicine) . In the combined group, ECA?109 and TE?13 cells were treated with nimotuzumab for 24 h before irradiation, and the cells were collected 2 h after irradiation. The radiosensitizing effects of nimotuzumab on ECA?109 and TE?13 cells were evaluated by clone formation assay. Cell apoptosis was detected by flow cytometry. Western blotting was used to evaluate the expression of EGFR, p?EGFR, DNA?PKcs, p?DNA?PKcs and γH2AX. Results The values of Dq( quasithreshold dose) , D0( mean lethal dose) and SF2(surviving fraction at 2 Gy) of ECA?109 and TE?13 cells in the combined group were significantly lower than those of the radiation group ( for ECA?109 cells, 1. 11 vs. 1. 72, 1. 40 vs. 2. 14, 0. 42 vs. 0. 66, respectively;for TE?13 cells, 0.41 vs. 0.46, 0.43 vs. 0.65, 0.40 vs. 0.71, respectively ( all P<0.05) . The sensitivity enhancement ratio (SER) of ECA?109 and TE?13 cells were 1.35 and 1.43, respectively. Flow cytometry showed that the apoptosis rate of ECA?109 and TE?13 cells in the combined group were significantly higher than those of the radiation group [ for ECA?109 cells, ( 41. 31 ± 1. 52)% vs. ( 9. 54 ± 0.52)%;for TE?13 cells, (46.28±0.28)% vs. (11.32±0.31)%, both P<0.01]. Western blotting showed that the expression levels of EGFR and DNA?PKcs were not significantly different in all groups ( all P>0.05) . Compared with those of the control group, p?EGFR and p?DNA?PKcs of the radiation group were significantly higher in both cell lines ( P<0.05) , and theγH2AX levels in the radiation group and medicine group were significantly higher than that of the control group ( P<0.05) . Compared with those of the radiation group and medicine group, p?EGFR and p?DNA?PKcs protein expression in the combined group were decreased significantly (P<0.05), while γH2AX protein expression was significantly increased (P<0.05). Conclusions Nimotuzumab can enhance the radiosensitivity of esophageal cancer ECA?109 and TE?13 cells. The potential mechanism may be related to the inhibition of EGFR phosphorylation and down?regulation of DNA damage repair proteins. The radiosensitizing effect of nimotuzumab is greater on poorly differentiated esophageal cancer cells.