Influence of intensity-modulated radiotherapy on tumor regression in nasopharyngeal carcinoma / 中华放射医学与防护杂志

Objective To retrospectively analyze the influence of intensity-modulated radiotherapy (IMRT) on tumor regression in primary nasopharyngeal carcinoma (NPC).Methods 272 patients with NPC received radical radiotherapy alone,196 by IMRT with a total treatment time of 6 weeks,and 76 by bilateral field conventional radiotherapy (CRT) with the total treatment timc of 7 weeks.Results By the end of radiotherapy,the primary tumor and neck lymph node residual rates of the IMRT group were 36.7％ and 44.2％,respectively,both significantly higher than those of the GRT group (21.1％ and 26.6％,x2 =6.15,3.99,P ＜ 0.05).Three months after the radiotherapy,residual lesions were observed at the nasopharynx or neck lymph nodes in 12 of the IMRT group,with a residual rate of 6.1％,not significantly different from that of the CRT group (9.2％,7/76).The 12 residual lesions of the IMRT group all vanished completely 4 -9 months after the radiotherapy.Conclusions There is an obvious difference in regressive mode between IMRT and CRT technique in NPC treatment.At the end of IMRT,the tumor residual rate is slightly increased.However,the delivered dose of gross tumor volume (GTV) is sufficient,and the boost dose should not be delivered indiscreetly.

Molecular Aspects of Radiotherapy

When tumor cells are exposed to ionizing radiation, various and complicated molecular biological changes take place leading to cell death, mutation, and recovery from sublethal damage. It has been known that DNA is the major critical target of radiation leading to cell death. The radiation-induced DNA damage activates ATM/ATR which then lead to activation and phosphorylation of downstream molecular signals, such as p53. Phosphorylation of p53 leads to inhibition of cell cycle progression, cell death through apoptosis and repair of damaged DNA. Recent evidence clearly demonstrated that p53 is directly involved in activation of cell cycle checkpoints resulting in G1 arrest and G2 arrest. During these arrests, the damaged DNA are repaired. However, when the radiation-induced DNA damage is excessive, cells undergo apoptotic cell death. Here again, p53 is involved in activation of pro-apoptotic signals such as Bax and caspases and inactivation of anti-apoptotic signals such as Bcl-2. Proper activation or intervention of these molecular signals may enable us to enhance the radiation damage in cancer cells and improve the efficacy of radiotherapy of malignant cancer.