常规分割放疗在中晚期非小细胞肺癌治疗中疗效有限,大分割放疗地位越来越重要,但仍有相当部分肿瘤细胞具有放射线抗拒,其分子机制未明。PI3K/AKT/mTOR信号通路与非小细胞肺癌常规分割放疗抗拒有关,但与大分割放疗抗拒关系尚未明确。调控PI3K/AKT/mTOR信号通路的基因表达及蛋白磷酸化水平有望增加NSCLC肿瘤细胞对大分割放疗的敏感性,并可能达到逆转放疗抗拒的效果;在PI3K/AKT/mTOR信号通路的诸多基因中,有望从临床样本中筛选获得预测NSCLC大分割放疗疗效的分子标记。
Radiotherapy is a primary treatment for lung cancer, especially for non-small cell lung cancer (NSCLC). Compared with conventional fractionated radiotherapy, hypofractionated radiotherapy (HFRT) is a powerful method in NSCLC treatment because of its convenience and excellent clinical efficacy. Although HFRT has been significantly developed for treating NSCLC, radiation resistance with an unknown molecular mechanism is still observed in tumors. The PI3K/AKT/mTOR signaling pathway significantly affects resistance to conventional fractionated radiotherapy. However, whether this pathway induces radiation resistance to HFRT remains unclear. The underlying molecular mechanisms between HFRT and the PI3K/AKT/mTOR signal pathway may be used as targets in radiation sensitivity or in the modification of radiation resistance in NSCLC patients. New predictive biomarkers can also be expected in the PI3K/AKT/mTOR signaling pathway when the clinical specimen is screened using HFRT.