CAJ | 학술논문

胶质瘤放化疗耐受现象的分子机制是一个多信号通路构成的复杂网络,近年来的研究表明细胞DNA损伤检控点ATM、ATR、Chk1、Chk2、Rad17、Rad1、Rad9、Hus1等及其调节通路在细胞增殖、基因组的稳定以及肿瘤的发生和肿瘤放化疗耐受机制中发挥重要的作用.干预细胞DNA损伤检控点能够增加放化疗耐受肿瘤细胞对放化疗的敏感性,提高疗效.
효질류방화료내수현상적분자궤제시일개다신호통로구성적복잡망락,근년래적연구표명세포DNA손상검공점ATM、ATR、Chk1、Chk2、Rad17、Rad1、Rad9、Hus1등급기조절통로재세포증식、기인조적은정이급종류적발생화종류방화료내수궤제중발휘중요적작용.간예세포DNA손상검공점능구증가방화료내수종류세포대방화료적민감성,제고료효.
The resistance mechanism of gliomas to chemotherapy and radiotherapy is a complex network of many signaling pathways. It remains unclearhow the pathways interact with each other and how they were regulated. Recent studies have shown that DNA damage checkpoint pathway ( ATM、 ATR、 Chk1、 Chk2、 Rad17、 Radl 、Rad9、Hus1 et al. ) plays an important role in cell proliferation、genomic stability、tumorigenesis and the resistance to chemoradiotherapy of tumors. Inhibiting DNA damage checkpoint can increase tumor sensitivity to chemoradiotherapy and therefore improve the therapeutic effect. We review here the role of ATM in chemoradiotherapy resistance of gliomas and its associated mechanisms.