Allalunis-Turner M J, Lintott L G, Barron G M, Day R S, Lees-Miller S P
Radiobiology, M. J.A-T., G. M. B. Program, Cross Cancer Institute, Edmonton, Alberta, Canada.
Cancer Res. 1995 Nov 15;55(22):5200-2.
Lack of DNA-dependent protein kinase (DNA-PK) activity confers radiosensitivity and defective DNA double-strand break repair. Nine human malignant glioma cell lines were studied to determine whether differences in DNA-PK activity reflect differences in inherent radiosensitivity or are predictive of tumor treatment response. DNA-PK activity was present in all cell extracts, as were the DNA-PK proteins, DNA-PK catalytic subunit, Ku p70, and Ku p80. No correlation was found between the levels of DNA-PK activity and inherent radiosensitivity or in the tumor treatment response. These preliminary results suggest that variation in DNA-PK activity may not be a determinant of clinical response in malignant glioma.
缺乏DNA依赖性蛋白激酶（DNA-PK）活性会导致放射敏感性增加和DNA双链断裂修复缺陷。研究了九种人类恶性胶质瘤细胞系，以确定DNA-PK活性的差异是否反映了内在放射敏感性的差异，或者是否可预测肿瘤治疗反应。所有细胞提取物中均存在DNA-PK活性，DNA-PK蛋白、DNA-PK催化亚基、Ku p70和Ku p80也同样存在。未发现DNA-PK活性水平与内在放射敏感性或肿瘤治疗反应之间存在相关性。这些初步结果表明，DNA-PK活性的变化可能不是恶性胶质瘤临床反应的决定因素。
