Long-term molecular changes in WHO grade II astrocytomas following radiotherapy.
- Author:
Wei-Ying YUE
1
;
Ke SAI
;
Qiu-Liang WU
;
Yun-Fei XIA
;
Su-Huan YU
;
Zhong-Ping CHEN
Author Information
- Publication Type:Journal Article
- MeSH: Adult; Astrocytoma; metabolism; pathology; radiotherapy; surgery; Brain Neoplasms; metabolism; pathology; radiotherapy; surgery; Cell Proliferation; radiation effects; Cell Transformation, Neoplastic; radiation effects; Cyclin-Dependent Kinase Inhibitor p21; metabolism; Cyclin-Dependent Kinase Inhibitor p27; metabolism; Female; Humans; Immunohistochemistry; Ki-67 Antigen; metabolism; Male; Middle Aged; Neoplasm Grading; Tumor Suppressor Protein p53; metabolism
- From:Chinese Journal of Cancer 2012;31(3):159-165
- CountryChina
- Language:English
- Abstract: Monitoring the long-term radiotherapy-associated molecular changes in low-grade gliomas (LGGs) facilitates the understanding of LGG response to radiotherapy. In this study, we used immunohistochemistry to analyze the expression of Ki-67, tumor protein P53 (TP53), P21, and P27 in 8 paired WHO grade II astrocytoma samples. The interval between radiotherapy (RT) and the second surgery was more than 3 months in all cases. The average Ki-67 labeling index (LI) was 5.3% in pre-RT samples and 11.54% in post-RT samples. Ki-67 LI was higher in the primary tumors that underwent malignant transformation observed at the second surgery after radiation. Post-RT Ki-67 LI decreased in 2 cases with an interval of less than 12 months between RT and the second surgery. TP53 expression was found in 3 out of 4 pre-RT samples with malignant transformation and in 1 out of 4 pre-RT samples without malignant transformation. Post-RT TP53 increased in 2 cases in which increased expression of P21 or P27 was also observed. Our study suggests that radiotherapy can inhibit WHO grade II astrocytoma proliferation as reflected by Ki-67 LI, but the effect attenuates with time. In addition, there is a tendency of malignant transformation for WHO grade II astrocytomas with a high Ki-67 level or TP53 expression in initial samples.
