in vitro Biological Response of Malignant Glioma Cell Lines to Gamma Knife Irradiation.
- Author:
Jeong Eun KIM
1
;
Sun Ha PAEK
;
Hyun Tai CHUNG
;
Dong Gyu KIM
;
Hee Won JUNG
Author Information
1. Department of Neurosurgery, Clinical Research Institute, Seoul National University College of Medicine, Seoul, Korea. hwnjung@snu.ac.kr
- Publication Type:In Vitro ; Original Article
- Keywords:
Malignant glioma;
In vitro;
Gamma knife;
Cell cycle
- MeSH:
Apoptosis;
Cell Cycle;
Cell Cycle Checkpoints;
Cell Line*;
Cell Survival;
Flow Cytometry;
Glioma*;
Humans;
Radiosurgery
- From:Journal of Korean Neurosurgical Society
2004;35(6):599-604
- CountryRepublic of Korea
- Language:English
-
Abstract:
OBJECTIVE: The effectiveness of gamma knife radiosurgery to malignant glioma has been controversial. The goal of this study is to elucidate the in vitro biological response of malignant glioma cells to gamma knife radiosurgery. METHODS: The human glioma cell lines U87 MG (p53-wild type) and U373 MG (p53-mutant type) were irradiated in vitro via Gamma Knife 23004B2 using specially designed well holder, with a maximal dose of 10, 20, 40, 80Gy. Those two cell lines were used to study a variety of gamma knife effects on morphological change by microscopic observation, on cell viability by MTT assay, on postirradiated apoptosis by annexin assay, and on cell cycle by flow cytometry. RESULTS: With increasing dosage, more spheroid cells were observed in tumor cells and this phenomenon peaked at the second day after gamma knife irradiation. MTT assay performed 3 hours after irradiation revealed reduced cell survival in the cells irradiated with over 20Gy (p=0.000). The annexin assay showed that apoptosis tended to increase on escalating the radiation dose in U87 cells. G2-M phase cell cycle arrest markedly increased 48 hours after irradiation, and this was more exaggerated in U373 MG than in U87 MG. CONCLUSION: These results suggest that the biological effect of gamma knife on malignant glioma cell line in vitro is mainly mediated by G2-M phase cell cycle arrest.