• Kevin C Yao, Tadashi Komata, Yasuko Kondo, Takao Kanzawa, Seiji Kondo, and Isabelle M Germano.
• Department of Neurosurgery, Mount Sinai School of Medicine, New York, New York, USA.
• J. Neurosurg. 2003 Feb 1; 98 (2): 378-84.

ObjectIonizing radiation is the gold-standard adjuvant treatment for glioblastoma multiforme (GBM), the most aggressive primary brain tumor. The mechanisms underlying neoplastic glial cell growth inhibition after administration of ionizing radiation, however, remain largely unknown. In this report, the authors characterize the response of GBM cells to ionizing radiation and elucidate factors that correlate with the radiosensitivity of these tumors.MethodsSix human GBM cell lines were subjected to increasing doses of radiation. Each demonstrated a dose-dependent suppression of cell proliferation. In the most radiosensitive cell line, the authors demonstrated a transient increase in the expression of the cyclin-dependent kinase inhibitors (CDKIs) p21 and p27, which corresponded with a G1 cell-cycle arrest. In contrast, the most radioresistant cell line demonstrated a decrease in p21 and p27 expression levels, which correlated with a failure to arrest. Apoptosis did not occur in any cell line following irradiation. Instead, autophagic cell changes were observed following administration of radiation, regardless of the relative radiosensitivity of the cell line.ConclusionsThese findings elucidate some of the molecular responses of GBMs to irradiation and suggest novel targets for future therapy.

38 keywords...

hide…