Failure of betamethasone to alter the radiation response of two cultured human glioma cell-lines.

Glucocorticoids, such as betamethasone, are often used to prevent possible acute reactions during radiation therapy of intracranial tumors (for example gliomas). The effect of the glucocorticoids is probably due to vascular changes decreasing the development of edemas. The radiosensitivity of two studied cell-lines of human malignant glioma origin did not significantly change when they were continuously exposed to betamethasone in the concentration range of 1-25 micrograms/ml. The radiosensitivity was measured with the extrapolation method, which gave an estimate of cell survival, and through direct measurements of growth delays from growth curves. The results obtained are in conformity with previously published results where clonogenic survival tests showed that the isomer dexamethasone did not change the radiosensitivity of these cells. Thus, no direct effects on the radiosensitivity of glioma cells are expected from glucocorticoid treatment and it is therefore unlikely that the poor results obtained from radiation therapy of malignant gliomas are due to an increased radioresistance brought on by the glucocorticoid treatment.