APOPTOSIS IN GLIAL TUMORS AS DETERMINED BY IN-SITU NONRADIOACTIVE LABELING OF DNA BREAKS

Tumor growth depends on cell division and cell death. To investigate t he role of apoptosis in tumor cell death, we examined 83 cases of glia l tumors using in situ nonradioactive tailing of DNA breaks. In additi on, since p53 protein may participate in the regulation of apoptosis i n glioblastoma, we compared the apoptosis ratio (AR) with the labeling index (LI) of p53 protein immunopositivity. The AR in glial tumor par enchyma ranged from 0 to 1.4%: mean AR +/- standard deviation was 0.4 +/- 0.4% (range, 0-1.4) for glioblastoma, 0.3 +/- 0.3% (range, 0.01-0. 83) for anaplastic astrocytoma, 0.1 +/- 0.1% (range, 0-0.41) for low-g rade astrocytoma, 0.006 +/- 0.008% (range, 0-0.02) for pilocytic astro cytoma, 0.2 +/- 0.2% (range, 0-0.62) for oligodendroglioma and 0.003 /- 0.004% (range, 0-0.01) for ependymoma. ARs were significantly highe r in higher-grade astrocytic tumors than in lower-grade tumors (Mann-W hitney U test: P = 0.0003), although wide variability in each group re sulted in overlapping between the groups. p53 protein immunopositivity (more than 25% of nuclei) was found in 15 of 32 glioblastoma cases, w hile in the remaining 17 none or only a low percentage (up to 6%) of t he nuclei were positive. In p53 protein-positive cases mean AR (0.51 /- 0.47%) was not significantly higher than that in p53 protein-negati ve cases (0.22 +/- 0.23%; P = 0.1681).