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p53 accumulation and apoptosis in embolized meningiomas
S Nakasu1, M Nakajima, T Nakazawa
1Department of Neurosurgery, Shiga University of Medical Science, Japan.
Acta Neuropathologica
|June 1, 1997
Summary
Preoperative embolization of meningiomas induces cell cycle arrest and apoptosis, not just necrosis. This suggests embolization impacts non-necrotic tumor cells, potentially mediated by p53 and p21.
Area of Science:
- Neurosurgery
- Oncology
- Cell Biology
Background:
- Preoperative embolization of meningiomas aims to reduce surgical blood loss.
- Its effect on non-necrotic tumor cell behavior, beyond necrosis induction, is poorly understood.
Purpose of the Study:
- To investigate the impact of preoperative embolization on the proliferative activity and cell cycle regulation of meningioma cells.
- To assess the roles of p53 and p21 in post-embolization tumor cell responses.
Main Methods:
- Immunohistochemistry was used to evaluate MIB-1 (proliferation), p53, and p21 expression in nine embolized meningiomas and controls.
- Terminal deoxynucleotidyl transferase-mediated dUTP-digoxigenin nick end labeling (TUNEL) was employed to detect apoptosis.
Main Results:
- MIB-1 positive cells and p53/p21 accumulation were observed in perinecrotic areas of embolized meningiomas.
- Apoptosis was detected in these same areas.
- While mean proliferation index was unchanged, co-expression of MIB-1 and p21 suggested cell cycle arrest.
Conclusions:
- Preoperative embolization of meningiomas induces not only necrosis but also apoptosis and cell cycle arrest.
- These effects, particularly cell cycle arrest, appear to be at least partly dependent on the p53 pathway.