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Apoptosis in astrocytic neoplasms
R S Carroll1, J Zhang, B W Chauncey
1Neurosurgical Laboratories, Brigham and Women's Hospital, Boston, MA, USA.
Abstract:
Apoptosis is a form of programmed cell death characterized by specific morphologic and biochemical properties. Tumorgenesis is the consequence not only of cell proliferation but also the loss of the ability to undergo apoptosis [2]. Bcl-2 is a protooncogene which has the ability to block apoptosis in many cell types. Astrocytic neoplasms are very aggressive tumors which many times fail to respond to surgery, radiation or chemotherapy. They frequently overexpress wild-type p53 which is associated with the expression of bcl-2, and thus they may have evolved a mechanism to subvert apoptosis and allow continued growth. We examined the apoptotic index in fifty-nine astrocytic tumors of various histological grades (Oncor ApopTag Plus In Situ Detection Kit) and compared this with the level of bcl-2 expression. Low grade astrocytomas (0.21 +/- 0.05; range 0.0-0.9) and anaplastic astrocytomas (0.27 +/- 0.13; range 0.0-2.6) had significantly less apoptosis than glioblastomas (0.70 +/- 0.13; range 0.0-2.1; Kruskal-Wallis test, P < or = 0.01). In contrast, bcl-2 expression was similar in all grades of astrocytic tumors and did not correlate with the apoptotic index. Cells of low grade and anaplastic astrocytomas are less likely to undergo apoptosis; however, this does not seem to be a direct consequence of the regulation of bcl-2 expression. The difference in growth potential despite differences in apoptotic index is likely to be attributed to differences in mitotic not apoptotic activity.
Insights
Programmed cell death (apoptosis) is crucial in preventing tumor growth. This study found that while astrocytic tumors show reduced apoptosis, bcl-2 expression doesn't correlate with this, suggesting other factors drive tumor progression.
Area of Science:
- Neuro-oncology
- Cell Biology
- Cancer Research
Background:
- Apoptosis, or programmed cell death, is a critical mechanism that prevents uncontrolled cell proliferation and tumor development.
- Astrocytic neoplasms are aggressive brain tumors often resistant to standard treatments.
- Overexpression of p53 and bcl-2 in astrocytomas suggests potential mechanisms for evading apoptosis and promoting tumor growth.
Purpose of the Study:
- To investigate the relationship between the apoptotic index and bcl-2 expression in astrocytic tumors of varying grades.
- To determine if bcl-2 expression is a key factor in the reduced apoptosis observed in astrocytic neoplasms.
Main Methods:
- Fifty-nine astrocytic tumors of different histological grades were analyzed.
- The apoptotic index was quantified using the Oncor ApopTag Plus In Situ Detection Kit.
- Bcl-2 expression levels were assessed and compared across tumor grades.
Main Results:
- Glioblastomas exhibited a significantly higher apoptotic index compared to low-grade and anaplastic astrocytomas (P < 0.01).
- Bcl-2 expression levels were consistent across all astrocytic tumor grades.
- No significant correlation was found between bcl-2 expression and the apoptotic index in these tumors.
Conclusions:
- Reduced apoptosis in low-grade and anaplastic astrocytomas is not directly mediated by bcl-2 expression.
- Differences in tumor growth potential among astrocytic grades may be more strongly influenced by mitotic activity than by apoptotic regulation.
- Further research into alternative pathways regulating apoptosis and proliferation is warranted for astrocytic neoplasms.