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Journal of Korean Neurosurgical Society 2002;31(4): 357-363.
p53 and Bcl-2 Expression and Apoptosis in Human Brain Tumors.
Hyeong Joong Yi, Choong Hyun Kim, Koang Hum Bak, Jae Min Kim, Yong Ko, Suck Jun Oh
Department of Neurosurgery, School of Medicine, Hanyang University, Seoul, Korea.
In this preliminary report, the authors investigated whether apoptosis is affected by p53 and/or Bcl-2 in the surgical specimens of the human brain tumors.
During the period from July 1998 to December 1999, seventy-six cases of surgically resected human brain tumors(meningioma 16, pituitary adenoma 13, glioblastoma 11, metastatic brain tumor 11, vestibular schwannoma 9, astrocytoma 8, anaplastic astrocytoma 6, and pineoblastoma 2) were studied. Apoptosis of the specimens was detected by DNA fragmentation analysis. Bcl-2 and p53 expression was analyzed by Western blot analysis.
Apoptosis was found in 16 tumors(21.1%), and Bcl-2 and p53 proteins were expressed in 18(23.7%) and 14(18.4%) tumors, respectively. Among 60 tumors with negative apoptosis, only 8 cases expressed p53(13.3%). Concerning the relationship between p53, Bcl-2 and apoptosis, the influence of Bcl-2 on p53 and apoptosis was not statistically significant(p=0.239). Among three groups of positive p53 expression, sole p53(+) group and combined with and without Bcl-2(+) groups, no significant difference of apoptosis induction was found(p=0.125). p53 seemed to play a more dominant role in the induction of apoptosis than Bcl-2. In 18 tumors with positive Bcl-2 expression, 16 cases(88.9%) did not show apoptosis and p53 expression was detected in 2 cases. Two cases which had Bcl-2 gene with apoptosis showed p53 expression. In our study, p53 was capable of inducing apoptosis despite the presence of Bcl-2 expression (p=0.028).
Apoptosis seemed not to be affected by Bcl-2 and the anti-apoptotic property of the Bcl-2 appeared to be attenuated by p53. Therefore, the use of p53 gene transfer to enhance the induction of apoptosis might be a potential treatment for human brain tumors irrespective of Bcl-2 expression.
Key Words: p53; Apoptosis; Bcl-2; Human brain tumors
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