Archives of pathology & laboratory medicine · 2001
Analysis of 2 antiapoptotic factors in gliomas: bcl-2 overexpression and p53 mutations.
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Rodriguez-Pereira C, Suarez-Peñaranda J M, Barros F, Sobrido M J, Vazquez-Salvado M, Forteza J
Аннотация
BACKGROUND: p53 mutations and immunoreactivity have been described in human gliomas. During the past few years, some authors have found bcl-2 overexpression in astrocytomas, although their correlation with histological grade is a matter of disagreement. A relation between bcl-2 overexpression and p53 immunoreactivity has also been suggested.
OBJECTIVES: To analyze the frequency of presentation of bcl-2 and p53, their clinicopathologic implications, and their possible coexpression.
METHODS: We studied p53 and bcl-2 with immunohistochemical and molecular methods in 61 gliomas (including 21 astrocytomas, 9 anaplastic astrocytomas, 29 glioblastomas, 1 oligodendroglioma, and 1 mixed glioma).
RESULTS: We discovered a high level of bcl-2 overexpression (57%). Overexpression of bcl-2 can be an early event in gliomas tumorigenesis, although no correlation was found with any of the clinicopathologic parameters studied. p53 mutations were present in a small proportion of gliomas (17%). p53 immunoreactivity was present in 34 cases (57%), and it was related to histological grade and a supratentorial location. A high percentage of tumors (26 cases, 42%) presented p53 immunoreactivity without p53 mutations.
CONCLUSIONS: Since there was no relation between bcl-2 overexpression and p53 mutations or p53 immunoreactivity, both factors may not act together in the genesis and evolution of gliomas.
OBJECTIVES: To analyze the frequency of presentation of bcl-2 and p53, their clinicopathologic implications, and their possible coexpression.
METHODS: We studied p53 and bcl-2 with immunohistochemical and molecular methods in 61 gliomas (including 21 astrocytomas, 9 anaplastic astrocytomas, 29 glioblastomas, 1 oligodendroglioma, and 1 mixed glioma).
RESULTS: We discovered a high level of bcl-2 overexpression (57%). Overexpression of bcl-2 can be an early event in gliomas tumorigenesis, although no correlation was found with any of the clinicopathologic parameters studied. p53 mutations were present in a small proportion of gliomas (17%). p53 immunoreactivity was present in 34 cases (57%), and it was related to histological grade and a supratentorial location. A high percentage of tumors (26 cases, 42%) presented p53 immunoreactivity without p53 mutations.
CONCLUSIONS: Since there was no relation between bcl-2 overexpression and p53 mutations or p53 immunoreactivity, both factors may not act together in the genesis and evolution of gliomas.