© 2001 by Society
© 2001 by the Society forNeuro-Oncology
Accumulation of 8-oxo-2'-deoxyguanosine and increased expression ofhMTH1 protein in brain tumors
Department of Neuropathology, Neurological Institute,Graduate School of Medical Sciences (T.Ii., A.F., M.K., T.Iw.), Department of Biochemistry, Medical Institute ofBioregulation (J.N., Y.N.), Kyushu University, Fukuoka, 812-8582, Japan;and Core Research for Evolutional Science andTechnology, Japan Science and Technology Corporation, Tokyo, 105-0011, Japan(T.Ii., A.F., Y.N., T.Iw.)
1 Address correspondence and reprint requests to Dr. Takashi Iida, Department ofNeuropathology, Neurological Institute, Graduate School of Medical Sciences,Kyushu University 60, Fukuoka, 812-8582, Japan.
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Abstract |
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Oxidative DNA damage generated by an attack of reactive oxygen speciescauses mutation or cell death that may lead to various diseases and may berelated to initiation or progression of carcinogenesis. 8-Oxo-2 deoxyguanosine(8-oxo-dG) is a major oxidative DNA damage product that can result inmutation, and hMTH1, human MutT homolog protein 1, has been identified as anenzyme that hydrolyzes 8-oxo-dGTP to the monophosphate, thus preventingaccumulation of 8-oxo-dG in DNA. With immunohistochemical approaches, weinvestigated accumulation of 8-oxo-dG and expression of hMTH1 in brain tumortissues obtained from surgical and autopsy cases, including 42 neuroepithelialtumors, 5 meningiomas, 2 metastatic brain tumors, and 1 schwannoma. 8-Oxo-dGaccumulation and hMTH1 expression were increased in various brain tumors.Nuclei of brain tumor cells were immunoreactive for 8-oxo-dG in all cases. Inmost cases, both nuclei and cytoplasm of the tumor cells were immunoreactivefor hMTH1. Both 8-oxo-dG accumulation and hMTH1 expression were most evidentin high-grade gliomas, indicating that oxidative stress was high in thesegliomas. Thus, the defense mechanism against such oxidative stress may beenhanced as well. These results suggest that oxidative stress may play a rolein tumor progression.
Received October 19, 2000; Accepted December 20, 2000
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