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Journal of Korean Neurosurgical Society 2003;33(2): 126-131.
Methylation Status of CpG Island of p16 in Benign, Atypical and Malignant Meningiomas.
Jeong Hoon Kim, Jae Sung Ahn, Sang Ryong Jeon, Yong Hee Shim, Chang Jin Kim, Jung Kyo Lee
1Department of Neurological Surgery, Asan Medical Center, College of Medicine, University of Ulsan, Seoul, Korea.
2Department of Diagnostic Pathology, Asan Medical Center, College of Medicine, University of Ulsan, Seoul, Korea.
Hypermethylation of p16, a tumor suppressor gene, has been frequently detected in a variety of cancer cells and is known to represent the level of p16 transcription. In human meningiomas, genetic alterations of p16 have shown to be infrequent. The purpose of this study is to investigate the role of p16 associated with the progression of meningiomas. METHODS: Sixty-eight meningiomas(randomly sampled 29 benign, 16 atypical and 23 malignant formalin-fixed, paraffin-embedded tissues) were analyzed. We examined the molecular mechanism of inactivation of p16 in these benign, atypical and malignant meningiomas by detecting the methylation status of p16 using methylation-specific polymerase chain reaction. RESULTS: One out of 29(3.4%) revealed hypermethylation of p16 in benign meningiomas. Atypical and malignant meningiomas showed hypermethylation of p16 in 2 out of 16 cases(12.5%) and in 5 out of 23 cases(21.7%), respectively. Immunohistochemical analysis of methylation-positive tumors demonstrated that tumor cells had reduced immunoreactivity compared to normal lymphocytes. CONCLUSIONS: Our results suggest that inactivation of p16 gene plays a role in the pathogenesis of meningioma and hypermethylation is one of the processes for gene inactivation.
Key Words: Hypermethylation; p16; Meningiomas; Methylation-specific PCR
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