並列タイトル等CNS WHO Grade 2 および Grade 3 髄膜腫における、MTAP免疫組織化学とFISH解析によるCDKN2Aコピー数および臨床病理学的特徴との相関性
一般注記type:Thesis
CDKN2A homozygous deletion has occasionally been reported in atypical and anaplastic meningiomas and is considered as one of the genetic alterations commonly involved in their recurrence and malignant progression. Methylthioadenosine phosphorylase (MTAP) immunohistochemistry is a promising surrogate marker for CDKN2A homozygous deletion in different cancers but has not been examined in meningiomas. We performed CDKN2A FISH and MTAP immunohistochemistry on specimens from 30 patients with CNS WHO grade 2 (n = 27) and 3 (n = 3) meningiomas, including specimens from primary and recurrent tumors and then determined whether MTAP immunohistochemistry correlated with CDKN2A homozygous deletion and clinicopathological features. CDKN2A homozygous deletion was detected in 12% (3/26) of CNS WHO grade 2 and 67% (2/3) of CNS WHO grade 3 meningiomas; 3 cases exhibited temporal and/or spatial heterogeneity. MTAP loss was in excellent concordance with CDKN2A homozygous deletion (sensitivity; 100%, specificity; 100%). MTAP loss/CDKN2A homozygous deletion correlated with cellular proliferation (mitotic rate; p = 0.001, Ki-67 labeling index; p = 0.03) and poor prognosis (overall survival; p = 0.01, progression free survival; p < 0.001). Thus, MTAP immunostaining can be a surrogate marker for CDKN2A homozygous deletion in meningiomas, and MTAP loss/CDKN2A homozygous deletion may be an important prognostic factor for meningiomas.
博士(医学)・甲第840号・令和4年3月15日
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This is a pre-copyedited, author-produced version of an article accepted for publication in Journal of neuropathology and experimental neurology following peer review. The version of record "Vol.81 issue 2 p.117-126 (2022 Jan 29)" is available online at: https://doi.org/10.1093/jnen/nlab127.
identifier:Journal of neuropathology and experimental neurology Vol.81 No.2 p.117-126 (2022 Feb)
identifier:00223069
identifier:http://ginmu.naramed-u.ac.jp/dspace/handle/10564/4023
identifier:Journal of neuropathology and experimental neurology, 81(2): 117-126
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