Piva R, Cavalla P, Bortolotto S, Cordera S, Grosso R, Richiardi P, Dutto A, Schiffer D
Department of Neuroscience, University of Turin, via Cherasco, 15 I-10126 Turin, Italy.
Int J Oncol. 1998 Jan;12(1):55-8. doi: 10.3892/ijo.12.1.55.
CDKN2/p16 inactivation is the most frequent alteration in the molecular regulation of G1-S transition. CDKN2/p16 homozygous deletions was studied in paraffin-embedded sections of 45 astrocytic tumours by multiplex PCR. Immunohistochemistry for p16 and proliferation marker Ki-67 MIB-1 was performed in adjacent sections; their labelling index (LI) have been calculated. CDKN2/p16 gene was not deleted in astrocytomas, while homozygous deletion was found in 26.7% anaplastic astrocytomas, and in 55.0% of glioblastomas. Analysis of CDKN2/p16 homozygous deletion in discrete areas of the same tumour, showed that the deletion occurred independently of the phenotypic aspect of the areas. Nevertheless a genotypic and phenotypic heterogeneity is present in few cases. p16 immunohistochemistry mostly corresponds to the genotypic pattern. No correlation was found between CDKN2/p16 homozygous deletion and MIB-1 LI.
CDKN2/p16失活是G1-S期转换分子调控中最常见的改变。通过多重PCR在45例星形细胞瘤石蜡包埋切片中研究了CDKN2/p16纯合缺失情况。在相邻切片中进行p16和增殖标志物Ki-67 MIB-1的免疫组织化学检测；计算了它们的标记指数（LI）。星形细胞瘤中未发现CDKN2/p16基因缺失，而在26.7%的间变性星形细胞瘤和55.0%的胶质母细胞瘤中发现了纯合缺失。对同一肿瘤不同区域的CDKN2/p16纯合缺失分析表明，缺失的发生与这些区域的表型无关。然而，少数病例存在基因型和表型异质性。p16免疫组织化学结果大多与基因型模式相符。未发现CDKN2/p16纯合缺失与MIB-1 LI之间存在相关性。
