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[目的]探讨不同种类脑肿瘤患者全血p16基因的缺失及5’CpG岛甲基化情况。[方法]利用PCR和PCR-based甲基化技术检测不同种类脑肿瘤(星形细胞瘤43例、脑膜瘤8例、垂体瘤5例)p16基因的缺失及p16基因5’CpG岛甲基化。[结果]12例脑星形细胞瘤p16E1和p16E2均缺失,占28%(12/43),2例仅缺失p16E1,占5%(2/43);p16E基因缺失多发生在Ⅲ-Ⅳ级脑星形细胞瘤中(Ⅲ级6/16,Ⅳ级8/14),Ⅰ、Ⅱ级与Ⅲ、Ⅳ级比较差异有统计学意义(P﹤0.05)。2例脑膜瘤p16E1基因缺失占25%(2/8)、1例垂体瘤发生p16E1基因缺失,占20%(1/5)。无p16基因缺失的39例脑星形细胞瘤中2例有P16基因5’CpG岛甲基化,占5%(Ⅲ级1/10,Ⅳ级1/6);Ⅰ、Ⅱ级与Ⅲ、Ⅳ级甲基化比较差异无统计学意义(P﹥0.05)。[结论]p16基因失活可能与脑星形细胞瘤的分化程度有关,p16基因缺失是p16基因失活的主要机制。
[Objective] To investigate the deletion of p16 gene and methylation of 5’CpG island in whole blood of patients with different types of brain tumors. [Method] The deletion of p16 gene and the 5’CpG island methylation of different kinds of brain tumors (astrocytoma 43, meningioma 8, pituitary tumor 5) were detected by PCR and PCR-based methylation . [Results] The percentages of p16E1 and p16E2 were all 12 (12/43) in 12 cases of astrocytoma, and only 2% of p16E1 was deleted in 2 cases (p < In astrocytoma (Grade Ⅲ, 6/16, Grade Ⅳ, 8/14), there were significant differences in grade Ⅰ, Ⅱ and Ⅲ, Ⅳ (P <0.05). The deletion of p16E1 gene was found in 2 of 25 cases (2/8) in 2 cases of meningioma and in 1 case of pituitary adenoma (20% (1/5)). There were 5 cases of P16 gene 5’CpG island methylation in 5 cases (grade 1/10, grade 1/6) in 39 cases of brain astrocytomas without p16 gene deletion; Grade Ⅰ, Ⅱ and Ⅲ, Ⅳ methylation was no significant difference (P> 0.05). [Conclusion] The inactivation of p16 gene may be related to the degree of differentiation of astrocytomas, and the loss of p16 gene is the main mechanism of p16 gene inactivation.