机构地区:[1]复旦大学上海医学院病理学系,200032 [2]复旦大学附属华山医院神经病理室 [3]华山医院神经外科
出 处:《中华病理学杂志》2009年第7期445-450,共6页Chinese Journal of Pathology
基 金:复旦大学附属华山医院科研启动基金
摘 要:目的探讨少突胶质细胞瘤染色体10/19q杂合性缺失及p53蛋白的表达情况,与星形细胞起源的肿瘤进行比较研究并探讨其意义。方法选择2004—2005年间,经病理组织学诊断为不同类型和级别的胶质瘤合计191例,包括:WHO1I级少突胶质细胞瘤116例,其中30例为新鲜组织;间变性少突胶质细胞瘤45例和不同级别星形细胞起源的肿瘤石蜡组织30例;采用PCR-微卫星技术检测染色体1p/19q杂合性缺失情况;采用免疫组织化学方法对184例胶质瘤石蜡切片p53蛋白表达情况进行半定量分析。结果86例WHOⅡ级少突胶质细胞瘤石蜡标本染色体1p缺失率为69.8%(60/86)、19q缺失率为64.0%(55/86)、1p/19q联合缺失率为57.0%(49/86);45例间变性少突胶质细胞瘤中,1P缺失率为71.1%(32/45)、19q缺失率为60.0%(27/45)、1p/19q联合缺失率为55.6%(25/45);两种级别间差异无统计学意义(P〉0.05)。30例WHOⅡ级少突胶质细胞瘤新鲜标本染色体1p缺失率为70.0%(21/30)、19q缺失率为63.3%(19/30)、1p/19q联合缺失率为60.0%(18/30),与石蜡标本的缺失率比较差异无统计学意义(P〉0.05)。30例星形细胞起源的肿瘤染色体对应三种缺失率分别为23.3%(7/30)、33.3%(10/30)及20.0%(6/30),与少突胶质细胞瘤差异有统计学意义(P〈0.05)。86例WHOⅡ级少突胶质细胞瘤中,仅7例有p53蛋白阳性表达(占8.1%);45例间变性少突胶质细胞瘤中,有14例呈阳性表达(31.1%),两者差异有统计学意义(P=0.007)。少突胶质细胞瘤053蛋白阳性表达明显低于星形细胞起源的肿瘤(P=0.001)。在间变性少突胶质细胞瘤中,染色体10/19q杂合性缺失与053蛋白阳性表达呈负相关(P〈0.05)。结论石蜡和新鲜组织均可用于染色体1p/19q杂合性缺失的检测。在Objeetive To study the status of loss of heterozygosity (LOH) of chromosome 1p/19q and p53 protein expression in oligodendroglioma, as compared to astrocytoma. Methods One hundred and ninety-one cases of glioma of different histologic types and grades, including 116 cases of low-grade of oligodendroglioma (86 paraffin-embedded and 30 fresh tissues) , 45 cases of anaplastic oligodendroglioma (al1paraffin-embedded tissues ) and 30 cases of astrocytoma of various grades (al1paraffin-embedded tissues), were enrolled into the study. The LOH of chromosome 1p/19q was investigated by polymerase chain reaction (PCR)-based microsatellite analysis. The p53 protein expression was demonstrated by immunohistochemical staining. Results The rates of 1p loss, 19q loss and 1p/19q loss were 69. 8% ,64%, and 57.0% respectively in the 86 paraffin-embedded low-grade oligodendroglioma samples, as compared to 71.1%, 60.0% and 55.6% respectively in the 45 paraffin-embedded anaplastic oligodendroglioma samples. There was no difference of LOH of 1p/19q between low-grade oligodendroglioma and anaplastic oligodendroglioma ( P 〉 0. 05 ). In the 30 cases of low-grade oligodendroglioma with fresh tissues available, the rates of 1p loss, 19q loss and 1p/19q loss were 70.0%, 63.3% and 60. 0% respectively. The LOH of 1p/19q between paraffin-embedded and fresh samples was not statistically significant (P 〉0. 05). In the 30 cases of astrocytoma, the rates of 1p loss, 19q loss and 1p/19q loss were 23.3%, 33.3% and 20. 0% respectively, which were significantly less than those in oligodendroglioma (P 〈 0. 05 ). The expression of p53 protein was significantly lower in low-grade oligodendroglioma (8. 1% ) than in anaplastie oligodendroglioma (31.1%, P = 0. 007 ). The expression of p53 protein in oligodendroglioma was also lower than in astrocytoma ( P = 0. 001 ). Furthermore, p53 protein expression negatively correlated with 1p/19q loss in anaplastic oligodendroglioma (P 〈 0. 05 ). Conclusions Both
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