Loss of maternal alleles on chromosome arm 11p in hepatoblastoma.
Loss of maternal alleles on chromosome arm 11p in hepatoblastoma.
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DOI：
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发表时间：
1994-10
期刊：
影响因子：
11.2
通讯作者：
Steffen Albrecht;D. Schweinitz;A. Waha;Jürgen Kraus;Andreas von Detailing;Torsten Pietsch
中科院分区：
文献类型：
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作者：
Steffen Albrecht;D. Schweinitz;A. Waha;Jürgen Kraus;Andreas von Detailing;Torsten Pietsch
肝母细胞瘤是儿童最常见的原发性恶性肝脏肿瘤，但对这些肿瘤的分子遗传变化知之甚少。先前的研究报道了一些肝母细胞瘤中染色体臂11p的杂合性缺失。我们使用聚合酶链反应在染色体臂11p上扩增多个微卫星来评估18例肝母细胞瘤的杂合性损失。其中6例发现11p杂合性缺失。共有重叠区域仅限于11p的端粒部分（11p15.5），因此排除了11p13的WT-1肿瘤抑制基因。缺失等位基因的亲本起源在所有6例中都可以确定，并且完全是母系的。这些结果表明，11p15.5的肿瘤抑制基因参与了肝母细胞瘤的发病过程，也表明该染色体区域是印迹的。
Hepatoblastoma is the most common primary malignant liver tumor in children, yet little is known about molecular genetic changes in these tumors. Previous studies report loss of heterozygosity on chromosome arm 11p in some hepatoblastomas. We used the polymerase chain reaction to amplify multiple microsatellites on chromosome arm 11p to assess loss of heterozygosity in 18 hepatoblastomas. Loss of heterozygosity on 11p was found in six of them. The common region of overlap was restricted to the telomeric portion of 11p (11p15.5) and therefore excluded the WT-1 tumor suppressor gene at 11p13. Parental origin of the lost allele could be determined in all six cases and was exclusively maternal. These results indicate that a tumor suppressor gene at 11p15.5 is involved in the pathogenesis of hepatoblastoma and also suggest that this chromosomal region is imprinted.