Sonoda Y, Murakami Y, Tominaga T, Kayama T, Yoshimoto T, Sekiya T
Oncogene Division, National Cancer Center Research Institute, Tokyo, Japan.
Jpn J Cancer Res. 1996 Apr;87(4):363-7. doi: 10.1111/j.1349-7006.1996.tb00231.x.
We analyzed DNAs from 35 gliomas (27 malignant, grades III and IV; 8 less malignant, grades I and II) for loss of heterozygosity (LOH) using microsatellite sequences on chromosome 10 as polymorphic markers. An LOH was found in 8 of 11 (73%) glioblastomas (grade IV) and 4 of 16 (25%) grade III gliomas, but not in the less malignant types. We detected three commonly deleted regions. One was located in a telomeric region of 10p and the others were relatively large regions of 10q. Our results suggested that three putative tumor suppressor genes on chromosome 10 are involved in the malignant progression of gliomas.
我们使用10号染色体上的微卫星序列作为多态性标记,分析了35例神经胶质瘤(27例恶性,III级和IV级;8例低恶性,I级和II级)的DNA,以检测杂合性缺失(LOH)。在11例胶质母细胞瘤(IV级)中有8例(73%)和16例III级神经胶质瘤中有4例(25%)发现了LOH,但在低恶性类型中未发现。我们检测到三个常见的缺失区域。一个位于10p的端粒区域,其他两个是10q上相对较大的区域。我们的结果表明,10号染色体上的三个假定的肿瘤抑制基因参与了神经胶质瘤的恶性进展。