Enomoto T, Fujita M, Inoue M, Nakazawa-Miyamoto A, Tanizawa O, Nomura T
Department of Radiation Biology, Osaka University Medical School, Japan.
Mol Carcinog. 1993;8(3):132-7. doi: 10.1002/mc.2940080303.
Alterations of the retinoblastoma (Rb) gene were evaluated in nine primary endometrial adenocarcinomas that we had previously analyzed for the presence of Ki-ras activations and p53 alterations and in three endometrial carcinoma cell lines. Loss of mRNA expression in the Rb gene was detected in two of the 12 tumors. Internal deletions of Rb cDNA were observed in two tumors; one was a deletion of exon 21 in a primary carcinoma, and the other was a deletion of exon 8 in one allele in one cell line. Loss of heterozygosity of the Rb gene, which was detectable by polymorphisms in introns 1 and 17, was analyzed using polymerase chain reaction-restriction fragment length polymorphism analysis in 29 endometrial carcinomas. Of 13 heterozygous cases, two cases (15%) showed loss of heterozygosity. We therefore suggest that alteration of the Rb gene, as well as activation of the Ki-ras gene and alterations of the p53 gene, plays a significant role in the etiology of endometrial adenocarcinoma.
我们对9例先前已分析过Ki-ras激活和p53改变情况的原发性子宫内膜腺癌以及3种子宫内膜癌细胞系中的视网膜母细胞瘤（Rb）基因改变进行了评估。在12例肿瘤中的2例检测到Rb基因mRNA表达缺失。在2例肿瘤中观察到Rb cDNA内部缺失；1例是原发性癌中外显子21缺失，另1例是1个细胞系中1个等位基因的外显子8缺失。利用聚合酶链反应-限制性片段长度多态性分析，在29例子宫内膜癌中分析了可通过内含子1和17多态性检测到的Rb基因杂合性缺失。在13例杂合病例中，2例（15%）出现杂合性缺失。因此，我们认为Rb基因改变以及Ki-ras基因激活和p53基因改变在子宫内膜腺癌的病因学中起重要作用。
