Azuma C, Saji F, Nobunaga T, Kamiura S, Kimura T, Tokugawa Y, Koyama M, Tanizawa O
Department of Obstetrics and Gynecology, Osaka University Medical School, Japan.
Cancer Res. 1990 Feb 1;50(3):488-91.
The association of complete hydatidiform mole with choriocarcinoma has long been recognized, but it is unknown whether the pathogenesis of the two are identical. We investigated the pathogenesis of these trophoblastic tumors by analyzing restriction fragment length polymorphisms using a minisatellite DNA probe to choriocarcinoma, the complete mole, and normal trophoblasts as well as the parental cells. The polymorphic fragments of the complete mole were all transmitted from the paternal DNA, but some polymorphic fragments of the paternal DNA were not recognized in the complete mole. This confirms at a molecular level the androgenetic origin of the complete mole. In some cases of choriocarcinoma, the pattern of inheritance of restriction fragment length polymorphisms was the same as that in the complete mole, whereas in others all the polymorphic fragments in tumor tissues were identical to those in the host DNA. These results suggest that the pathogenesis of choriocarcinoma varies, being completely different from that of the complete hydatidiform mole in some cases.
完全性葡萄胎与绒毛膜癌的关联早已为人所知,但两者的发病机制是否相同尚不清楚。我们通过使用针对绒毛膜癌、完全性葡萄胎、正常滋养层细胞以及亲代细胞的小卫星DNA探针分析限制性片段长度多态性,来研究这些滋养层肿瘤的发病机制。完全性葡萄胎的多态性片段均来自父源DNA,但父源DNA的一些多态性片段在完全性葡萄胎中未被识别。这在分子水平上证实了完全性葡萄胎的孤雄生殖起源。在某些绒毛膜癌病例中,限制性片段长度多态性的遗传模式与完全性葡萄胎相同,而在其他病例中,肿瘤组织中的所有多态性片段与宿主DNA中的片段相同。这些结果表明,绒毛膜癌的发病机制各不相同,在某些情况下与完全性葡萄胎的发病机制完全不同。