Wake N, Fujino T, Hoshi S, Shinkai N, Sakai K, Kato H, Hashimoto M, Yasuda T, Yamada H, Ichinoe K
Department of Obstetrics and Gynaecology, School of Medicine, Hokkaido University, Sapporo, Japan.
Placenta. 1987 May-Jun;8(3):319-26. doi: 10.1016/0143-4004(87)90056-7.
Complete hydatidiform moles may originate from either the fertilization of an empty egg by a haploid sperm followed by duplication (producing a monospermic, homozygous mole) or the fertilization of such an egg by two haploid sperms (producing a dispermic, heterozygous mole). This difference in the mechanism leading to the formation of complete moles raises the question of whether the risk of subsequent malignancy is influenced by the zygosity of the mole. We have compared the incidence of postmolar sequelae in patients with homozygous and heterozygous moles. Using chromosomal heteromorphisms, human lymphocyte antigen (HLA) and phosphoglucuromutase 1 (PGM1) polymorphisms, we established the androgenetic origin of complete mole in 84 of 91 cases. Homozygosity was confirmed in 51 moles, and we found ten heterozygous moles. Five of ten patients with heterozygous moles developed postmolar trophoblastic disease, whereas only two of the 51 patients with homozygous moles had postmolar trophoblastic disease (an additional five patients showed signs of degenerating residual trophoblasts). The XY sex chromosome constitution of the two in vitro choriocarcinoma cell lines examined here provides further evidence of the propensity to malignancy of heterozygous moles.
完全性葡萄胎可能源于一个空卵被一个单倍体精子受精后复制（产生单精子、纯合性葡萄胎），或者源于这样一个卵被两个单倍体精子受精（产生双精子、杂合性葡萄胎）。导致完全性葡萄胎形成的机制上的这种差异引发了一个问题，即后续发生恶性肿瘤的风险是否受葡萄胎合子性的影响。我们比较了纯合性和杂合性葡萄胎患者葡萄胎后后遗症的发生率。利用染色体异态性、人类淋巴细胞抗原（HLA）和磷酸葡萄糖醛酸变位酶1（PGM1）多态性，我们在91例病例中的84例中确定了完全性葡萄胎的父系起源。在51个葡萄胎中证实为纯合性，我们发现了10个杂合性葡萄胎。10例杂合性葡萄胎患者中有5例发生了葡萄胎后滋养层细胞疾病，而51例纯合性葡萄胎患者中只有2例发生了葡萄胎后滋养层细胞疾病（另外5例显示有退化的残留滋养层细胞的迹象）。此处检测的两个体外绒癌细胞系的XY性染色体组成进一步证明了杂合性葡萄胎发生恶性肿瘤的倾向。
