title: [The propensity to malignancy of dispermic, heterozygous moles].
abstract: 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 2 haploid sperm (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. In the research reported here, we compared the incidence of postmolar sequelae between patients with homozygous and heterozygous moles. Using chromosomal heteromorphism, HLA and PGM1 polymorphisms, we established the androgenetic origin of complete mole in 82 of 91 cases. Homozygosity was confirmed in 51 moles, and we found 10 heterozygous moles. Five of 10 patients with heterozygous moles developed postmolar trophoblastic disease, whereas only 2 of the 51 patients with homozygous moles had postmolar trophoblastic disease (an additional 5 patients showed signs of degenerating residual trophoblasts). A high incidence of sequelae after the expulsion of heterozygous moles suggests that the heterozygous constitution of allelic genes plays an important role in the process of malignant transformation of trophoblasts.
mesh_terms: D005260:Female; D005306:Fertilization; D006680:HLA Antigens / Q000032:analysis; D006579:Heterozygote; D006720:Homozygote; D006801:Humans; D006828:Hydatidiform Mole / Q000209:etiology* / Q000235:genetics; D010733:Phosphoglucomutase / Q000235:genetics; D011247:Pregnancy; D012307:Risk Factors; D014594:Uterine Neoplasms / Q000209:etiology* / Q000235:genetics
chemical_list: D006680:HLA Antigens; D010733:Phosphoglucomutase