title: New concepts and questions in gestational trophoblastic disease.
abstract: Hydatidiform moles can be divided into two distinct syndromes: partial, or transitional, and classic. Both classic and partial moles appear to result from abnormal fertilization but differ in the type of abnormal fertilization, karyotype, histology, epidemiology and malignant potential. Using chromosomal banding polymorphism, classic hydatidiform moles have been shown to be androgenetic in origin, developing from a sperm with the egg nucleus either absent or inactivated. No maternal chromosomes are transmitted to the classic mole. Studies using HLA and enzyme heterozygosity have suggested that fertilization occurs by a haploid sperm with duplication of its chromosomes and without cell division, giving the 46XX karyotype found in classic moles. About 4% of classic moles are 46XY and are also androgenetic but result from dispermic fertilization. The partial mole consists of hydropic villi, but some normal villi also are present. An embryo, cord and fetal membranes generally can also be found, and the karyotype frequently is aneuploid (usually triploid) and not the 46XX or 46XY of the classic mole. In contrast to the classic mole, the partial mole has a maternal chromosomal contribution. Preliminary data suggest that many partial moles arise from dispermic fertilization, with participation of the maternal genome giving a triploid karyotype. The malignant potential of the partial mole is still controversial, but preliminary data indicate that 2.1% of partial moles require treatment as compared to 10% of classic moles.
mesh_terms: D002822:Choriocarcinoma / Q000209:etiology* / Q000473:pathology / Q000648:ultrastructure; D005260:Female; D006801:Humans; D006828:Hydatidiform Mole / Q000209:etiology* / Q000473:pathology / Q000648:ultrastructure; D007621:Karyotyping; D008297:Male; D011247:Pregnancy; D012730:Sex Chromosomes; D014594:Uterine Neoplasms / Q000209:etiology* / Q000473:pathology / Q000648:ultrastructure