PT - JOURNAL ARTICLE AU - M V Zaragoza AU - E Millie AU - R W Redline AU - T J Hassold TI - Studies of non-disjunction in trisomies 2, 7, 15, and 22: does the parental origin of trisomy influence placental morphology? AID - 10.1136/jmg.35.11.924 DP - 1998 Nov 01 TA - Journal of Medical Genetics PG - 924--931 VI - 35 IP - 11 4099 - http://jmg.bmj.com/content/35/11/924.short 4100 - http://jmg.bmj.com/content/35/11/924.full SO - J Med Genet1998 Nov 01; 35 AB - Recently, there have been several molecular studies of trisomic fetuses and liveborns which have examined the parent and meiotic stage of origin of nondisjunction. However, little is known about the possible phenotypic effects of the origin of trisomy. For trisomic spontaneous abortions, no distinct phenotype has been described, although some have been reported to have features, such as trophoblastic hyperplasia, similar to hydatidiform moles. In the present report, we describe molecular and histological studies of spontaneous abortions with trisomies 2, 7, 15, or 22, conditions occasionally linked to trophoblastic hyperplasia. Our results provide strong evidence for chromosome specific mechanisms of nondisjunction, with trisomy 2 having a high frequency of paternally derived cases and trisomy 7 typically originating postzygotically. In studies correlating parental origin of trisomy with phenotype, we found no difference in the proportion of cases with trophoblastic hyperplasia, fetal tissue, nucleated red blood cells, or hydropic villi among paternally or maternally derived trisomies 2, 7, 15, or 22. However, paternally derived trisomies tended to abort earlier than maternally derived trisomies. This suggests that parental origin might affect the developmental stage at which abortion occurs but not other features of placental phenotype.