Androgenesis as a Cause of Hydatidiform Mole 2

Abstract

Q-band chromosome studies were done in 3 molar conceptuses and their parents, with special attention to six pairs of chromosomes (No. 3, 13--15, 21, and 22) in which polymorphic variants occur frequently. Those six pairs of chromosomes were uniformly homomorphic in moles, whereas at least one of them was heteromorphic in both paternal and maternal cells. Closer analyses provided evidence strongly suggesting that the moles inherited two morphologically identical haploid sets from the father and none from the mother. Thus androgenesis seemed causally related to pathogenesis of complete hydatidiform moles.

A Further Cytogenetic Study of Hydatidiform Mole, with Reference to its Androgenetic Origin

“…However, homomorphism shown by this mole leads to the suggestion that it is also of androgenetic origin. Thus, the present study resulted in the confirmation of the previous data provided by Kaj ii and Ohama (1977), Wake et al (1978) and Jacobs et al (1978), in favor of the view that androgenesis is a cause of complete moles.…”

“…Such chorionic lesions have been a subject of special attention primarily on account of possible malignant transformation into choriocarcinoma. Current cytogenetic investigations have presented interesting evidence showing that complete moles are androgenetic in origin ( Kaj ii and Ohama 1977;wake et al 1978;Jacobs et al 1978). The chromosome findings were compatible with views of either fertilization by a diploid sperm resulted from nondivision at the second meiotic division, or fertilization by a haploid sperm followed by duplication of its chromosomes.…”

“…The literature refers to three cytogenetic papers regarding complete moles in which the presence in duplicate of a paternally derived haploid set was verified by the use of chromosome polymorphisms (Ka j ii and Ohama 1977; Wake et al 1978;Jacobs et al 1978). It has been demonstrated in these studies that a total of 20 cases of complete moles including present ones is androgenetic in origin.…”

Patterns of Hybrid Loss of Imprinting Reveal Tissue- and Cluster-Specific Regulation

“…Hydatidiform moles are typically androgenetic (e.g. due to loss of the oocyte pronucleus) [64]. In the last decade, molar pregnancies with a normal 1∶1 parental genomic contribution have been reported [65], [66], and are thought to account for the majority of recurrent familial cases of this syndrome [67].…”

Diploid hydatidiform moles with fetal red blood cells in molar villi. 2—genetics

“…3 Genetically CHMs are diploid, but unusual in that they are androgenetic, the entire nuclear genome being paternal in origin. 4,5 PHMs are generally triploid, 1 occasionally tetraploid, and arise by fertilization of an egg by two or more sperm. 6,7 These differences in ploidy can often be exploited to confirm the pathological diagnosis of CHM or PHM.…”