The propensity to malignancy of dispermic heterozygous moles

Genomic Imprinting: Implications for Human Disease

“…On a genome-wide scale, the complete hydatidiform mole and benign ovarian dermoid cyst arise from cells that are completely Ag or Pg in origin, respectively. 105,106 In addition, numerous tumors are associated with the preferential loss of a particular parental chromosome, indicating the involvement of imprinted genes. Examples include neuroblastoma (maternal chromosome 1p36 and paternal chromosome 2), 107 acute myeloblastic leukemia (paternal chromosome 7), 108 Wilms' tumor (maternal chromosome 11p15.5), 109 rhabdomyosarcoma (maternal chromosome 11p15.5), 110 and sporadic osteosarcoma (maternal chromosome 13).…”

Trophoblastic disease

“…Attempts to identify those women at greatest risk for postmolar disease by the use of cell proliferation markers, the expression of proto-oncogenes such as c-erb-B2, and flow cytometry [20][21][22] have failed, but it has been maintained that heterozygous (dispermic) moles have a much higher risk of subsequent postmolar complications than do homozygous (monospermic) moles. 23 Doubts have, however, been cast upon this claim by the failure to find any association between the presence of a Y chromosome (detected by the polymerase chain reaction or by chromosome in situ hybridization) in a mole and an excess incidence of postmolar disease. 24,25 Invasive hydatidiform mole An invasive hydatidiform mole is one which penetrates into the myometrium or invades the uterine vasculature.…”

Molecular diagnosis of gestational trophoblastic disease

“…A tetraploid complete mole also exists and harbors a paternal-only genome. It is of potential clinical interest that early studies suggest that a complete mole with a dispermic/heterozygous genome has a greater tendency towards malignant transformation than a monospermic/ homozygous one [17][18][19][20], although this is disputed by others [21].…”