Update on the pathology of gestational trophoblastic disease

Abstract

Gestational trophoblastic disease can be a challenging area for pathologic evaluation. An update with a focus on pathologic challenges is presented.

Exaggerated placental site reaction mimicking a trophoblastic tumor: a case report

“…So, all the clinical, surgical, histological, and Immunohistochemical findings were compatible with a non-neoplastic trophoblastic disease, that is EPS. We did not think about it initially because it was not evident 19 . Our first clinical suspicion was about a submucosal leiomyoma, not consistent with the elevated serum levels of hCG.…”

A challenging case of twin pregnancy with complete hydatidiform mole and co-existing normal live fetus – A case report and review of the literature

“…The second is a singleton triploid fetus with partial hydatidiform mole placenta (69 chromosomes, 23 maternal and 46 paternal) and the third is a twin gestation in which one fetus is diploid with normal placenta (46 chromosomes, 23 maternal and 23 paternal) and the other is triploid with partial hydatidiform mole placenta (69 chromosomes, 23 maternal and 46 paternal) (Matsui et al, 2000, Piura et al, 2008). In complete hydatidiform moles there is a lack of identifiable embryonic or fetal tissues and the chorionic villi exhibit generalized hydatidiform swelling and diffuse trophoblastic hyperplasia (Heller, 2018). Cytogenic studies have demonstrated that complete moles most commonly display a 46xx karyotype and molar chromosomes are entirely of paternal origin (Hoffner and Surti, 2012).…”

α,β-Thujone suppresses human placental choriocarcinoma cells via metabolic disruption

“…In the clinic, human chorionic gonadotrophin (hCG) is a diagnostic marker of choriocarcinoma as it is mainly produced by JEG-3 choriocarcinoma cells (Handschuh et al 2007, Fournier 2016). An increase in hCG concentration implies the advanced tumor stage and predictable metastasis in choriocarcinoma patients (Heller 2018). Despite the establishment of the etoposide, methotrexate, actinomycin, cyclophosphamide, vincristine (EMA/ CO) regimen as a conventional chemotherapeutic strategy against choriocarcinoma, 20-30% of high-risk patients do not respond to this regimen (Bower et al 1997).…”