[From human andro- and parthenogenesis (hydatidiform moles and benign ovarian teratomas) to cancer]

Gynecol Obstet Fertil. 2005 Jul-Aug;33(7-8):469-82. doi: 10.1016/j.gyobfe.2005.05.023.
[Article in French]

Abstract

Genomic imprinting is a process that appeared in mammals. This phenomenon blocks the normal development of parthenogenic and androgenic conceptuses, that is to say benign ovarian teratomas and hydatidiform moles respectively. Pathological modifications of these conceptuses depend on whether the chromosomes come from the mother or father. These pathologies are associated with an accidental anomaly during gametogenesis and/or fertilizing. These reproductive anomalies are sporadic and some familial cases may exist suggesting a genetic control of such diseases. The human andro- and parthenogenetic conceptuses, but more frequently the moles, may be invasive (choriocarcinoma). An imbalance of the imprinting genes may initiate the deregulation of other genes, including oncogenes and anti-oncogenes, which can explain the cancerous modification. Immunological and environmental factors must be also considered (presence of the only paternal chromosomes in the choriocarcinoma). Numerous works on this subject are published and some recent important discoveries underline the roles of genes HOX, Tim P3, E-cad and p-16, and the recurrent chromosome anomalies 7q21+and 8p21- in the mole to choriocarcinoma processing. Although these phenomena are complex and heterogeneous, the andro- and parthenogenote conceptuses are particularly interesting models with which to understand developmental disorders and cancerous progression.

Publication types

  • English Abstract
  • Review

MeSH terms

  • Embryonic Development / genetics*
  • Female
  • Genomic Imprinting*
  • Humans
  • Hydatidiform Mole / etiology
  • Hydatidiform Mole / genetics*
  • Ovarian Neoplasms / etiology
  • Ovarian Neoplasms / genetics*
  • Parthenogenesis
  • Pregnancy
  • Teratoma / etiology
  • Teratoma / genetics*
  • Uterine Neoplasms / etiology
  • Uterine Neoplasms / genetics*