title: Comparison of dysplasia profiles in stimulated ovaries and in those with a genetic risk for ovarian cancer.
abstract: OBJECTIVE
  Ovarian epithelial dysplasia (OED) was first described after prophylactic oophorectomy for genetic risk of ovarian cancer. In light of Fathalla's incessant ovulation theory, this study was set up to describe the presence of ovarian abnormalities (dysplasia) after ovulation induction and to compare dysplasia profiles in stimulated and genetic risk ovaries.
  
  
  METHODS
  One-hundred and twenty-four patients who had undergone salpingo-oophorectomies or ovarian cystectomies between 1990 and 2005 were reviewed. They were divided into three groups: (1) previous in vitro fertilisation (n=35); (2) prophylactic oophorectomies for genetic risk (n=27) and (3) fertile non-cancerous controls (n=62). Eleven cytological and architectural epithelial features were defined and a dysplasia score was calculated to quantify ovarian epithelial abnormalities.
  
  
  RESULTS
  Mean dysplasia score was significantly higher in the genetic risk and stimulated ovary groups than in controls (9.55 versus 3.62, p<0.0001; 7.51 versus 3.62, p<0.0002, respectively). Cytological and architectural abnormalities were more frequent in the genetic risk group, while the profile of abnormalities was different in the genetic risk and stimulated groups.
  
  
  CONCLUSIONS
  These findings support a possible relationship between OED and the use of ovulation-stimulating drugs. The increased dysplasia score in stimulated and genetic risk ovaries might be consistent with progression towards neoplastic transformation, and may justify the use of the term dysplasia or intraepithelial ovarian neoplasia. The observation of dysplasia in the stimulated group may differentiate women at risk. Conversely, the fact that the dysplasia profile after stimulation differs from that in genetic risk ovaries suggests that ovarian stimulation may predispose to a different evolution.
authors.affiliation: Department of Surgery, Centre Jean Perrin, Clermont-Ferrand, France.
authors.forename: J
authors.initials: J
authors.lastname: Dauplat
authors.forename: G
authors.initials: G
authors.lastname: Chene
authors.forename: C
authors.initials: C
authors.lastname: Pomel
authors.forename: M M
authors.initials: MM
authors.lastname: Dauplat
authors.forename: G
authors.initials: G
authors.lastname: Le Bouëdec
authors.forename: F
authors.initials: F
authors.lastname: Mishellany
authors.forename: N
authors.initials: N
authors.lastname: Lagarde
authors.forename: Y J
authors.initials: YJ
authors.lastname: Bignon
authors.forename: P
authors.initials: P
authors.lastname: Jaffeux
authors.forename: B
authors.initials: B
authors.lastname: Aublet-Cuvelier
authors.forename: P
authors.initials: P
authors.lastname: Dechelotte
authors.forename: J L
authors.initials: JL
authors.lastname: Pouly
authors.forename: F
authors.initials: F
authors.lastname: Penault-Llorca
mesh_terms: D000290:Adnexa Uteri / Q000601:surgery; D000328:Adult; D005260:Female; D005307:Fertilization in Vitro / Q000009:adverse effects; D019398:Genes, BRCA1; D024522:Genes, BRCA2; D020022:Genetic Predisposition to Disease; D006801:Humans; D008875:Middle Aged; D009154:Mutation; D010051:Ovarian Neoplasms / Q000209:etiology / Q000235:genetics / Q000473:pathology / Q000601:surgery*; D010052:Ovariectomy; D010053:Ovary / Q000473:pathology*; D010062:Ovulation Induction / Q000009:adverse effects*; D011230:Precancerous Conditions / Q000209:etiology / Q000473:pathology* / Q000601:surgery