title: Endometrioid endometrial carcinoma with atrophic endometrium and poor prognosis.
abstract: OBJECTIVE
  Type I endometrial carcinomas are characterized by endometrioid histology, develop from hyper-plastic endometrium, and have a good prognosis. Type II, nonendometrioid carcinomas, arise in atrophic endometrium and have a poor prognosis. However, approximately 20% of cases do not fit within this dualistic model and include endometrioid carcinomas associated with recurrence and possibly with atrophy. We aimed to evaluate grade 1 endometrioid endometrial carcinomas with atrophic endometrium, a putative third type of endometrial carcinoma.
  
  
  METHODS
  Histologic slides of all grade 1 endometrioid endometrial cancers from the Radboud University Medical Centre and Canisius-Wilhelmina Hospital from 1999-2009 and from the Mayo Clinic from 2002-2008 were reviewed. Comparisons were made between patients with atrophic and hyperplastic endometrium.
  
  
  RESULTS
  After review, 527 patients were identified. In 88 patients (16.8%), background endometrium was atrophic and 387 patients (73.3%) had hyperplastic endometrium. Fifty-two patients (9.9%) had proliferative endometrium or no background endometrium and were excluded. Atrophy correlated with older age, low body mass index, advanced International Federation of Gynecology and Obstetrics stage, malignant cells in peritoneal cytology, lymph node metastases, cervical involvement, lymphovascular space invasion, and deep myometrial invasion. Multivariable analysis showed that age (hazard ratio 1.06, 95% confidence interval [Cl] 1.01-1.12), International Federation of Gynecology and Obstetrics stage (hazard ratio 8.47, 95% Cl 1.73-41.57), and background endometrium (hazard ratio 3.11, 95% Cl 1.11-8.70) were predictors of progression-free survival.
  
  
  CONCLUSIONS
  Atrophic endometrium is an independent prognostic factor for patients with grade 1 endometrioid endometrial carcinoma. Endometrioid carcinoma with atrophy may not follow the hypothesized progression model for type I tumors and may arise through unique carcinogenic pathways.
  
  
  METHODS
  II.
authors.affiliation: Department of Obstetrics and Gynecology, Radboud University Nijmegen Medical Centre, and the Department of Pathology, Canisius-Wilhelmina Hospital, Nijmegen, The Netherlands. Y.Geels@obgyn.umcn.nl
authors.forename: Yvette P
authors.initials: YP
authors.lastname: Geels
authors.forename: Johanna M A
authors.initials: JM
authors.lastname: Pijnenborg
authors.forename: Saskia H
authors.initials: SH
authors.lastname: van den Berg-van Erp
authors.forename: Johan
authors.initials: J
authors.lastname: Bulten
authors.forename: Daniel W
authors.initials: DW
authors.lastname: Visscher
authors.forename: Sean C
authors.initials: SC
authors.lastname: Dowdy
authors.forename: Leon F A G
authors.initials: LF
authors.lastname: Massuger
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D001284:Atrophy; D018269:Carcinoma, Endometrioid / Q000401:mortality / Q000473:pathology*; D004714:Endometrial Hyperplasia / Q000401:mortality / Q000473:pathology*; D016889:Endometrial Neoplasms / Q000401:mortality / Q000473:pathology*; D004717:Endometrium / Q000473:pathology*; D005260:Female; D005500:Follow-Up Studies; D006801:Humans; D008875:Middle Aged; D011379:Prognosis; D015996:Survival Rate