Ovarian Brenner tumour

A morphologic and immunohistochemical analysis suggesting an origin from fallopian tube epithelium

Elisabetta Kuhn, Ayse Ayhan, Ie Ming Shih, Jeffrey D. Seidman, Robert J Kurman

Research output: Contribution to journalArticle

Abstract

Background Brenner tumours (BTs), like other epithelial ovarian tumours, are thought to develop from the ovarian surface epithelium. Aim and Methods We hypothesised that BTs arise from transitional metaplasia near the tuboperitoneal junction which, when embedded in the ovary as Walthard cell nests, may progress to BTs. The aim of this study was to validate this hypothesis by a morphologic and immunohistochemical (IHC) analysis. Results The IHC analysis revealed that fallopian tube secretory cells, transitional metaplasia, Walthard cell nests and the epithelial component of BTs shared a similar IHC profile, consistently expressing AKR1C3 (an enzyme involved in androgen biosynthesis) and androgen receptor, but not calretinin. The tumour stromal cells that immediately surrounded the epithelial nests showed strong expression of calretinin, inhibin and steroidogenic factor 1 (markers of steroidogenic cells) in the majority of BTs. Using a highly sensitive immunofluorescent staining method, we detected small groups of cilia in transitional metaplasia and Walthard cell nests, multifocal stretches of cilia and/or ciliated vacuoles in benign BTs and well-developed cilia in atypical proliferative BTs. Conclusions Our findings suggest a tubal origin of BTs through transitional metaplasia and Walthard cell nests, based on their anatomic proximity, similar IHC profile and the presence of cilia. In addition, we hypothesise a role of androgenic stimulation in the pathogenesis of BT, based on the IHC staining pattern of calretinin, inhibin and steroidogenic factor 1 expressed in the luteinised stromal cells surrounding the epithelial nests of the tumours, and AKR1C3 and androgen receptor expressed in both the epithelial and stromal components.

Original languageEnglish (US)
Pages (from-to)3839-3849
Number of pages11
JournalEuropean Journal of Cancer
Volume49
Issue number18
DOIs
StatePublished - Dec 2013

Fingerprint

Brenner Tumor
Fallopian Tubes
Epithelium
Cilia
Metaplasia
Calbindin 2
Steroidogenic Factor 1
Inhibins
Androgen Receptors
Stromal Cells
Staining and Labeling
Neoplasms
Vacuoles
Androgens
Ovary
Epithelial Cells

Keywords

  • Brenner tumour
  • Histogenesis
  • Metaplasia
  • Ovarian tumour
  • Pathogenesis
  • Transitional
  • Tuboperitoneal junction

ASJC Scopus subject areas

  • Cancer Research
  • Oncology

Cite this

Ovarian Brenner tumour : A morphologic and immunohistochemical analysis suggesting an origin from fallopian tube epithelium. / Kuhn, Elisabetta; Ayhan, Ayse; Shih, Ie Ming; Seidman, Jeffrey D.; Kurman, Robert J.

In: European Journal of Cancer, Vol. 49, No. 18, 12.2013, p. 3839-3849.

Research output: Contribution to journalArticle

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abstract = "Background Brenner tumours (BTs), like other epithelial ovarian tumours, are thought to develop from the ovarian surface epithelium. Aim and Methods We hypothesised that BTs arise from transitional metaplasia near the tuboperitoneal junction which, when embedded in the ovary as Walthard cell nests, may progress to BTs. The aim of this study was to validate this hypothesis by a morphologic and immunohistochemical (IHC) analysis. Results The IHC analysis revealed that fallopian tube secretory cells, transitional metaplasia, Walthard cell nests and the epithelial component of BTs shared a similar IHC profile, consistently expressing AKR1C3 (an enzyme involved in androgen biosynthesis) and androgen receptor, but not calretinin. The tumour stromal cells that immediately surrounded the epithelial nests showed strong expression of calretinin, inhibin and steroidogenic factor 1 (markers of steroidogenic cells) in the majority of BTs. Using a highly sensitive immunofluorescent staining method, we detected small groups of cilia in transitional metaplasia and Walthard cell nests, multifocal stretches of cilia and/or ciliated vacuoles in benign BTs and well-developed cilia in atypical proliferative BTs. Conclusions Our findings suggest a tubal origin of BTs through transitional metaplasia and Walthard cell nests, based on their anatomic proximity, similar IHC profile and the presence of cilia. In addition, we hypothesise a role of androgenic stimulation in the pathogenesis of BT, based on the IHC staining pattern of calretinin, inhibin and steroidogenic factor 1 expressed in the luteinised stromal cells surrounding the epithelial nests of the tumours, and AKR1C3 and androgen receptor expressed in both the epithelial and stromal components.",
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