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Frequent nuclear expression of β-catenin protein but rare β-catenin mutation in pulmonary sclerosing haemangioma
  1. P-M Chiang1,
  2. R-H Yuan2,3,
  3. H-C Hsu1,
  4. T-L Mao1,
  5. R-H Hu2,
  6. P-L Lai1,
  7. Y-M Jeng1
  1. 1
    Department of Pathology, National Taiwan University Hospital, and College of Medicine, National Taiwan University, Taipei, Taiwan
  2. 2
    Department of Surgery, National Taiwan University Hospital, and College of Medicine, National Taiwan University, Taipei, Taiwan
  3. 3
    Department of Surgery, Tao-Yuan General Hospital, Department of Health, Executive Yuan, Republic of China
  1. Dr Yung-Ming Jeng, Department of Pathology, National Taiwan University Hospital, 7, Chung-Shan South Road, Taipei, Taiwan; mrna0912{at}yahoo.com.tw

Abstract

Background: Pulmonary sclerosing haemangioma (PSH) is an uncommon tumour that is composed of glandular/papillary lining cells and polygonal cells. The biological behaviour of this tumour has been investigated; however, the molecular pathogenesis of PSH remains unknown.

Aims: To characterise the role of the Wnt/β-catenin pathway in the genesis of PSH.

Methods: 37 PSH samples were investigated immunohistochemically for detection of the β-catenin protein and direct sequencing of exon 3 of the β-catenin gene.

Results: Nuclear expression of β-catenin was found in the lining component of 23 tumours (62%) and in the polygonal component of 11 tumours (30%). The expression of β-catenin was stronger in the lining component, but weaker in the polygonal component. Interestingly, all the tumours with expression of β-catenin in the polygonal component also expressed β-catenin in the lining component. However, mutation of exon 3 of the β-catenin gene was detected in only one tumour that expressed nuclear β-catenin in lining and polygonal components.

Conclusions: The Wnt/β-catenin pathway is involved in the genesis of PSH, but mutation of exon 3 of the β-catenin gene rarely contributes to the activation of the Wnt/β-catenin pathway in PSH.

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Footnotes

  • Competing interests: None.

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