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J Clin Pathol 61:707-712 doi:10.1136/jcp.2008.055954
  • My approach

Loss of basal cell keratin 14 reflects increased risk of recurrence in surgically resected sinonasal inverted papilloma

  1. S Gunia1,
  2. D Liebe2,
  3. S Koch1
  1. 1
    Department of Pathology, HELIOS Klinikum Bad Saarow, Charité-University Medicine Teaching Hospital, Bad Saarow, Germany
  2. 2
    Department of Otorhinolaryngology, HELIOS Klinikum Bad Saarow, Charité-University Medicine Teaching Hospital, Bad Saarow, Germany
  1. Dr S Gunia, Department of Pathology, HELIOS Klinikum Bad Saarow, Charité-University Medicine Teaching Hospital, Pieskower Straße 33, 15526 Bad Saarow, Germany; sven.gunia{at}helios-kliniken.de
  • Accepted 22 February 2008

Abstract

Aims: To evaluate selected markers in terms of their possible relation to the development of recurrence in microsurgically resected sinonasal inverted papilloma (SIP) in order to advance understanding of the mechanisms pathogenetically involved, and to identify novel biomarkers for individual risk assessment in SIP.

Methods: Retrospective computerised database analysis and thorough review of medical charts was performed in order to identify all patients with newly diagnosed SIP who underwent microinvasive endonasal surgery at the HELIOS Klinikum Bad Saarow and at the Klinikum Hoyerswerda (Germany) between 1985 and 2005, yielding a total of 73 patients with newly diagnosed SIP. Among these, 22 patients (30.1%) developed recurrence during follow-up. Recurrent SIP were also microsurgically resected. Therefore, archival paraffin-wax-embedded tissues comprising a total of 95 SIP were immunostained for a panel of selected antigens (Ki67/CK5/CK14/E-cadherin/CD56) functionally involved in cellular adhesion structures or in proliferative activity. Adjacent non-papillomatous sinonasal mucosa was available in all cases and served as normal controls.

Results: Increased proliferative activity (Ki67) and loss of basal cell keratin 14 (CK14) expression were related to the development of recurrence in microsurgically resected SIP.

Conclusion: These findings might advance understanding of the pathogenesis behind the development of recurrence in microsurgically resected SIP by focusing on so far neglected alterations of cell-matrix connections at the epithelial-stromal interface in SIP, and might hint at CK14 representing a possible novel biomarker for individual risk assessment in microsurgically resected SIP.

Footnotes

  • Competing interests: None.