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Open Access Research article

Expression pattern of class I histone deacetylases in vulvar intraepithelial neoplasia and vulvar cancer: a tissue microarray study

Nicolas Samartzis1, Patrick Imesch1*, Konstantin J Dedes1, Eleftherios P Samartzis1, André Fedier1, Daniel Fink1, Rosmarie Caduff2 and Mathias K Fehr3

Author Affiliations

1 Department of Gynecology, University Hospital Zurich, Frauenklinikstrasse 10, 8091 Zurich, Switzerland

2 Department of Pathology, University Hospital Zurich, Schmelzbergstrasse 12, 8091 Zurich, Switzerland

3 Department of Gynecology and Obstetrics, Hospital of Frauenfeld, 8051 Frauenfeld, Switzerland

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BMC Cancer 2011, 11:463  doi:10.1186/1471-2407-11-463

Published: 26 October 2011

Abstract

Background

Epigenetic regulation is an important mechanism leading to cancer initiation and promotion. Histone acetylation by histone deacetylases (HDACs) represents an important part of it. The development of HDAC inhibitors has identified the utility of HDACs as a therapeutic target. Little is known about the epigenetic regulation of vulvar intraepithelial neoplasia (VIN) and vulvar squamous cell cancer (VSCC). In this study, the expression of class I HDACs (HDAC 1, 2 and 3) was compared in a series of VIN and VSCC tissues.

Methods

A tissue micro array (TMA) with specimens from 106 patients with high-grade VIN and 59 patients with vulvar cancer was constructed. The expression of HDACs 1, 2 and 3 were analyzed with immunohistochemistry (IHC). The nuclear expression pattern was evaluated in terms of intensity and percentage of stained nuclei and was compared between vulvar preinvasive lesions and vulvar cancer.

Results

HDAC 2 expression was significantly higher in VIN than in VSCC (p < 0.001, Fisher's test). Also, 88.7% (n = 94/106) of VIN samples and only 54.5% (n = 31/57) of VSCC samples were scored at the maximum level. Conversely, HDAC 3 expression was significantly higher in VSCC (93%, 53/57) compared to VIN (73.6%, 78/106, p = 0.003), whereas only a small difference in the expression of HDAC 1 was found between these two entities of vulvar neoplasia.

Conclusions

These results suggest that epigenetic regulation plays a considerable role in the transformation of VIN to invasive vulvar neoplasia.

Keywords:
Histone deacetylase; epigenetics; vulvar intraepithelial neoplasia; vulvar squamous cell cancer; tissue microarray; immunohistochemistry