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Oral acantholytic squamous cell carcinoma shares clinical and histological features with angiosarcoma

Oliver Driemel1 email, Urs DA Müller-Richter2 email, Samer G Hakim3 email, Richard Bauer1 email, Alexander Berndt4 email, Johannes Kleinheinz5 email, Torsten E Reichert1 email and Hartwig Kosmehl6 email

1Department of Oral and Maxillofacial Surgery, University of Regensburg, Franz-Josef-Strauss-Allee 11, 93053, Regensburg, Germany

2Department of Oral and Maxillofacial Plastic Surgery, University of Würzburg, Pleicherwall 2, 97070, Würzburg, Germany

3Department of Maxillofacial Surgery, University Medical Center Schleswig-Holstein, Campus Lübeck, Ratzeburger Allee 160, 23538, Lübeck, Germany

4Department of Pathology, University of Jena, Ziegelmühlenweg 1, 07740, Jena, Germany

5Department of Maxillofacial Surgery, University of Münster, Waldeyerstraße 30, 48149, Münster, Germany

6Institute of Pathology, HELIOS Hospital Erfurt, Nordhäuser Strasse 74, 99089, Erfurt, Germany

author email corresponding author email

Head & Face Medicine 2008, 4:17doi:10.1186/1746-160X-4-17

Published: 31 July 2008

Abstract

Background

acantholytic squamous cell carcinomas (ASCC) and intraoral angiosarcoma share similar histopathological features. Aim of this study was to find marker for a clear distinction.

Methods

Four oral acantholytic squamous cell carcinomas and one intraoral angiosarcoma are used to compare the eruptive intraoral growth-pattern, age-peak, unfavourable prognosis and slit-like intratumorous spaces in common histological staining as identical clinical and histopathological features. Immunohistochemical staining for pancytokeratin, cytokeratin, collagen type IV, γ2-chain of laminin-5, endothelial differentiation marker CD31 and CD34, F VIII-associated antigen, Ki 67-antigen, β-catenin, E-cadherin, α-smooth-muscle-actin and Fli-1 were done.

Results

Cytokeratin-immunoreactive cells can be identified in both lesions. The large vascularization of ASCC complicates the interpretation of vascular differential markers being characteristic for angiosarcoma. Loss of cell-cell-adhesion, monitored by loss of E-cadherin and β-catenin membrane-staining, are indetified as reasons for massive expression of invasion-factor ln-5 in ASCC and considered responsible for unfavourable prognosis of ASCC. Expression of Fli-1 in angiosarcoma and cellular immunoreaction for ln-5 in ASCC are worked out as distinguishing features of both entities.

Conclusion

Fli-1 in angiosarcoma and ln-5 in ASCC are distinguishing features.


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