1. ¹Institute for Pathology, University Hospital of Basel, Basel, Switzerland
2. ²Department of Gynecology and Obstetrics, University Hospital of Basel, Basel, Switzerland
3. ³Institute of Pathology, Kantonsspital St Gallen, St Gallen, Switzerland
4. ⁴Department of Gynecology and Obstetrics, Innsbruck Medical University, Innsbruck, Austria
5. ⁵Department of Pathology, University Medical Center Hamburg Eppendorf, Hamburg, Germany

Correspondence: Dr G Singer, MD, Institute of Pathology, University Hospital of Basel, Schönbeinstrasse 40, Basel CH-4031, Switzerland. E-mail: gsinger@uhbs.ch

^*These authors contributed equally to this work.

Received 22 December 2005; Revised 11 January 2006; Accepted 12 January 2006.

Abstract

Success of epidermal growth factor receptor (EGFR) targeting agents in different cancer types is related to EGFR gene mutations and/or copy number gains. We investigated the EGFR gene status and protein expression by DNA mutational analysis, fluorescence in situ hybridization (FISH), and immunohistochemistry in tumor tissues from 80 patients with primary and corresponding recurrent ovarian serous carcinomas. The patients were classified into six groups with ascending EGFR gene copy numbers. EGFR amplification and high polysomy (FISH+) was present in a significant fraction of the primary (20%) and recurrent (22%) ovarian carcinomas. On mutational analysis, only one tumor with a silent EGFR mutation was observed, and this was the only carcinoma with high-level amplification. EGFR protein immunoexpression was seen in 28% of primary and 33% of recurrent carcinomas and correlated to amplification in the primary tumors (P=0.003). In recurrent carcinoma, moderate and strong EGFR expression was associated with amplification (P=0.034). These molecular events potentially have impact on the responsiveness to EGFR targeting agents in ovarian cancer.