1. ¹Department of Obstetrics and Gynecology, Helsinki University Central Hospital, Haartmaninkatu 2, Helsinki 00290, Finland
2. ²Department of Oncology, Helsinki University Central Hospital, Haartmaninkatu 4, Helsinki 00290, Finland
3. ³Department of Pathology, University of Helsinki, PO Box 21 (Haartmaninkatu 3), Helsinki 00014, Finland

Correspondence: Dr R Butzow, E-mail: ralf.butzow@hus.fi

Received 7 July 2004; Revised 12 October 2004; Accepted 18 October 2004; Published online 7 December 2004.

Abstract

KIT and PDGFRA are receptor tyrosine kinases that can be specifically inactivated by small-molecule tyrosine kinase inhibitors, notably imatinib mesylate. In ovarian carcinoma, expression of KIT and PDGFRA protein has been documented, but the frequency and the molecular background of expression are poorly known. We analysed the expression of KIT and PDGFRA by immunohistochemistry in 522 serous ovarian carcinomas, and mutations of KIT and PDGFRA by denaturing high-performance liquid chromatographyin 125 and 187 serous ovarian carcinomas, respectively. No mutations of KIT or PDGFRA were detected. KIT expression was detected in 12% of carcinomas: low expression in 10% and high expression in 2% of cases. Using normal serous epithelium as a reference, decreased PDGFRA expression was detected in 12% and increased expression in 13% of carcinomas. Both KIT and PDGFRA expression were associated with high tumour grade, high proliferation index and poor patient outcome. By fluorescence in situ hybridisation, no KIT amplification was found in carcinomas with high KIT expression, but two cases showed a relative gain of chromosome 4. In conclusion, no mutations of KIT or PDGFRA were found, but a subset of serous ovarian carcinoma showed overexpression of the proteins, which was associated with aggressive tumour characteristics.