Research
Endometrial stromal tumors: immunohistochemical and molecular analysis of potential targets of tyrosine kinase inhibitors
- † Equal contributors
1 Pathology Department, Hospital Espírito Santo E.P.E, Évora, Portugal
2 Centro de Investigación del Cáncer-IBMCC USAL-CSIC, Salamanca, Spain
3 Pathology Department, USP-Institut Universitari Dexeus, Barcelona, Spain
4 Pathology Department, Hospital de Bellvitge, Barcelona, Spain
5 Pathology Department, Hospital Universitari Germans Trias i Pujol, Badalona, Spain
6 Pathology Department, Hospital Universitario Central de Asturias, Oviedo, Spain
7 Anatomical Pathology Department, Hospital Universitario de la Laguna, Canarias, Spain
8 Pathology Department, Complejo Hospitalario Universitario de Badajoz, Badajoz, Spain
9 Pathology Department, Hospital Clinic de Barcelona, Barcelona, Spain
10 Pathology Department, Hospital do Espírito Santo E.P.E, Évora, Portugal
11 Pathology Department, Hospital Son Espases, Palma de Mallorca, Spain
12 Medical Oncology Service, Catalan Institute of Oncology - Hospital Germans Trias i Pujol, Badalona, Spain
Clinical Sarcoma Research 2013, 3:3 doi:10.1186/2045-3329-3-3
Published: 7 March 2013Abstract
Background
The systemic treatment of malignant endometrial stromal tumors (EST) is not well established. A few reports describe objective responses to imatinib, which suggest a novel therapeutic strategy for these tumors. Due to these facts, we aimed to perform a retrospective analysis of possible molecular targets of tyrosine kinase inhibitors (TKI) in EST: KIT, PDGFRA and EGFR.
Methods
52 endometrial stromal sarcomas and 13 undifferentiated endometrial sarcomas were examined and reviewed. Mutational analysis were performed for exons 9, 11, 13, and 17 of the KIT gene, exons 12 and 18 of the PDGFRA gene and exons 18, 19, 20 and 21 of the EGFR gene. The incidence and distribution of the KIT, PDGFRA, and EGFR expression were examined by immunohistochemistry, and EGFR amplification was assessed by fluorescence in situ hybridization.
Results
No mutations in KIT, PDGFRA and EGFR genes were detected. Overexpression of KIT, PDGFRA, EGFR, was detected in 2 (3%), 23 (35.4%), 7 (10.8%) cases respectively, whereas amplification of EGFR gene was not found.
Conclusions
Absence of significant expression, amplification and activating mutations on these tyrosine kinase receptors suggest that it is unlikely that EST can benefit from therapies such as TKI on the systemic setting.
