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Endometrial stromal tumors: immunohistochemical and molecular analysis of potential targets of tyrosine kinase inhibitors

Ruth Sardinha1, Teresa Hernández2, Susana Fraile2, Francesc Tresserra3, August Vidal4, Maria Carmén Gómez5, Aurora Astudillo6, Nieves Hernández7, Javier Saenz de Santamaría8, Jaume Ordi9, Luis Gonçalves10, Rafael Ramos11, Carmen Balañá12 and Enrique de Álava2*

  • * Corresponding author: Enrique de Álava

  • † Equal contributors

Author Affiliations

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

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Clinical Sarcoma Research 2013, 3:3  doi:10.1186/2045-3329-3-3

Published: 7 March 2013



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.


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.


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.


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.

Endometrial stromal tumors; Tyrosine kinase inhibitors; KIT; PDGFRA; EGFR; Systemic treatment