期刊论文详细信息
Clinical Sarcoma Research
Endometrial stromal tumors: immunohistochemical and molecular analysis of potential targets of tyrosine kinase inhibitors
Enrique de Álava8  Carmen Balañá7  Rafael Ramos6  Luis Gonçalves4  Jaume Ordi5  Javier Saenz de Santamaría2  Nieves Hernández1,10  Aurora Astudillo1,11  Maria Carmén Gómez9  August Vidal1,12  Francesc Tresserra3  Susana Fraile8  Teresa Hernández8  Ruth Sardinha1 
[1] Pathology Department, Hospital Espírito Santo E.P.E, Évora, Portugal;Pathology Department, Complejo Hospitalario Universitario de Badajoz, Badajoz, Spain;Pathology Department, USP-Institut Universitari Dexeus, Barcelona, Spain;Pathology Department, Hospital do Espírito Santo E.P.E, Évora, Portugal;Pathology Department, Hospital Clinic de Barcelona, Barcelona, Spain;Pathology Department, Hospital Son Espases, Palma de Mallorca, Spain;Medical Oncology Service, Catalan Institute of Oncology - Hospital Germans Trias i Pujol, Badalona, Spain;Centro de Investigación del Cáncer-IBMCC USAL-CSIC, Salamanca, Spain;Pathology Department, Hospital Universitari Germans Trias i Pujol, Badalona, Spain;Anatomical Pathology Department, Hospital Universitario de la Laguna, Canarias, Spain;Pathology Department, Hospital Universitario Central de Asturias, Oviedo, Spain;Pathology Department, Hospital de Bellvitge, Barcelona, Spain
关键词: Systemic treatment;    EGFR;    PDGFRA;    KIT;    Tyrosine kinase inhibitors;    Endometrial stromal tumors;   
Others  :  861493
DOI  :  10.1186/2045-3329-3-3
 received in 2012-12-13, accepted in 2013-03-04,  发布年份 2013
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【 摘 要 】

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.

【 授权许可】

   
2013 Sardinha et al; licensee BioMed Central Ltd.

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