Expression of EMSY gene in sporadic ovarian cancer

The majority of familial breast and ovarian cancers arise from mutations in the BRCA1 and BRCA2 genes. Amplification at the 11q13.5 locus is commonly observed in breast and ovarian cancers. In 2003, Hughes-Davies et al. identified a novel gene (EMSY) at this locus which binds BRCA2 within a region d...

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Bibliographic Details
Published inMolecular biology reports Vol. 38; no. 1; pp. 359 - 363
Main Authors Altinisik, Julide, Karateke, Ates, Coksuer, Hakan, Ulutin, Turgut, Buyru, Nur
Format Journal Article
LanguageEnglish
Published Dordrecht Dordrecht : Springer Netherlands 2011
Springer Netherlands
Springer Nature B.V
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Summary:The majority of familial breast and ovarian cancers arise from mutations in the BRCA1 and BRCA2 genes. Amplification at the 11q13.5 locus is commonly observed in breast and ovarian cancers. In 2003, Hughes-Davies et al. identified a novel gene (EMSY) at this locus which binds BRCA2 within a region deleted in some cancers. Although little is known about the cellular role of EMSY, indirect evidence suggests that this nuclear protein is capable of silencing the activation potential of BRCA2. In this study we aimed to investigate expression of the EMSY gene and its protein product in sporadic ovarian cancer. Real-time quantitative RT-PCR was performed in 50 ovarian cancer and 17 normal ovarian tissue samples. Overexpression of the EMSY gene was found in 6/50 cases (12%), but in none of the control samples. To determine the EMSY protein by Western blotting, semi-quantitative analysis of the EMSY protein was performed using the Scion Image Gel Analysis Program. Statistical analysis was performed using SPSS 11.5. All patients having EMSY overexpression also displayed increased levels of the EMSY protein. Sporadic ovarian cancer shows overexpression of EMSY at a prevalence similar to that found in breast cancer and the overexpression is correlated with the protein level.
Bibliography:http://dx.doi.org/10.1007/s11033-010-0116-0
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ISSN:0301-4851
1573-4978
DOI:10.1007/s11033-010-0116-0