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HER2 expression in ovarian carcinoma: caution and complexity in biomarker analysis
  1. Hugh McCaughan,
  2. InHwa Um,
  3. Simon P Langdon,
  4. David J Harrison,
  5. Dana Faratian
  1. Edinburgh Breakthrough Research Unit, Division of Pathology, Institute of Genetics and Molecular Medicine, University of Edinburgh, Edinburgh, UK
  1. Correspondence to Dr Dana Faratian, Division of Pathology, Institute of Genetics and Molecular Medicine, University of Edinburgh, Crewe Road South, Edinburgh EH4 2XU, UK; d.faratian{at}

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We read with interest the recent article by Yan et al,1 in which a small cohort (n=85) of ovarian tumours were assessed for HER2 amplification by immunohistochemistry (IHC), fluorescence in situ hybridisation (FISH) and chromogenic in situ hybridisation. HER2 amplification and protein overexpression were identified in 35.3% (6/17) and 29.4% (5/17) of primary mucinous carcinomas, respectively, with none of the other histological subtypes demonstrating HER2 amplification or overexpression. In another recent study, Tan et al.2 used array-based comparative genomic hybridisation to establish the genomic profiles and regions of recurrent copy number change in 50 pure ovarian clear cell carcinomas (OCCCs). In that study, 7/50 (14%) OCCCs were found to harbour HER2 gene amplification and protein overexpression, representing <2% of the ovarian cancer population as a whole. The authors in both studies quite rightly conclude that HER2 may therefore be a potential therapeutic target in non-serous ovarian tumours. However, since there is documented evidence of HER2 overexpression in other histological subtypes of ovarian cancer, including serous carcinomas3–5 and some HER2-directed therapies (such as pertuzumab), may be effective against tumours which express non-amplified levels of the receptor,6 we sought to better define the frequency, quantity and distribution of HER2 expression …

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  • Competing interests None.

  • Ethics approval The study was approved by Lothian Research Ethics Committee (08/S1101/41).

  • Provenance and peer review Not commissioned; externally peer reviewed.

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