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Prognostic impact of discordance between triple-receptor measurements in primary and recurrent breast cancer
Institution:1. Department of Breast Medical Oncology, The University of Texas M. D. Anderson Cancer Center, Houston, TX, USA;2. Department of Gynecology and Obstetrics, University of Muenster, Medical Center, Muenster, Germany;3. Division of Quantitative Sciences;4. Department of Pathology;5. Department of Surgical Oncology;6. Department of Radiation Oncology;7. Department of Systems Biology, The University of Texas M. D. Anderson Cancer Center, Houston, TX, USA
Abstract:BackgroundWe evaluated discordance in expression measurements for estrogen receptor (ER), progesterone receptor (PR), and HER2 between primary and recurrent tumors in patients with recurrent breast cancer and its effect on prognosis.MethodsA total of 789 patients with recurrent breast cancer were studied. ER, PR, and HER2 status were determined by immunohistochemistry (IHC) and/or FISH. Repeat markers for ER, PR, and HER2 were available in 28.9%, 27.6%, and 70.0%, respectively. Primary and recurrent tumors were classified as triple receptor-negative breast cancer (TNBC) or receptor-positive breast cancer (RPBC, i.e. expressing at least one receptor). Discordance was correlated with clinical/pathological parameters.ResultsDiscordance for ER, PR, and HER2 was 18.4%, 40.3%, and 13.6%, respectively. Patients with concordant RPBC had significantly better post-recurrence survival (PRS) than discordant cases; patients with discordant receptor status had similarly unfavorable survival as patients with concordant TNBC. IHC scores for ER and PR showed weak concordance between primary and recurrent tumors. Concordance of HER2–FISH scores was higher.ConclusionsConcordance of quantitative hormone receptor measurements between primary and recurrent tumors is modest consistent with suboptimal reproducibility of measurement methods, particularly for IHC. Discordant cases have poor survival probably due to inappropriate use of targeted therapies. However, biological change in clinical phenotype cannot be completely excluded.
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