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This Article Full Text Full Text (PDF) All Versions of this Article: ERC-08-0065v1 ERC-08-0065v2 16/1/73    most recent Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Singer, C. F Articles by Kubista, E. Search for Related Content PubMed PubMed Citation Articles by Singer, C. F Articles by Kubista, E.

¹ Division of Special Gynecology, Department of Obstetrics and Gynecology² Division of Oncology, Department of Internal Medicine³ , Department of Surgery⁴ Division of Gynecopathology, Department of Clinical Pathology, Medical University of Vienna, Waehringer Guertel 18-20, 1090 Vienna, Austria

(Correspondence should be addressed to C F Singer; Email: christian.singer{at}meduniwien.ac.at)

ERBB2 amplification and consecutive overexpression is a predictor for poor prognosis in breast cancer patients. In addition, incomplete resection of ERBB2-overexpressing tumors leads to increased proliferation of residual breast cancer cells. While the local release of cytokines is thought to be responsible for the malignant behavior of remaining tumor tissue, the exact mechanism is still unknown. We have analyzed epidermal growth factor receptor (EGFR), activated (p)EGFR, and activated (p)ERBB2 protein expression in ERBB2-overexpressing and in non-ERBB2-overexpressing tumors from patients who underwent breast surgery and consecutive re-excision for involved margins, and compared expression levels by immunohistochemistry. While overall ERBB2 protein expression in the initial and the re-excised sample were comparable, we observed an increase in pERBB2 in ductal carcinomas in situ in both, ERBB2-overexpressing (16/21 vs 24/24; P=0.018, ² test) and non-ERBB2-overexpressing tumors (3/28 vs 5/12; P=0.025, ² test). pERBB2 was not increased in invasive tumors, regardless on whether the samples had been taken from a ERBB2-overexpressing (9/25 vs 6/17; P=0.261, ² test) or a non-ERBB2-overexpressing tumor (1/27 vs 0/8; P=0.581, ² test). EGFR expression was only detected in 1/47 ERBB2-overexpressing primary tumors and 2/48 non-ERBB2-overexpressing tumors, and was undetectable in re-excised specimen. Taken together, we have demonstrated an increase in ERBB2 receptor activation in incompletely resected preinvasive breast cancer. We hypothesize that receptor phosphorylation is caused by growth factor stimulation in response to intraoperative tissue damage, and perioperative inhibition of specific cytokines could become a promising therapeutic strategy.