PATHOLOGY & ONCOLOGY RESEARCHVol. 12 No. 3, 2006

 Article

HER-2/neu Genotype of Breast Cancer May Change in Bone Metastasis

Tamás LÕRINCZ1, József TÓTH2, Gayane BADALIAN1, József TÍMÁR3, Miklós SZENDRŐI1

1Department of Orthopedics, Semmelweis University, Budapest, Hungary
2Department of Human and Experimental Pathology, National Institute of Oncology, Budapest, Hungary
3Department of Tumor Progression, National Institute of Oncology, Budapest, Hungary

 

The genotype of breast cancer (BRC) is considered to be relatively stable during tumor progression, accordingly, determination of the estrogen receptor and HER-2/neu status is currently based on the primary tumor. However, recent data suggest that the gene expression profile of the metastatic lesion can be different compared to that of the primary BRC. Accordingly, it is possible that the HER-2/neu status is different in the metastatic lesion and the primary BRC. Since the bone is the most frequent metastatic site during the progression of BRC, we have analyzed the HER-2/neu status of 48 bone metastatic BRC cases by immunohistochemistry and fluorescent in situ hybridization, and it was possible to compare it to the primary site in 23 cases. The frequency of HER-2/neu amplification of BRC in the primary tumors was found to be 17.4% compared to 10.5% in bone metastases. Half of BRC cases with HER-2/neu amplification lost this genotype in bone metastases (4/23 versus 2/23, respectively) and even in the 2 cases where HER-2/neu amplification was retained in the metastases, the copy number was found to be decreased compared to the primary tumor. Based on our data and previous reports in the literature, we suggest to perform HER-2/neu testing both on primary tumor and samples obtained from BRC metastases, at least in case of primary tumors with HER-2/neu amplification, before introduction of HER-2/neu-targeting therapy. Pathology & Oncology Research, Vol 12, Nr 3, 149-152, 2006

Key words: breast cancer; bone metastatic; HER-2


Received: May 23, 2006; accepted: Aug 31, 2006
Correspondence: József TÍMÁR, Department of Tumor Progression, National Institute of Oncology, Ráth György u. 7-9. Budapest H-1122, Hungary; Tel: 36-1-224-8786, Fax: 36-1-224-8706; E-mail: jtimar@oncol.hu

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