Neurotensin Receptor 1 (NTSR1) Overexpression in Breast Carcinomas Is Common and Independent of ER/PR/Her2 Expression

Abstract

Neurotensin (NT) is a 13-amino acid peptide with trophic effects on some neoplasms. Its bioactivities are mainly mediated by neurotensin receptor 1 (NTSR1). Both NT and NTSR1 were found to be upregulated in breast cancer. NT/NTSR1 thus becomes a potential therapeutic target. We studied whether any correlation exists between the expression of NTSR1 in breast carcinomas and the expression of ER, PR, and Her2. A total 85 cases of invasive ductal (62) and lobular (23) breast carcinomas were studied. Based on their ER/PR profiles, the ductal carcinomas (DCs) were subcategorized into ER+/PR+ (21), ER+/PR (20), and ER/PR (21). All of the lobular carcinomas (LCs) were ER+/PR+. 21.57% of all DCs and 5.56% of LCs were Her2 positive. 77.78% of ER/PR DCs were also Her2 negative (triple negative). The expression of NTSR1 was detected by immunohistochemistry and was semiquantitated (as negative, 1+, 2+, 3+). Both 2+ and 3+ were collectively defined as overexpression. The expression of NTSR1 was weak and focal in non-neoplastic mammary epithelial cells. It is increased in 74.19% of DCs (80.95% in ER+/PR+, 75% in ER+/PR, and 66.67% in ER/PR group), and in 95.65% of LCs. The overexpression of NTSR1 is similar between ER+ DCs and ER DCs (75% vs 66.67%, p > 0.05) as well as between PR+ DCs and PR DCs (80.95% in ER+/PR+ DCs vs 75% in ER+/PR DCs, p > 0.05). And it was seen in 77.78% of Her2+ DCs, 78.38% of Her2 DCs, 94.12% of Her2 LCs, and 78.57% of triple negative DCs. Overall, NTSR1 is commonly overexpressed in both ductal and lobular breast carcinomas and is independent of the ER/PR/Her2 profiles of the tumors. The present data supports the potential benefit of developing NTSR1 blockers in the adjuvant therapy of breast carcinomas, particularly for those triple negative tumors.

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X. Gui, S. Liu, Z. Meng and Z. Gao, "Neurotensin Receptor 1 (NTSR1) Overexpression in Breast Carcinomas Is Common and Independent of ER/PR/Her2 Expression," Journal of Cancer Therapy, Vol. 4 No. 7A, 2013, pp. 12-17. doi: 10.4236/jct.2013.47A003.

Conflicts of Interest

The authors declare no conflicts of interest.

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