Folate receptor-α expression in triple-negative and non-triple-negative invasive breast carcinoma
作者
Ragaa A. Salem,Nadia Galal Elhefnawy,Faten Ragheb,Iman H. Hewedi,Lobna Sadek Shash,Dalia M. Ismail
出处
期刊:Egyptian Journal of Pathology日期:2017-12-01卷期号:37 (2): 268-273
标识
DOI:10.1097/01.xej.0000526546.49017.77
摘要
Background and objective Breast cancer is a heterogeneous disease with variable behavior and response to therapy. It is grouped into three main molecular subtypes: estrogen receptor and/or progesterone receptor expressing, human epidermal growth factor receptor-2 expressing, or triple-negative breast cancer (TNBC). There are currently no established targeted therapies for TNBC. The folate receptor-α (FRA) is a glycosylphosphatidylinositol-linked protein overexpressed in certain malignancies, along with its low coordinate expression in normal tissue. Therefore, FRA is an attractive target for directed therapies. The aim of this study was to assess immunohistochemical expression of FRA in invasive breast carcinomas and to explore its association with TNBC and non-triple-negative breast cancer (NTNBC), trying to specify the subset of patients with breast cancer who might benefit most from anti-folate receptors targeted therapy. Materials and methods This retrospective study was conducted on 60 invasive breast carcinoma tissue samples: 30 cases of TNBC cases and 30 cases of NTNBC. All were retrieved from archives of the Pathology Laboratory of Ain Shams Specialized Hospital. Immunohistochemistry using rabbit polyclonal anti-FRA antibody was performed to detect the expression of FRA, which was subsequently correlated with different pathological parameters. Results Statistically significant higher expression of FRA was noted in TNBC group in comparison with NTNBC group ( P =0.02). On the contrary, no significant correlation was found between FRA expression and tumor size, tumor type, tumor grade, or lymph node status. Conclusion FRA expression is strongly associated with TNBC cases, and such association suggests its potential role in tumorigenesis. As such, novel premises for treatment of TNBC are anticipated by targeting its molecule.