FOXP3 expression and nodal metastasis of breast cancer

Springer Science and Business Media LLC - Tập 36 - Trang 405-409 - 2013
Yesim Gökmen-Polar1, Mangesh A. Thorat1, Payal Sojitra1, Rashmil Saxena1, Sunil Badve1,2,3
1Department of Pathology and Laboratory Medicine, IU School of Medicine, Indianapolis, USA
2Department of Internal Medicine, IU School of Medicine, Indianapolis, USA
3Department of Pathology, Indiana University School of Medicine, Indianapolis, USA

Tóm tắt

T regulatory cells, a subset of T lymphocytes, function to suppress immune responses. FOXP3, a member of the forkhead family of transcription factors, is a good marker for T regulatory cells. Since sentinel nodes are important sites of immunomodulation in breast cancer, we studied the association between T regulatory cells and nodal metastasis using FOXP3 expression in sentinel nodes with and without metastatic breast carcinoma. Following sample size calculations, we selected 140 sentinel nodes from breast cancer patients; 70 with metastasis (sentinel node+) and 70 without metastasis (sentinel node–). FOXP3 expression in sentinel nodes was studied by immunohistochemistry. Cortical cells expressing FOXP3 were counted in 10 high power fields. In the evaluable cases, the node positive (n = 66) and negative (n = 69) groups were well balanced for all clinicopathological parameters except histological type. The mean number of T regulatory cells expressing FOXP3 (per 10 hpf) was 139 in the node positive and 132 in the node negative group (P = 0.540). The mean number of T regulatory cells was 162 in patients ≤35 years of age (n = 8) compared to 133 in older patients (P = 0.250). Primary tumor pathological characteristics like tumor type, grade, size, and ER, PR, and HER2 status did not correlate with FOXP3 expression. The number of FOXP3-expressing T regulatory cells does not differ significantly between sentinel node+ and sentinel node– samples. It was also not affected by primary tumor characteristics like tumor type, grade, size, hormone receptor, and HER2 status.

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