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Prognostic significance of FOXP3+tumor-infiltrating lymphocytes in Basrah women of breast cancer

Journal: Scientific Journal of Medical Research (Vol.2, No. 5)

Publication Date:

Authors : ; ;

Page : 1-6

Keywords : FOXP3; Breast; Cancer; Lymphocyte;

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Abstract

Objective: FOXP3 is a forkhead box transcription factor, a defining hall mark of Treg cells, and its functions as the master regulator in the development and function of regulatory T cell. Treg cells are sub set of T lymphocytes that the main functions regulate the immune response through suppress the proliferation and cytokines production of effector T lymphocyte. The infiltration of FOXP3+ regulatory T cells into invasive tumors has been reported to be associated with survival in a variety of cancers. The prognostic significance of FOXP3+ tumor infiltrating lymphocytes (TILs) in breast cancer, however, remains controversial. We investigated whether there were significant numbers of FOXP3-positive Tregs in breast cancer using immunohistochemistry, and whether the presence of FOXP3-positive Tregs was associated with other prognostic factors, such as stage or histologic grade, receptor status, lymph node involve and metastasis. Methods: A tissue microarray (TMA) including 24 ductal and 11 lobular breast cancers was stained with antibodies recognizing FOXP3 by immunohistochemical techniques. Foxp3+Lymphocyte counts were correlated with clinicopathological parameters. Results: The Foxp3-positive was more prevalent whereas Foxp3-negative was rare. Lymph node displayed significantly (p < 0.01) higher FOXP3+ lymphocyte infiltration and no metastasis was also significant (P˂0.02) associated with higher FOXP3+ TIL counts. In contrast, FOXP3+ lymphocyte infiltration was not linked with other clinic pathological parameters. Conclusion: Our results showed a significant increase in the proportion of these cells in the tissue of breast cancer patients. The prognostic value of FOXP3+ TILs in breast cancer differs depending on lymph node and metastasis.

Last modified: 2018-07-06 19:30:28