High expression of CX3CL1 by tumor cells correlates with a good prognosis and increased tumor-infiltrating CD8+ T cells, natural killer cells, and dendritic cells in breast carcinoma

被引:100
作者
Park, Min Ho [1 ,3 ]
Lee, Ji Shin [2 ,3 ]
Yoon, Jung Han [1 ,3 ]
机构
[1] Chonnam Natl Univ, Dept Surg, Sch Med, Kwangju, South Korea
[2] Chonnam Natl Univ, Dept Pathol, Sch Med, Kwangju, South Korea
[3] Res Inst Med Sci, Kwangju, South Korea
基金
新加坡国家研究基金会;
关键词
CX3CL1; breast carcinoma; CD8+T cells; natural killer cells; dendritic cells; prognosis; ANTITUMOR IMMUNE-RESPONSE; COLORECTAL-CANCER; FRACTALKINE; SYSTEM; LYMPHOCYTES; ACTIVATION; CHEMOKINES; RECEPTORS; CD1A;
D O I
10.1002/jso.23095
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Background CX3CL1 is the only CX3C chemokine that can chemoattract T cells, natural killer (NK) cells, and dendritic cells (DCs). The role of CX3CL1 in breast carcinoma remains unknown. Methods Immunohistochemical staining for CX3CL1, CD8, CD57, and CD1a was performed on 204 breast carcinoma specimens using tissue microarray blocks to determine whether CX3CL1 expression correlated with a good prognosis and antitumor immunity. Results The number of stromal CD8+ T cells, intratumoral CD1a+ DCs, and stromal CD57+ NK cells were significantly increased in the high CX3CL1 expression group compared with those in the low CX3CL1expression group. Patients with high CX3CL1 expression had a significantly better disease-free and overall survival than those with low CX3CL1 expression (P?=?0.002 and P?<?0.001, respectively). CX3CL1 expression was identified as one of the independent prognostic factors for disease-free and overall survival (P?=?0.046 and P?=?0.010, respectively). Conclusion The expression of CX3CL1 by tumor cells appears to enhance the recruitment of CD8+ T cells, CD57+ NK cells, and CD1a+ DCs, thereby bringing about a better prognosis in breast carcinoma. CX3CL1 is a new prognostic biomarker and may be a novel candidate for development of a more effective therapeutic strategy for breast carcinoma. J. Surg. Oncol. 2012; 106:386392. (c) 2012 Wiley Periodicals, Inc.
引用
收藏
页码:386 / 392
页数:7
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