Document Type
Article
Publication Date
8-2017
Abstract
Tumor-associated macrophages (TAMs) are major constituents of the tumor microenvironment in solid tumors and have been implicated as mediators of tumor progression, invasion and metastasis. Correspondingly, accumulation of TAMs is associated with unfavorable clinical outcomes in numerous types of solid tumors. E-selectin is a hallmark of inflammation and a key adhesion molecule that accommodates the initial contact of circulating immune cells with the inflamed vessel surface. Currently, the association between E-selectin and TAMs is not fully elucidated; therefore, the present study investigated the association between vessel inflammation, TAM infiltration, and clinical outcome in breast cancer. A total of 53 procedure-naïve invasive breast cancer cases were immunohistochemically analyzed for the presence of cluster of differentiation (CD)68+ TAMs, E-selectin+ vessels and tumor inflammation. The association between CD68 and E-selectin expression, and tumor inflammation as well as overall survival was evaluated using Kaplan-Meier survival curves and multivariable Cox's proportional hazards regression analysis. The abundance of TAMs was identified to be positively associated with tumor inflammation, estrogen receptor and E-selectin expression levels. A greater prevalence of TAMs and tumor inflammation was significantly associated with shorter overall survival times. E-selectin expression levels were significantly higher in tumor vessels among elderly patients, but were not associated with overall survival. The abundance of TAMs was associated with the presence of E-selectin-expressing inflamed tumor vessels and tumor inflammation, as well as overall survival in patients with invasive breast carcinoma. © 2017, Spandidos Publications. All rights reserved.
Recommended Citation
Morita, Yoshihiro; Zhang, Roy; Leslie, Macall; Adhikari, Smita; Hasan, Nafis; Chervoneva, Inna; Rui, Hallgeir; and Tanaka, Takemi, "Pathologic evaluation of tumor-associated macrophage density and vessel inflammation in invasive breast carcinomas" (2017). Department of Pharmacology and Experimental Therapeutics Faculty Papers. Paper 84.
https://jdc.jefferson.edu/petfp/84
Comments
This article has been peer reviewed. It is the author’s final published version in Oncology Letters
Volume 14, Issue 2, August 2017, Pages 2111-2118.
The published version is available at DOI: 10.3892/ol.2017.6466. Copyright © Spandidos Publications