Abstract
Tumor-associated macrophages (TAMs) are known markers playing complex roles in tumorigenesis. However, the function of TAMs in a variety of malignancies is not yet fully understood. The aim of this pilot study was to quantify the density of TAMs in Ewing sarcoma and to determine the correlation between TAMs and clinicopathological parameters. Using immunohistochemistry, the expressions of CD68 and CD163 were examined in 24 tissue samples of Ewing sarcoma of bone. The density of CD68 and CD163-positive TAMs was analyzed quantitatively and semi-quantitatively and statistically correlated with clinical parameters. CD163-positive TAMs outnumbered CD68-positive cells (median of 130 vs 96, respectively). No statistically significant relatio nship was found between density of CD68-positive cells, clinical parameters or prognosis. However, high levels of CD163-positive TAMs were associated with localized disease (P=0.008). In cases with a higher density of CD163-positive cells, a trend toward longer survival was revealed (P=0.063). This is the first study that has quantified CD163 expression in TAMs in Ewing sarcoma and showed its possible prognostic value. CD163 was confirmed to be a more specific marker of macrophages than CD68. CD163 is not an exclusive hallmark of M2 macrophages.
Highlights
Ewing sarcoma (ES) represents the second most common primary bone cancer of childhood, adolescence and young adults
At the time of diagnosis, ten patients (41.7%) had American Joint Committee on Cancer (AJCC) Stage 4, which refers to distant metastatic disease at onset
Univariate Cox proportional hazard regression analysis revealed a strong trend toward longer survival in relation to a higher density of CD163-positive Tumor-associated macrophages (TAMs), with Hazard Ratio 0.99, these results did not reach statistical significance (P=0.063, Fig. 2)
Summary
Ewing sarcoma (ES) represents the second most common primary bone cancer of childhood, adolescence and young adults. ES has a predilection for Caucasians and typically arises in bone marrow, but extra skeletal soft tissues can be affected[1] It is an extremely aggressive tumor with a high propensity for local recurrences and distant metastases. Macrophages play a crucial role in this interaction, having the ability to promote tumor growth, invasion, angiogenesis and metastasis[8,9,10,11]. These tumor-associated macrophages (TAMs) contribute to tumor relapse following anticancer therapy[12]. M2 macrophages produce IL-10, IL-1 receptor antagonist, CC ligand 22 (CCL22), matrix metalloproteinases and scavenger and mannose receptor This way promotes tissue remodeling and angiogenesis, which supports tumor progression[24,25]. The densities of TAMs were analyzed quantitatively and semi-quantitatively and number of infiltrating TAMs as well as expression levels of TAMs were correlated with clinicopathological parameters and prognosis
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