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Tumor-associated macrophages (TAMs) are prominent components of tumor stroma that promotes tumorigenesis. Many soluble factors participate in the deleterious cross-talk between TAMs and transformed cells; however mechanisms how tumors orchestrate their production remain relatively unexplored. c-Myb is a transcription factor recently described as a negative regulator of a specific immune signature involved in breast cancer (BC) metastasis. Here we studied whether c-Myb expression is associated with an increased presence of TAMs in human breast tumors. Tumors with high frequency of c-Myb-positive cells have lower density of CD68-positive macrophages. The negative association is reflected by inverse correlation between  MYB  and  CD68/CD163  markers at the mRNA levels in evaluated cohorts of BC patients from public databases, which was found also within the molecular subtypes. In addition, we identified potential  MYB -regulated TAMs recruiting factors that in combination with  MYB  and  CD163  provided a valuable clinical multigene predictor for BC relapse. We propose that identified transcription program running in tumor cells with high  MYB  expression and preventing macrophage accumulation may open new venues towards TAMs targeting and BC therapy.

Low infiltration of tumor-associated macrophages in high c-Myb-expressing breast tumors