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Low infiltration of tumor-associated macrophages in high c-Myb-expressing breast tumors
N. Volodko, T. Gutor, O. Petronchak, R. Huley, M. Dúcka, J. Šmarda, L. Borsig, P. Beneš, L. Knopfová,
Language English Country Great Britain
Document type Journal Article, Research Support, Non-U.S. Gov't
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- MeSH
- Antigens, Differentiation, Myelomonocytic metabolism MeSH
- Antigens, CD metabolism MeSH
- Datasets as Topic MeSH
- Adult MeSH
- Kaplan-Meier Estimate MeSH
- Cohort Studies MeSH
- Middle Aged MeSH
- Humans MeSH
- Macrophages immunology metabolism MeSH
- Tumor Microenvironment genetics immunology MeSH
- Breast Neoplasms genetics immunology mortality pathology MeSH
- Prognosis MeSH
- Cell Proliferation MeSH
- Proto-Oncogene Proteins c-myb metabolism MeSH
- Breast pathology MeSH
- Receptors, Cell Surface metabolism MeSH
- Gene Expression Regulation, Neoplastic immunology MeSH
- Aged, 80 and over MeSH
- Aged MeSH
- Gene Expression Profiling MeSH
- Check Tag
- Adult MeSH
- Middle Aged MeSH
- Humans MeSH
- Aged, 80 and over MeSH
- Aged MeSH
- Female MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
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.
References provided by Crossref.org
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- $a 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.
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