ArticleScientific reports2019
Low infiltration of tumor-associated macrophages in high c-Myb-expressing breast tumors.
Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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Who cites it
8 citing papers in PubMed, 11 citations in OpenAlex.
- Tumor Cell-Intrinsic c-Myb Upregulation Stimulates Antitumor Immunity in a Murine Colorectal Cancer Model.Cancer immunology research · 2023Article
- Transcription factor c-Myb: novel prognostic factor in osteosarcoma.Clinical & experimental metastasis · 2022Article
- Bone marrow-independent adventitial macrophage progenitor cells contribute to angiogenesis.Cell death & disease · 2022Article
- TRIB1 regulates tumor growth via controlling tumor-associated macrophage phenotypes and is associated with breast cancer survival and treatment response.Theranostics · 2022Article
- c-Myb interferes with inflammatory IL1α-NF-κB pathway in breast cancer cells.Neoplasia (New York, N.Y.) · 2021Article
- Macrophage Biology and Mechanisms of Immune Suppression in Breast Cancer.Frontiers in immunology · 2021Review
- CD163Clinical & translational immunology · 2020Article
- Mannose receptor 1 expression does not determine the uptake of high-density mannose dendrimers by activated macrophages populations.PloS one · 2020Article
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.