Low infiltration of tumor-associated macrophages in high c-Myb-expressing breast tumors
Jazyk angličtina Země Anglie, Velká Británie Médium electronic
Typ dokumentu časopisecké články, práce podpořená grantem
PubMed
31406165
PubMed Central
PMC6690941
DOI
10.1038/s41598-019-48051-1
PII: 10.1038/s41598-019-48051-1
Knihovny.cz E-zdroje
- MeSH
- antigeny diferenciační myelomonocytární metabolismus MeSH
- CD antigeny metabolismus MeSH
- datové soubory jako téma MeSH
- dospělí MeSH
- Kaplanův-Meierův odhad MeSH
- kohortové studie MeSH
- lidé středního věku MeSH
- lidé MeSH
- makrofágy imunologie metabolismus MeSH
- nádorové mikroprostředí genetika imunologie MeSH
- nádory prsu genetika imunologie mortalita patologie MeSH
- prognóza MeSH
- proliferace buněk MeSH
- protoonkogenní proteiny c-myb metabolismus MeSH
- prsy patologie MeSH
- receptory buněčného povrchu metabolismus MeSH
- regulace genové exprese u nádorů imunologie MeSH
- senioři nad 80 let MeSH
- senioři MeSH
- stanovení celkové genové exprese MeSH
- Check Tag
- dospělí MeSH
- lidé středního věku MeSH
- lidé MeSH
- senioři nad 80 let MeSH
- senioři MeSH
- ženské pohlaví MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- Názvy látek
- antigeny diferenciační myelomonocytární MeSH
- CD antigeny MeSH
- CD163 Antigen MeSH
- CD68 antigen, human MeSH Prohlížeč
- MYB protein, human MeSH Prohlížeč
- protoonkogenní proteiny c-myb MeSH
- receptory buněčného povrchu 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.
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