ArticleNature cell biology2014
A breast cancer stem cell niche supported by juxtacrine signalling from monocytes and macrophages.
Article in Nature cell biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 299 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
299 citing papers in PubMed, 1 synthesis or guideline pooled it, 469 citations in OpenAlex.
- The mechanism of breast cancer stem cells and tumor microenvironment promoting radioresistance in breast cancer and its intervention strategies.Frontiers in immunology · 2026Pooled it
- Deciphering the role of sirtuins in cancer immunoregulation through molecular cross-talk and docking-based interaction.Molecular biology reports · 2026Review
- The pivotal role of macrophages in tumorigenesis and pioneering cancer immunotherapy across pre-clinical and clinical frontiers.Journal of cancer research and clinical oncology · 2026Review
- Regulated cell death plasticity in cancer: thresholds, reversibility, and therapeutic failure.Journal of translational medicine · 2026Review
- Review
- The metabolic plasticity of cancer stem cells: bidirectional crosstalk with organ-resident cells.Experimental & molecular medicine · 2026Review
- Review
- Comparative single cell analysis of wound and cancer identifies the metabolic dialogues between tumor initiating stem cells and macrophages.bioRxiv : the preprint server for biology · 2026Article
- Prognostic value and predictive biomarkers of synergistic interaction between tumor-associated macrophages and cancer stem cells in colorectal cancer.Molecular and clinical oncology · 2026Article
- Tumor-Associated Macrophages as Therapeutic Targets: Deciphering Interaction Networks and Advancing Clinical Translation.MedComm · 2026Review
- Cellular neighborhoods in cancer.Nature cancer · 2026Article
- Macrophages Drive Ferroptosis Resistance after Radiotherapy.Cancer communications (London, England) · 2026Article
- Identification, functional insights and therapeutic targeting of EMT tumour states.Nature reviews. Cancer · 2026Review
- MisTIC: Missegmented Transcript Inference Correction for Improved Spatial Transcriptomics Analysis.bioRxiv : the preprint server for biology · 2025Article
- Genetic profiling of the circulating proteome in common diseases suggests causal proteins and improves risk prediction.Nature communications · 2025Article
- Review
- How stem cells respond to infection, inflammation and ageing.Nature reviews. Immunology · 2025Review
- The lncrnas: innovative multifunctional players of drug resistance in colorectal cancer.Cancer cell international · 2025Review
- Clinical significance and expression of ALDH1 in triple-negative breast cancer.Diagnostic pathology · 2025Article
- The Tumor Environment in Peritoneal Carcinomatosis and Malignant Pleural Effusions: Implications for Therapy.Cancers · 2025Review
239 more citing papers are in PubMed but not listed here.
Corrections and comments
- Erratum issued
Authors and funding
11 authors at 5 institutions in 1 country.
Funding
Abstract
The cell-biological program termed the epithelial-mesenchymal transition (EMT) confers on cancer cells mesenchymal traits and an ability to enter the cancer stem cell (CSC) state. However, the interactions between CSCs and their surrounding microenvironment are poorly understood. Here we show that tumour-associated monocytes and macrophages (TAMs) create a CSC niche through juxtacrine signalling with CSCs. We performed quantitative proteomic profiling and found that the EMT program upregulates the expression of CD90, also known as Thy1, and EphA4, which mediate the physical interactions of CSCs with TAMs by directly binding with their respective counter-receptors on these cells. In response, the EphA4 receptor on the carcinoma cells activates Src and NF-κB. In turn, NF-κB in the CSCs induces the secretion of a variety of cytokines that serve to sustain the stem cell state. Indeed, admixed macrophages enhance the CSC activities of carcinoma cells. These findings underscore the significance of TAMs as important components of the CSC niche.
Indexed as
Identifiers
What OpenQuestion holds
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.