ArticleScientific reports2016
Macrophages Enhance Migration in Inflammatory Breast Cancer Cells via RhoC GTPase Signaling.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers, 1 of them a synthesis that pooled it.
What it found
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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.
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Who cites it
34 citing papers in PubMed, 1 synthesis or guideline pooled it, 48 citations in OpenAlex.
- Modulation of tumor-associated macrophage activity with radiation therapy: a systematic review.Strahlentherapie und Onkologie : Organ der Deutschen Rontgengesellschaft ... [et al] · 2023Pooled it
- Reprogramming the Immune Landscape of Inflammatory Breast Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Review
- The spatial immune landscape predicts outcome and reveals the central role of tumor-associated macrophages in inflammatory breast cancer biology.Breast cancer research : BCR · 2026Article
- Article
- Genomic and transcriptomic analyses identify distinctive features of triple-negative inflammatory breast cancer.NPJ precision oncology · 2024Article
- Protocols for Co-Culture Phenotypic Assays with Breast Cancer Cells and THP-1-Derived Macrophages.Journal of mammary gland biology and neoplasia · 2024Article
- Article
- Micro-engineering and nano-engineering approaches to investigate tumour ecosystems.Nature reviews. Cancer · 2023Review
- Article
- Blood-brain barrier remodeling in an organ-on-a-chip device shows Dkk1 to be a regulator of early metastasis.Advanced nanobiomed research · 2023Article
- High-Throughput Cellular Heterogeneity Analysis in Cell Migration at the Single-Cell Level.Small (Weinheim an der Bergstrasse, Germany) · 2023Article
- EGFR is a master switch between immunosuppressive and immunoactive tumor microenvironment in inflammatory breast cancer.Science advances · 2022Article
- The presence of retraction clefts correlates with lymphovascular invasion and lymph node metastasis and predicts poor outcome: Analysis of 2497 breast cancer patients.Annals of diagnostic pathology · 2022Article
- Paracrine IL-6 Signaling Confers Proliferation between Heterogeneous Inflammatory Breast Cancer Sub-Clones.Cancers · 2022Article
- Circulating inflammatory cells in patients with metastatic breast cancer: Implications for treatment.Frontiers in oncology · 2022Review
- Inflammatory Breast Cancer: The Secretome of HCMVFrontiers in oncology · 2022Article
- Going with the Flow: Modeling the Tumor Microenvironment Using Microfluidic Technology.Cancers · 2021Review
- Rho-Kinase as a Target for Cancer Therapy and Its Immunotherapeutic Potential.International journal of molecular sciences · 2021Review
- Immune landscape of inflammatory breast cancer suggests vulnerability to immune checkpoint inhibitors.Oncoimmunology · 2021Article
- Estrogen Receptor β-Mediated Inhibition of Actin-Based Cell Migration Suppresses Metastasis of Inflammatory Breast Cancer.Cancer research · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors at 2 institutions in 1 country.
Funding
Abstract
Inflammatory breast cancer (IBC) is the most lethal form of breast cancer. All IBC patients have lymph node involvement and one-third of patients already have distant metastasis at diagnosis. This propensity for metastasis is a hallmark of IBC distinguishing it from less lethal non-inflammatory breast cancers (nIBC). Genetic profiling studies have been conducted to differentiate IBC from nIBC, but no IBC cancer-cell-specific gene signature has been identified. We hypothesized that a tumor-extrinsic factor, notably tumor-associated macrophages, promotes and contributes to IBC's extreme metastatic phenotype. To this end, we studied the effect of macrophage-conditioned media (MCM) on IBC. We show that two IBC cell lines are hyper-responsive to MCM as compared to normal-like breast and aggressive nIBC cell lines. We further interrogated IBC's hyper-responsiveness to MCM using a microfluidic migration device, which permits individual cell migration path tracing. We found the MCM "primes" the IBC cells' cellular machinery to become extremely migratory in response to a chemoattractant. We determined that interleukins -6, -8, and -10 within the MCM are sufficient to stimulate this enhanced IBC migration effect, and that the known metastatic oncogene, RhoC GTPase, is necessary for the enhanced migration response.
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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.