Tumor entrained neutrophils inhibit seeding in the premetastatic lung
Open accessAbstract
Primary tumors have been shown to prepare distal organs for later colonization of metastatic cells by stimulating organ-specific infiltration of bone marrow derived cells. Here we demonstrate that neutrophils accumulate in the lung prior to the arrival of metastatic cells in mouse models of breast cancer. Tumor-entrained neutrophils (TENs) inhibit metastatic seeding in the lungs by generating H(2)O(2) and tumor secreted CCL2 is a critical mediator of optimal antimetastatic entrainment of G-CSF-stimulated neutrophils. TENs are present in the peripheral blood of breast cancer patients prior to surgical resection but not in healthy individuals. Thus, whereas tumor-secreted factors contribute to tumor progression at the primary site, they concomitantly induce a neutrophil-mediated inhibitory process at the metastatic site.
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Immune cells can attenuate metastasis.
“On one hand, there is evidence that immune cells have the capability to attenuate metastasis[54–59], which provides insight into how to restore or enhance their ability to combat cancer.”
From Microfluidics: A New Tool for Modeling Cancer–Immune Interactions (2016) · cites this paper as [57]
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- Authors
- Granot, Z., Henke, E., Comen, E. A., King, T. A., Norton, L., & Benezra, R.
- Affiliations
- Memorial Sloan Kettering Cancer Center (US)
- Corresponding author
- Benezra, Robert
- Venue
- Cancer Cell
- Publisher
- Elsevier BV
- Published
- 2011-09
- Volume
- 20
- Issue
- 3
- Pages
- 300-314
- ISSN
- 1535-6108 (ISSN-L)
- PMC
- PMC3172582
- OpenAlex
- W2112744561
- Cited by
- 782
- References
- 43
- Citations by year
- 2026: 34 · 2025: 60 · 2024: 49 · 2023: 57 · 2022: 64 · 2021: 95 · 2020: 69 · 2019: 49 · 2018: 60 · 2017: 51 · 2016: 57 · 2015: 41 · 2014: 20 · 2013: 43 · 2012: 31
- FWCI
- 13.48
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- www.elsevier.com/tdm/userlicense/1.0/ (tdm)
- www.elsevier.com/legal/tdmrep-license (tdm)
- www.elsevier.com/open-access/userlicense/1.0/ (vor, 685 d)
- doi.org/10.15223/policy-017 (stm-asf)
- doi.org/10.15223/policy-037 (stm-asf)
- doi.org/10.15223/policy-012 (stm-asf)
- doi.org/10.15223/policy-029 (stm-asf)
- doi.org/10.15223/policy-004 (stm-asf)
- Locations
- Cancer Cell (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health
- Breast Cancer Research Foundation
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Immune cells in cancer
- Health Sciences › Medicine › Oncology › Cancer Cells and Metastasis
- Life Sciences › Immunology and Microbiology › Immunology › Neutrophil, Myeloperoxidase and Oxidative Mechanisms
- Keywords
- breast cancer metastasis, lung metastasis, pre-metastatic niche, neutrophil accumulation, hydrogen peroxide, MCP-1, granulocyte colony-stimulating factor, bone marrow-derived cells, tumor-secreted factors
- MeSH terms
- Animals, Bone Marrow Cells, Breast Neoplasms, Cytotoxicity, Immunologic, Female, Humans, Hydrogen Peroxide, Lung, Lung Neoplasms, Mice, Inbred BALB C, Mice, Inbred C57BL, Molecular Sequence Data, Neoplasm Invasiveness, Neutrophils, Granulocyte Colony-Stimulating Factor, Transforming Growth Factor beta, Reactive Oxygen Species, Chemokine CCL2, RNA Interference, RNA, Small Interfering, Cell Line, Tumor, Mice
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