Macrophage Diversity Enhances Tumor Progression and Metastasis
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Summary
There is persuasive clinical and experimental evidence that macrophages promote cancer initiation and malignant progression, and specialized subpopulations of macrophages may represent important new therapeutic targets.
- Type
- review
- Published
- 2010-04-02
- Cited by
- 5,024
- References
- 128
- Access
- Open access
- OpenAlex
- https://openalex.org/W2058648826
- Semantic Scholar
- https://api.semanticscholar.org/CorpusID:24282306
Keywords
Biology, Extravasation, Macrophage, Angiogenesis, Cancer research
References
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- Serum levels of granulocyte colony-stimulating factor (G-CSF) and macrophage colony-stimulating factor (M-CSF) in pancreatic cancer patients
- Analysis of multiple biomarkers shows that lymphoma-associated macrophage (LAM) content is an independent predictor of survival in follicular lymphoma (FL).
- Analysis of stromal signatures in the tumor microenvironment of ductal carcinoma in situ
- The S100A8–serum amyloid A3–TLR4 paracrine cascade establishes a pre-metastatic phase
- Stromal cell-derived CSF-1 blockade prolongs xenograft survival of CSF-1-negative neuroblastoma
- Anti-colony-stimulating factor-1 antibody staining in primary breast adenocarcinomas correlates with marked inflammatory cell infiltrates and prognosis.
- Systemic endocrine instigation of indolent tumor growth requires osteopontin.
- Significant correlation of monocyte chemoattractant protein‐1 expression with neovascularization and progression of breast carcinoma
- Corrupt policemen: inflammatory cells promote tumor angiogenesis
- VEGFR1 Activity Modulates Myeloid Cell Infiltration in Growing Lung Metastases but Is Not Required for Spontaneous Metastasis Formation
- NF-κB: linking inflammation and immunity to cancer development and progression
Cited by
- Alternative activation of tumor-associated macrophages by IL-4
- The inhibition of the integrin VLA-4 in MV3 melanoma cell binding by non-anticoagulant heparin derivatives.
- Microarray Analysis of Colorectal Cancer Stromal Tissue Reveals Upregulation of Two Oncogenic miRNA Clusters
- Cancer‐associated fibroblast and M2 macrophage markers together predict outcome in colorectal cancer patients
- Caspase signalling in the absence of apoptosis drives Jnk‐dependent invasion
- N-myc Downstream-regulated Gene 1 Promotes Tumor Inflammatory Angiogenesis through JNK Activation and Autocrine Loop of Interleukin-1α by Human Gastric Cancer Cells*
- Inflammation in the context of oral cancer.
- LDL receptor-related protein-1: a regulator of inflammation in atherosclerosis, cancer, and injury to the nervous system.
- Cathepsin S-mediated autophagic flux in tumor-associated macrophages accelerate tumor development by promoting M2 polarization
- The Emerging Immunological Role of Post-Translational Modifications by Reactive Nitrogen Species in Cancer Microenvironment
- Tumor-Derived Interleukin-1 Promotes Lymphangiogenesis and Lymph Node Metastasis through M2-Type Macrophages
- Versican silencing improves the antitumor efficacy of endostatin by alleviating its induced inflammatory and immunosuppressive changes in the tumor microenvironment.
- The oncolytic virus dl922-947 reduces IL-8/CXCL8 and MCP-1/CCL2 expression and impairs angiogenesis and macrophage infiltration in anaplastic thyroid carcinoma
- Natural Killer Cell-Based Therapies Targeting Cancer: Possible Strategies to Gain and Sustain Anti-Tumor Activity
- Role of deltaNp63pos CD44vpos cells in the development of N‐nitroso‐tris‐chloroethylurea‐induced peripheral‐type mouse lung squamous cell carcinomas
- Tumour stroma‐derived lipocalin‐2 promotes breast cancer metastasis
- Tumor-associated macrophages in human breast cancer parenchyma negatively correlate with lymphatic metastasis after neoadjuvant chemotherapy.
- Tumor-promoting effect of IL-23 in mammary cancer mediated by infiltration of M2 macrophages and neutrophils in tumor microenvironment.
- Radiotherapy in the age of cancer immunology: Current concepts and future developments.
- Macrophage heterogeneity and energy metabolism.
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