Macrophages: obligate partners for tumor cell migration, invasion, and metastasis.

By J. Condeelis, J. Pollard. Cell, 2006

2,730 citations recorded by the source corpus.

Subfields: Immunology, Oncology

View Paper: https://www.semanticscholar.org/paper/7c669182fc38a963a0764ac80093c9089393f383

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Immunology

1. A. Mantovani
2. J. Pollard
3. Lisa M. Coussens
4. D. Hanahan
5. P. Allavena
6. J. Joyce
7. A. Sica
8. F. Balkwill

In Oncology

1. J. Pollard
2. A. Mantovani
3. R. Weinberg
4. Lisa M. Coussens
5. D. Hanahan
6. J. Joyce
7. P. Allavena
8. Zena Werb

Citations in the corpus

• Collective Invasion in Breast Cancer Requires a Conserved Basal Epithelial Program (2013, background): “One solution is for cancer cells to rely upon the motility of migratory stromal cells, such as fibroblasts (Gaggioli et al., 2007) or macrophages (Condeelis and Pollard, 2006; DeNardo et al., 2009).”
• Trophic macrophages in development and disease (2009, background): “However, clinical and experimental evidence indicates that in most cases, macrophages promote the progression and malignancy of tumour”
• The transcription factor ZEB1 (δEF1) promotes tumour cell dedifferentiation by repressing master regulators of epithelial polarity (2007, background): “One attractive hypothesis is that tumour infiltrating macrophages, which are abundantly detected at the tumour–host interface, express cytokines that may induce ZEB1 expression (Condeelis and Pollard, 2006).”
• Tumor cell metabolism: cancer's Achilles' heel. (2008, background): “TAMs facilitate angiogenesis, promote tumor cell migration, and exert local immunosuppressive effects (Condeelis and Pollard, 2006).”
• Abrogation of TGF beta signaling in mammary carcinomas recruits Gr-1+CD11b+ myeloid cells that promote metastasis. (2008, background): “They are different from terminally differentiated tumor-associated macrophages (TAM), identified as Mac-1 (CD11b) and F4/80+, which have been shown to promote tumor progression and metastasis through elevated CSF-1 production and enhanced EGF signaling in cancer cells (Condeelis and Pollard, 2006).”
• Cancer as an overhealing wound: an old hypothesis revisited (2008, background): “Secretion of MMPs and other proteinases by macrophages at the invading front of a tumour also enhances cancer-cell motility and invasio”
• Cancer-Associated Fibroblasts Are Activated in Incipient Neoplasia to Orchestrate Tumor-Promoting Inflammation in an NF-kappaB-Dependent Manner. (2010, background): “Therefore, we suspected that macrophages, which are known to support tumor angiogenesis (Condeelis and Pollard, 2006), might be differentially recruited to PDSC5 tumors injected with CAFs.”
• A mechanically active heterotypic E-cadherin/N-cadherin adhesion enables fibroblasts to drive cancer cell invasion (2017, background): “Three classes of duration time were defined: longer than 60 min (>60), between 30 to 60 min (30-60) and less than 30 min (<30).”