Tumour-educated macrophages promote tumour progression and metastasis

By J. Pollard. Nature Reviews. Cancer, 2004

3,457 citations recorded by the source corpus.

Subfields: Biomedical Engineering, Immunology, Psychiatry and Mental health

View Paper: https://www.semanticscholar.org/paper/07974bf0adf39c88f709fb87792cf512ec89f492

How researchers see this paper

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

In Biomedical Engineering

1. J. Condeelis
2. J. Pollard
3. Rakesh K. Jain
4. Dai Fukumura
5. J. Joyce
6. J. Segall
7. J. Wyckoff
8. E. Stanley

In Immunology

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

In Psychiatry and Mental health

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

Citations in the corpus

• Different tumor microenvironments contain functionally distinct subsets of macrophages derived from Ly6C(high) monocytes. (2010, background): “TAMs can promote tumor growth by affecting angiogenesis, immune suppression, and invasion and metastasis (2, 3).”
• M1 and M2 macrophages derived from THP-1 cells differentially modulate the response of cancer cells to etoposide (2015, background): “Among these tumor infiltrated immune cells, macrophages are the most abundant, called tumor associated macrophages (TAMs) [9].”
• Cancer-related inflammation, the seventh hallmark of cancer: links to genetic instability. (2009, background): “[58,61,63,94].”
• Paradoxical roles of the immune system during cancer development (2006, background): “These experimental data, combined with the positive correlation in human cancers between CSF1 levels, macrophage recruitment and poor prognosi”
• Clodronate-liposome-mediated depletion of tumour-associated macrophages: a new and highly effective antiangiogenic therapy approach (2006, background): “Macrophages are perfectly apt to promote these processes, as their monocytic precursors migrate to specific locations such as hypoxic tumour tissues (Mantovani et al, 2004; Murdoch et al, 2004; Pollard, 2004), where they differentiate and synthesise angiogenic molecules.”
• Tumor cell biodiversity drives microenvironmental reprogramming in liver cancer (2019, background): “A uthor M anuscript A uthor M anuscript A uthor M anuscript A uthor M anuscript VEGF in Div-High tumors may induce polarization of CAFs, TAMs and TECs, and drive tumor progression (Goel and Mercurio, 2013; Kalluri, 2016; Pollard, 2004).”
• Tumor‐induced tolerance and immune suppression by myeloid derived suppressor cells (2008, background): “Inflammatory leukocytes reach tumor stroma (9), suggesting an ongoing cancer-related inflammation.”
• The Yin‐Yang of tumor‐associated macrophages in neoplastic progression and immune surveillance (2008, background): “A recent report showed that co-cultivation of tumor cells with macrophages leads to enhanced invasiveness of the malignant cells due to TNF-a-dependent matrix metalloproteinase (MMP) induction in the macrophages (30).”
• Tumor microvasculature and microenvironment: targets for anti-angiogenesis and normalization. (2007, background): “…influence many steps of tumor progression, such as tumor cell proliferation, invasion, angiogenesis, metastasis, and even malignant transformation (Elenbaas and Weinberg, 2001; Fukumura et al., 1998; Li et al., 2003; Liotta and Kohn, 2001; Pollard, 2004; Ruiter et al., 2001; Tlsty, 2001).”
• Anti-PlGF inhibits growth of VEGF(R)-inhibitor-resistant tumors without affecting healthy vessels. (2007, methodology): “Tumor perfusion was analyzed using fluorescent microspheres (Luttun et al., 2002b).”