Macrophage polarization in tumour progression.

By A. Sica, P. Larghi, A. Mancino, Luca Rubino, C. Porta, M. Totaro, M. Rimoldi, Subhra K. Biswas, P. Allavena, A. Mantovani. Seminars in Cancer Biology, 2008

1,239 citations recorded by the source corpus.

Subfields: Immunology, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/184c569bbdb763a14f6f7b54156a7e21ad9a035c

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. A. Sica
3. J. Pollard
4. R. Noy
5. S. Grivennikov
6. F. Greten
7. S. Badylak
8. J. Condeelis

In Molecular Biology

1. A. Mantovani
2. A. Sica
3. J. Pollard
4. Shomyseh Sanjabi
5. M. Laflamme
6. R. Noy
7. F. Greten
8. Xiangming Zou

Citations in the corpus

• Chemotaxis in cancer (2011, background): “Inside the tumour and under the influence of tumour-derived chemokines, both macrophages and neutrophils can polarize away from a tumour-suppressing phenotype (M1 and N1, respectively) towards a more tumour-promoting phenotype (M2 or N2, respectively”
• Macrophages in Tumor Microenvironments and the Progression of Tumors (2012, background): “For example, during tumor progression, the macrophage phenotype changes from classically activated to alternatively activated [23].”
• Microglial cell origin and phenotypes in health and disease (2011, background): “Alternative activation states can be deleterious in other disease states, particularly cance”
• Repertoire of microglial and macrophage responses after spinal cord injury (2011, background): “Recent studies on macrophage polarization in vitro and in non-neural tissues, in conditions such as tumours, kidney disease and atherosclerosis, have extended our understanding of macrophage polarization and the role of the tissue microenvironment in this proces”
• Akt Signaling Pathway in Macrophage Activation and M1/M2 Polarization (2017, background): “found in the tumor stroma or in inflamed tissues (6, 7), or induced by abundant glucocorticoids, termed M(GC), such as late stages of sepsis (8, 9) or in cancer (9, 10).”
• The polarization of immune cells in the tumour environment by TGFβ (2010, background): “In late stages of tumour development, TAMs and MDSCs can produce TGFβ and are classically involved in cancer progression and metastasi”
• Tumor-Associated Macrophages and Neutrophils in Tumor Microenvironment (2016, background): “In turn, TAMs contribute to high IL-10 and TGF-β levels in the TME [20] and they express inflammatory cytokines (e.”
• Tumor-Associated Macrophages as Major Players in the Tumor Microenvironment (2014, background): “The polarization of macrophages toward the pro-angiogenic phenotype is regulated by hypoxia and the various signals derived from tumor and stromal cells [11,62].”
• Proangiogenic scaffolds as functional templates for cardiac tissue engineering (2010, background): “At one end, M1-polarized MΦ are proinflammatory; at the other extreme, M2-polarized MΦ are considered antiinflammatory, marked by the release of growth factor and tissue remodeling (19, 33).”
• Macrophages, innate immunity and cancer: balance, tolerance, and diversity. (2010, background): “Possible explanations for this discrepancy are based on the functional feature of macrophages, which are considered highly plastic cells able to finely modulate their programs in response to different microenvironmental conditions [48].”
• The application of nanoparticles in cancer immunotherapy: Targeting tumor microenvironment (2020, background): “Given these two activated states, macrophages are regarded as “a double-edged sword” with both pro-tumor and anti-tumor ability [47, 48].”
• Macrophage polarization: An opportunity for improved outcomes in biomaterials and regenerative medicine (2012, background): “mature tumors are of a more suppressive, M2-like, phenotype [36,39].”
• TNF and increased intracellular iron alter macrophage polarization to a detrimental M1 phenotype in the injured spinal cord. (2014, neutral): “…chemokine 0.001 (Martinez et al., 2006) Ifng IFN-g 274 M1 inducing cytokine 0.001 (Martinez et al., 2006) Lta Lymphotoxin-a 265 Th1 cytokine 0.003 (Sica et al., 2008) Tnf TNF 252 M1 cytokine 0.02 (Martinez et al., 2006) Cd70 CD70 138 M1 cytokine* 0.02 (Martinez et al., 2006) Tnfsf10 TRAIL 131 M1…”