Cancer-related inflammation

By A. Mantovani, P. Allavena, A. Sica, F. Balkwill. Nature, 2008

11,101 citations recorded by the source corpus.

Subfields: Immunology, Oncology

View Paper: https://www.semanticscholar.org/paper/b3a9e344a32ad6ca402d9149ac74b2b1df9e3076

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. M. Karin
4. P. Allavena
5. J. Pollard
6. Lisa M. Coussens
7. D. Hanahan
8. J. Joyce

In Oncology

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

Citations in the corpus

• The interaction of anticancer therapies with tumor-associated macrophages (2015, background): “2; Mantovani et al., 2008; Ruffell et al., 2012; Sica and Mantovani, 2012; Coussens et al., 2013; De Palma and Lewis, 2013; Colegio et al., 2014; Noy and Pollard, 2014).”
• Early-Life Adversity and Physical and Emotional Health across the Lifespan: A Neuro-Immune Network Hypothesis (2015, background): “These conditions range from traditional psychiatric disorders, like depression and substance misuse, to allergic, metabolic, cardiovascular, neoplastic, and rheumatic diseases (12,13,114,115).”
• Rethinking Ovarian Cancer: Recommendations for Improving Outcomes (2011, neutral): “Tumour cells typically trigger inflammatory cytokine networks as a means of escaping immune recognition in spite of surrounding inflammatio”
• The head and neck cancer immune landscape and its immunotherapeutic implications. (2016, background): “shown to promote immune-mediated tumor clearance (38–41), effectors of innate immunity can lead to an inflammatory response and increase regional blood flow and angiogenesis, possibly contributing to tumor growth and progression (42).”
• Macrophages, innate immunity and cancer: balance, tolerance, and diversity. (2010, background): “expression of cytotoxic mediators, such as NO, and cytokines (TNFa, IL-1 and IL-12) [2,48]).”
• Tumor-Associated Macrophages in Tumor Immunity (2020, background): “Circulating inflammatory monocytes could be recruited by multiple chemokines (CCL2 and CCL5) and cytokines (CSF-1 and members of the VEGF family) to tumor (9).”
• Cancer-Associated Fibroblasts Are Activated in Incipient Neoplasia to Orchestrate Tumor-Promoting Inflammation in an NF-kappaB-Dependent Manner. (2010, background): “Studies investigating the link between inflammation and cancer have been particularly revealing, demonstrating that inflammatory immune cells are recruited to neoplasias, where they in many cases markedly promote tumor progression by facilitating multiple hallmark capabilities (de Visser et al., 200”
• Oxidative stress, inflammation, and cancer: how are they linked? (2010, background): “In addition, it has long been known that tumor growth is promoted by tumor-associated macrophages (TAM), a major leukocyte population present in tumors [65,307-310].”
• The tumor microenvironment. (2012, background): “The major leukocytes that have been identified as vital to this interaction or progression of inflammation to cancer are termed TAMs- tumor associated macrophages [37].”
• Checkpoint Blockade Cancer Immunotherapy Targets Tumour-Specific Mutant Antigens (2014, methodology): “Our findings provide some of the first experimental support for the clinical observations that (1) checkpoint blockade therapy amplifies, in some cases, preexisting anti-tumour T-cell responses(8,9,21,22); (2) whereas anti-CTLA-4 treatment eliminates regulatory T cells, promotes T-cell priming, and ”
• Cyclooxygenase-Dependent Tumor Growth through Evasion of Immunity (2015, background): “Inflammation has emerged as a major factor promoting cancer development (Coussens et al., 2013; Grivennikov et al., 2010; Mantovani et al., 2008; Rakoff-Nahoum and Medzhitov, 2009).”