Cancer-related inflammation.
TLDR
The molecular pathways of this cancer-related inflammation are now being unravelled, resulting in the identification of new target molecules that could lead to improved diagnosis and treatment.Citations
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Inhibition of CXCR2 profoundly suppresses inflammation-driven and spontaneous tumorigenesis
Thomas Jamieson,Mairi Clarke,Colin W. Steele,Michael S. Samuel,Jens Neumann,Andreas Jung,David J. Huels,Michael F. Olson,Sudipto Das,Robert J. B. Nibbs,Owen J. Sansom +10 more
TL;DR: CXCR2 is a potent protumorigenic chemokine receptor that directs recruitment of tumor-promoting leukocytes into tissues during tumor-inducing and tumor-driven inflammation and may have therapeutic and prophylactic potential in the treatment of cancer.
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Cancer and inflammation: Promise for biologic therapy
Sandra Demaria,Eli Pikarsky,Michael Karin,Lisa M. Coussens,Yen-Ching Chen,Emad M. El-Omar,Giorgio Trinchieri,Steven M. Dubinett,Jenny T. Mao,Eva Szabo,Arthur M. Krieg,George J. Weiner,Bernard A. Fox,George Coukos,Ena Wang,Robert T. Abraham,Michele Carbone,Michael T. Lotze +17 more
TL;DR: Although no therapeutic strategies to prevent or treat cancers based on insights into inflammatory pathways are currently approved for the common epithelial malignancies, there remains substantial interest in agents targeting COX2 or PPARγ, ethyl pyruvate and steroids, and several novel agents on the horizon.
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RIP3: a molecular switch for necrosis and inflammation.
TL;DR: The current understanding of the mechanisms that drive RIP3-dependent necrosis and its role in different inflammatory diseases is reviewed.
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S100A8/A9 activate key genes and pathways in colon tumor progression
TL;DR: Evidence is presented that S100A8/A9 interact with RAGE and carboxylated glycans on colon tumor cells and promote activation of MAPK and NF-κB signaling pathways, revealing a novel role for myeloid-derived S 100A8-A9 in activating specific downstream genes associated with tumorigenesis and in promoting tumor growth and metastasis.
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The role of the complement system in cancer
TL;DR: In this Review, immune and nonimmune functions of complement proteins and the tumor-promoting effect of complement activation are discussed.
References
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Journal ArticleDOI
Inflammation and cancer
Lisa M. Coussens,Zena Werb +1 more
TL;DR: It is now becoming clear that the tumour microenvironment, which is largely orchestrated by inflammatory cells, is an indispensable participant in the neoplastic process, fostering proliferation, survival and migration.
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Inflammation and cancer: back to Virchow?
TL;DR: A rationale for the use of cytokine and chemokine blockade, and further investigation of non-steroidal anti-inflammatory drugs, in the chemoprevention and treatment of malignant diseases is provided.
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Involvement of chemokine receptors in breast cancer metastasis.
Anja Müller,Bernhard Homey,Hortensia Soto,Nianfeng Ge,Daniel Catron,Matthew E. Buchanan,Terri McClanahan,Erin Murphy,Wei Yuan,Stephan N. Wagner,Jose Luis Barrera,Alejandro Mohar,Emma Verastegui,Albert Zlotnik +13 more
TL;DR: It is reported that the chemokine receptors CXCR4 and CCR7 are highly expressed in human breast cancer cells, malignant breast tumours and metastases and their respective ligands CXCL12/SDF-1α and CCL21/6Ckine exhibit peak levels of expression in organs representing the first destinations of breast cancer metastasis.
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Macrophage polarization: tumor-associated macrophages as a paradigm for polarized M2 mononuclear phagocytes
Alberto Mantovani,Silvano Sozzani,Silvano Sozzani,Massimo Locati,Paola Allavena,Antonio Sica +5 more
TL;DR: These functionally polarized cells, and similarly oriented or immature dendritic cells present in tumors, have a key role in subversion of adaptive immunity and in inflammatory circuits that promote tumor growth and progression.
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Nuclear factor-kappaB in cancer development and progression.
TL;DR: This article showed that NF-kappaB provides a mechanistic link between inflammation and cancer, and is a major factor controlling the ability of both pre-neoplastic and malignant cells to resist apoptosis-based tumour-surveillance mechanisms.