Cancer-related inflammation.
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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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Journal ArticleDOI
Does the Immune System Naturally Protect Against Cancer
TL;DR: There are compelling pieces of evidence that a primary function of the immune system is to confer protection against cancer, and a promising strategy to treat cancer consists in potentiating the naturally occurring immune response of the patient, through blockade of theimmune checkpoint molecules CTLA-4, PD-1, or PD-L1.
Journal ArticleDOI
How cell death shapes cancer
Verena Labi,Miriam Erlacher +1 more
TL;DR: Evidence is reviewed in support of the oncogenic role of stress-induced apoptosis in human cancers, exemplified in therapy-induced secondary malignancies and myelodysplastic syndromes in patients with congenital bone marrow failure Syndromes.
Book ChapterDOI
Generation and characterization of murine alternatively activated macrophages.
TL;DR: In this chapter, in vitro derivation of polarized bone marrow macrophages and methods to analyze the resulting phenotype are described including Q-PCR, Western blotting, and enzyme assays to determine argI and iNOS expression and activity, as well as production of IL-12p40 and IL-10 and determination ofIL-12/IL-10 ratios.
Journal ArticleDOI
The integration of inflammaging in age-related diseases.
TL;DR: The concept of inflammaging is described, being a chronic, systemic, low grade and therefore for a long time subclinical, inflammatory process, and how it is integrated in the context of ARD.
Journal ArticleDOI
C1q acts in the tumour microenvironment as a cancer-promoting factor independently of complement activation
Roberta Bulla,Claudio Tripodo,Damiano Rami,Guang Sheng Ling,Chiara Agostinis,Carla Guarnotta,Sonia Zorzet,Paolo Durigutto,Marina Botto,Francesco Tedesco +9 more
TL;DR: It is shown that C1q, but not C4, is expressed in the stroma and vascular endothelium of several human malignant tumours andBone marrow chimeras between C1qa−/− and WT mice identify non-BM-derived cells as the main local source of C1Q that can promote cancer cell adhesion, migration and proliferation.
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.
Journal ArticleDOI
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.
Journal ArticleDOI
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.
Journal ArticleDOI
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.
Journal ArticleDOI
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.