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Open AccessJournal ArticleDOI

The immunobiology of cancer immunosurveillance and immunoediting

TLDR
The full understanding of the immunobiology of cancer immunosurveillance and immunoediting will hopefully stimulate development of more effective immunotherapeutic approaches to control and/or eliminate human cancers.
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This article is published in Immunity.The article was published on 2004-08-01 and is currently open access. It has received 2550 citations till now. The article focuses on the topics: Immunoediting & Immunosurveillance.

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Cancer-related inflammation.

TL;DR: 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.
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Immunity, Inflammation, and Cancer

TL;DR: The principal mechanisms that govern the effects of inflammation and immunity on tumor development are outlined and attractive new targets for cancer therapy and prevention are discussed.
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Cancer Immunoediting: Integrating Immunity’s Roles in Cancer Suppression and Promotion

TL;DR: A unifying conceptual framework called “cancer immunoediting,” which integrates the immune system’s dual host-protective and tumor-promoting roles is discussed.
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NF-kappaB: linking inflammation and immunity to cancer development and progression.

TL;DR: The hypothesis is put forward that activation of nuclear factor-κB by the classical, IKK-β (inhibitor-of-NF-β kinase-β)-dependent pathway is a crucial mediator of inflammation-induced tumour growth and progression, as well as an important modulator of tumour surveillance and rejection.
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Naturally arising Foxp3-expressing CD25+CD4+ regulatory T cells in immunological tolerance to self and non-self.

TL;DR: Naturally arising CD25+CD4+ regulatory T cells actively maintain immunological self-tolerance, and are a good target for designing ways to induce or abrogate immunological tolerance to self and non-self antigens.
References
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Journal ArticleDOI

Inflammation and cancer

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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Immunologic self-tolerance maintained by activated T cells expressing IL-2 receptor alpha-chains (CD25). Breakdown of a single mechanism of self-tolerance causes various autoimmune diseases.

TL;DR: The authors showed that CD4+CD25+ cells contribute to maintaining self-tolerance by downregulating immune response to self and non-self Ags in an Ag-nonspecific manner, presumably at the T cell activation stage.
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Tolerance, danger, and the extended family.

TL;DR: The possibility that the immune system does not care about self and non-self, that its primary driving force is the need to detect and protect against danger, and that it does not do the job alone, but receives positive and negative communications from an extended network of other bodily tissues is discussed.
Journal ArticleDOI

Cancer immunoediting: from immunosurveillance to tumor escape.

TL;DR: The historical and experimental basis of cancer immunoediting is summarized and its dual roles in promoting host protection against cancer and facilitating tumor escape from immune destruction are discussed.
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