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Open AccessJournal ArticleDOI

Tumor stress, cell death and the ensuing immune response

TLDR
The state-of-the-art of cancer immunity is summarized and how tumor cell death dictates the links between innate and acquired immunity is described.
Abstract
A cornucopia of physiological and pathological circumstances including anticancer chemotherapy and radiotherapy can induce cell death. However, the immunological consequences of tumor cell demise have remained largely elusive. The paradigm opposing 'apoptosis versus necrosis' as to their respective immunogenicity does not currently hold to predict long-term immunity. Moreover, the notion that tumor cells may be 'stressed' before death to be recognized by immune cells deserves to be underlined. 'Eat-me', 'danger' and 'killing' signals released by stressed tumor under the pressure of cytotoxic compounds may serve as links between the chemotherapy-elicited response of tumor cells and subsequent immune responses. This review will summarize the state-of-the-art of cancer immunity and describe how tumor cell death dictates the links between innate and acquired immunity.

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Interferon-γ reverses the immunosuppressive and protumoral properties and prevents the generation of human tumor-associated macrophages

TL;DR: IFNγ overcomes TAM‐induced immunosuppression by preventing TAM generation and functions, highlighting that IFNγ used locally at the tumor site could potentiate the efficacy of antitumor immunotherapies based on the generation of effector T cells.
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Apoptosis in cancer: key molecular signaling pathways and therapy targets.

TL;DR: This review provides references concerning the apoptotic molecules, their interactions, the mechanisms involved in apoptosis resistance, and also the modulation of apoptosis for the treatment of cancer.
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Molecular Interactions between Dying Tumor Cells and the Innate Immune System Determine the Efficacy of Conventional Anticancer Therapies

TL;DR: Data suggests that HMGB1- and TLR4-dependent immune responses elicited by conventional cancer treatment may increase the probability to achieve a durable therapeutic success.
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HMGB1: a two-headed signal regulating tumor progression and immunity

TL;DR: A surprising role for innate receptors, including toll like receptor 4 (TLR4), in the response to conventional cancer radio and chemotherapy has also recently emerged, providing new insight into the mechanisms by which these treatments actually work.
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Immunogenicity of anthracyclines: moving towards more personalized medicine.

TL;DR: In this paper, the effects of anthracyclines on the host immune system and how this knowledge can be exploited for anticancer therapy are discussed. But, the authors do not discuss how to exploit this knowledge to improve the efficacy of chemotherapy.
References
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Journal ArticleDOI

The hallmarks of cancer.

TL;DR: This work has been supported by the Department of the Army and the National Institutes of Health, and the author acknowledges the support and encouragement of the National Cancer Institute.
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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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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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Release of chromatin protein HMGB1 by necrotic cells triggers inflammation

TL;DR: It is reported that Hmgb1-/- necrotic cells have a greatly reduced ability to promote inflammation, which proves that the release of HMGB1 can signal the demise of a cell to its neighbours, and cells undergoing apoptosis are programmed to withhold the signal that is broadcast by cells that have been damaged or killed by trauma.
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