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Cited by 334

The DOI matches its Crossref record; 101 of the 101 references it cites were found in a registry or an index.

The Dark Side of IFN-γ: Its Role in Promoting Cancer Immunoevasion

Open access
Mojic, Marija, Takeda, Kazuyoshi, Hayakawa, Yoshihiro·2017·International Journal of Molecular Sciences

Abstract

Interferon-γ (IFN-γ) is a pleiotropic cytokine that has long been praised as an important effector molecule of anti-tumor immunity, capable of suppressing tumor growth through various mechanisms. On the contrary to such a bright side of IFN-γ, it has also been involved in promoting an outgrowth of tumor cells with immunoevasive phenotype suggesting an existence of a dark “tumor-promoting” side effect of IFN-γ. In this review, we will summarize this multi-functional role of IFN-γ in tumor context, how it promotes changes in tumor phenotype towards increased fitness for growth in immunocompetent host. Furthermore, we summarize how IFN-γ is involved in homeostatic or cancer-triggered mechanisms to establish an immunosuppressive tumor microenvironment.

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Metadata

Authors
Mojic, M., Takeda, K., & Hayakawa, Y.
Venue
International Journal of Molecular Sciences
Publisher
MDPI AG
Published
2017-12-28
Volume
19
Issue
1
Pages
89
ISSN
1422-0067 (ISSN-L)
OpenAlex
W2781052937
Cited by
334
References
101
FWCI
10.12
Type
journal article
Language
en
Open access
gold

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CoChat. (2026). Citation check: The Dark Side of IFN-γ: Its Role in Promoting Cancer Immunoevasion. https://app.cochat.ai/papers/10.3390/ijms19010089
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Mojic, M., Takeda, K., & Hayakawa, Y. (2017). The Dark Side of IFN-γ: Its Role in Promoting Cancer Immunoevasion. International Journal of Molecular Sciences. https://doi.org/10.3390/ijms19010089

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Bibliographic data: Semantic Scholar, OpenAlex, Crossref.

Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.