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Cited by 355

The DOI matches its Crossref record; 125 of the 125 references it cites were found in a registry or an index.

Immunosuppression associated with chronic inflammation in the tumor microenvironment

Open access
Wang, Dingzhi, DuBois, Raymond N.·2015·Carcinogenesis

Abstract

Chronic inflammation contributes to cancer development via multiple mechanisms. One potential mechanism is that chronic inflammation can generate an immunosuppressive microenvironment that allows advantages for tumor formation and progression. The immunosuppressive environment in certain chronic inflammatory diseases and solid cancers is characterized by accumulation of proinflammatory mediators, infiltration of immune suppressor cells and activation of immune checkpoint pathways in effector T cells. In this review, we highlight recent advances in our understanding of how immunosuppression contributes to cancer and how proinflammatory mediators induce the immunosuppressive microenvironment via induction of immunosuppressive cells and activation of immune checkpoint pathways.

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Crossref · 10.1093/carcin/bgv123

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Metadata

Authors
Wang, D., & DuBois, R. N.
Venue
Carcinogenesis
Published
2015-09-08
Volume
36
Issue
10
Pages
1085-1093
ISSN
  • 0143-3334 (ISSN-L)
  • 1460-2180
OpenAlex
W2234490399
Cited by
355
References
125
FWCI
9.62
Type
journal article
Language
en
Open access
green

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CoChat. (2026). Citation check: Immunosuppression associated with chronic inflammation in the tumor microenvironment. https://app.cochat.ai/papers/10.1093/carcin/bgv123
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Wang, D., & DuBois, R. N. (2015). Immunosuppression associated with chronic inflammation in the tumor microenvironment. Carcinogenesis. https://doi.org/10.1093/carcin/bgv123

Data sources

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.