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Cited by 169

The DOI matches its Crossref record; 16 of the 16 references it cites were found in a registry or an index.

The Role of Interleukin 17 in Tumour Proliferation, Angiogenesis, and Metastasis

Open access
Yang, Bob, Kang, Heechan, Fung, Anthony, Zhao, Hailin, Wang, Tianlong, Ma, Daqing·2014·Mediators of Inflammation

Abstract

With 7.6 million deaths globally, cancer according to the World Health Organisation is still one of the leading causes of death worldwide. Interleukin 17 (IL-17) is a cytokine produced by Th17 cells, a T helper cell subset developed from an activated CD4+ T-cell. Whilst the importance of IL-17 in human autoimmune disease, inflammation, and pathogen defence reactions has already been established, its potential role in cancer progression still needs to be updated. Interestingly studies have demonstrated that IL-17 plays an intricate role in the pathophysiology of cancer, from tumorigenesis, proliferation, angiogenesis, and metastasis, to adapting the tumour in its ability to confer upon itself both immune, and chemotherapy resistance. This review will look into IL-17 and summarise the current information and data on its role in the pathophysiology of cancer as well as its potential application in the overall management of the disease.

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Metadata

Authors
Yang, B., Kang, H., Fung, A., Zhao, H., Wang, T., & Ma, D.
Venue
Mediators of Inflammation
Publisher
Wiley
Published
2014
Volume
2014
Pages
1-12
ISSN
  • 0962-9351 (ISSN-L)
  • 1466-1861
OpenAlex
W2104226707
Cited by
169
References
16
FWCI
6.03
Type
journal article
Language
en
Open access
gold

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CoChat. (2026). Citation check: The Role of Interleukin 17 in Tumour Proliferation, Angiogenesis, and Metastasis. https://app.cochat.ai/papers/10.1155/2014/623759
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Yang, B., Kang, H., Fung, A., Zhao, H., Wang, T., & Ma, D. (2014). The Role of Interleukin 17 in Tumour Proliferation, Angiogenesis, and Metastasis. Mediators of Inflammation. https://doi.org/10.1155/2014/623759

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

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