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Cited by 213

The DOI matches its Crossref record; 47 of the 47 references it cites were found in a registry or an index.

Targeting the hypoxia-inducible factor (HIF) pathway in cancer

Open access
Poon, Evon, Harris, Adrian L., Ashcroft, Margaret·2009·Expert Reviews in Molecular Medicine

Abstract

The central component of hypoxia sensing in the cell is the hypoxia-inducible factor (HIF) transcriptional complex. HIF activity is deregulated in many human cancers, especially those that are highly hypoxic. Hypoxic tumour cells are usually resistant to radiotherapy and most conventional chemotherapeutic agents, rendering them highly aggressive and metastatic. Overexpression of HIF-α, the regulatory subunit of HIF, is associated with increased vascular density, severity of tumour grade, treatment failure and a poor prognostic outcome with conventional therapies. Therefore HIF is an attractive, although challenging, therapeutic target, and several different strategies have been developed to target HIF directly or indirectly in recent years. This review outlines the preclinical and clinical advances in this arena and discusses which cancers may benefit from HIF-targeted therapy.

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Metadata

Authors
Poon, E., Harris, A. L., & Ashcroft, M.
Venue
Expert Reviews in Molecular Medicine
Published
2009-08
Volume
11
Pages
e26-e26
ISSN
1462-3994 (ISSN-L)
OpenAlex
W2143643440
Cited by
213
References
47
FWCI
5.83
Type
journal article
Language
en
Open access
bronze

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CoChat. (2026). Citation check: Targeting the hypoxia-inducible factor (HIF) pathway in cancer. https://app.cochat.ai/papers/10.1017/s1462399409001173
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Poon, E., Harris, A. L., & Ashcroft, M. (2009). Targeting the hypoxia-inducible factor (HIF) pathway in cancer. Expert Reviews in Molecular Medicine. https://doi.org/10.1017/s1462399409001173

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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.