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Cited by 314

The DOI matches its Crossref record; 86 of the 86 references it cites were found in a registry or an index.

Disrupting Insulin-Like Growth Factor Signaling as a Potential Cancer Therapy

Sachdev, D., Yee, D.·2008·AACR Education book

Abstract

The type I insulin-like growth factor receptor (IGF-IR) plays multiple roles in several cancers and increased circulating levels of insulin-like growth factor-I (IGF-I) are associated with increased risk of breast, colon, and prostate cancers. Because IGF-II and insulin signal via the insulin receptor (IR) to stimulate the growth of cancer cells, inhibition of IR might be necessary to totally disrupt the action of IGFs and their receptors. This review describes the well-recognized roles of IGF-IR in driving the malignant phenotype, examines the evidence that perhaps IR should also be targeted to inhibit the effects of the IGF ligands and insulin in cancer, describes the strategies to disrupt IGF signaling in cancer, and highlights some key issues that need to be considered as clinical trials targeting IGF-IR proceed.

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Crossref · 10.1158/aacr.edb-mct-06-0080

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Metadata

Authors
Sachdev, D., & Yee, D.
Venue
AACR Education book
Published
2008-04-12
Volume
2008
Issue
1
Pages
39-58
ISSN
1943-6475 (ISSN-L)
OpenAlex
W2031253131
Cited by
314
References
86
FWCI
32.90
Type
journal article
Language
en
Open access
closed

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CoChat. (2026). Citation check: Disrupting Insulin-Like Growth Factor Signaling as a Potential Cancer Therapy. https://app.cochat.ai/papers/10.1158/aacr.edb-mct-06-0080
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Sachdev, D., & Yee, D. (2008). Disrupting Insulin-Like Growth Factor Signaling as a Potential Cancer Therapy. AACR Education book. https://doi.org/10.1158/aacr.edb-mct-06-0080

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.