The DOI matches its Crossref record; 35 of the 35 references it cites were found in a registry or an index.
Insulin-like growth factor 1 receptor is a potential therapeutic target for gastrointestinal stromal tumors
Open accessAbstract
A subset of gastrointestinal stromal tumors (GISTs) lack gain-of-function mutations in c- KIT and PDGFR α. These so-called wild-type (WT) GISTs tend to be less responsive to imatinib-based therapies and have a poor prognosis. We identified amplification of IGF1R in a SNP analysis of GIST and thus studied its potential as a therapeutic target in WT and mutant GIST. Expression of IGF1R and downstream effectors in clinical GIST samples was examined by using immunoblots and immunohistochemistry. The roles of IGF1R signaling in GIST and viability were analyzed by using NVP-AEW541, an inhibitor of IGF1R, alone and in combination with imatinib, or via siRNA silencing of IGF1R. IGF1R was strongly overexpressed, and IGF1R amplification was detected at a significantly higher frequency in WT GISTs, including a pediatric WT GIST, compared with mutant GISTs ( P = 0.0173 and P = 0.0163, respectively). Inhibition of IGF1R activity in vitro with NVP-AEW541 or down-regulation of expression with siIGF1R led to cytotoxicity and induced apoptosis in GIST cell lines via AKT and MAPK signaling. Combination of NVP-AEW541 and imatinib in GIST cell lines induced a strong cytotoxicity response. Our results reveal that IGF1R is amplified and the protein is overexpressed in WT and pediatric GISTs. We also demonstrate that the aberrant expression of IGF1R may be associated with oncogenesis in WT GISTs and suggest an alternative and/or complementary therapeutic regimen in the clinical management of all GISTs, especially in a subset of tumors that respond less favorably to imatinib-based therapy.
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Efficacy and safety of imatinib mesylate in advanced gastrointestinal stromal tumors
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Self-citationmTOR Inhibition Induces Upstream Receptor Tyrosine Kinase Signaling and Activates Akt
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The insulin-like growth factor system and cancer
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Coactivation of receptor tyrosine kinases affects the response of tumor cells to targeted therapies
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Cited by
Gastrointestinal stromal tumours: origin and molecular oncology
Corless, C. L., Barnett, C. M., & Heinrich, M. C. (2011) · Nature Reviews Cancer · doi:10.1038/nrc3143 · Cited by 891
Insulin-like growth factors: Ligands, binding proteins, and receptors
LeRoith, D., Holly, J. M. P., & Forbes, B. E. (2021) · Molecular Metabolism · doi:10.1016/j.molmet.2021.101245 · Cited by 303
Receptor Tyrosine Kinase-Targeted Cancer Therapy
Yamaoka, T., Kusumoto, S., Ando, K., Ohba, M., & Ohmori, T. (2018) · International Journal of Molecular Sciences · doi:10.3390/ijms19113491 · Cited by 297
Targeting the insulin growth factor receptor 1
Arnaldez, F. I., & Helman, L. J. (2012) · Hematology/Oncology Clinics of North America · doi:10.1016/j.hoc.2012.01.004 · Cited by 88
Metadata
- Authors
- Tarn, C., Rink, L., Merkel, E., Flieder, D., Pathak, H., Koumbi, D., Testa, J. R., Eisenberg, B., von Mehren, M., & Godwin, A. K.
- Venue
- Proceedings of the National Academy of Sciences
- Published
- 2008-06-17
- Volume
- 105
- Issue
- 24
- Pages
- 8387-8392
- ISSN
- 0027-8424 (ISSN-L)
- 1091-6490
- OpenAlex
- W1971736092
- Cited by
- 252
- References
- 35
- FWCI
- 25.40
- Type
- journal article
- Language
- en
- Open access
- green
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- Tarn, C., Rink, L., Merkel, E., Flieder, D., Pathak, H., Koumbi, D., Testa, J. R., Eisenberg, B., von Mehren, M., & Godwin, A. K. (2008). Insulin-like growth factor 1 receptor is a potential therapeutic target for gastrointestinal stromal tumors. Proceedings of the National Academy of Sciences. https://doi.org/10.1073/pnas.0803383105
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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.
