The DOI matches its Crossref record; 48 of the 48 references it cites were found in a registry or an index.
Somatic Mutations Lead to an Oncogenic Deletion of Met in Lung Cancer
Abstract
Activating mutations in receptor tyrosine kinases play a critical role in oncogenesis. Despite evidence that Met kinase is deregulated in human cancer, the role of activating mutations in cancers other than renal papillary carcinoma has not been well defined. Here we report the identification of somatic intronic mutations of Met kinase that lead to an alternatively spliced transcript in lung cancer, which encodes a deletion of the juxtamembrane domain resulting in the loss of Cbl E3-ligase binding. The mutant receptor exhibits decreased ubiquitination and delayed down-regulation correlating with elevated, distinct Met expression in primary tumors harboring the deleted receptor. As a consequence, phospho-Met and downstream mitogen-activated protein kinase activation is sustained on ligand stimulation. Cells expressing the Met deletion reveal enhanced ligand-mediated proliferation and significant in vivo tumor growth. A hepatocyte growth factor competitive Met antagonist inhibits receptor activation and proliferation in tumor cells harboring the Met deletion, suggesting the important role played by ligand-dependent Met activation and the potential for anticancer therapy. These results support a critical role for Met in lung cancer and somatic mutation–driven splicing of an oncogene that leads to a different mechanism for tyrosine kinase activation through altered receptor down-regulation in human cancer. (Cancer Res 2006; 66(1): 283-9)
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EGFR Mutations in Lung Cancer: Correlation with Clinical Response to Gefitinib Therapy
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Gain-of-Function Mutations of c- kit in Human Gastrointestinal Stromal Tumors
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Met, metastasis, motility and more
Birchmeier, C., Birchmeier, W., Gherardi, E., & Vande Woude, G. F. (2003) · Nature Reviews Molecular Cell Biology · doi:10.1038/nrm1261 · Cited by 2,602
PDGFRA Activating Mutations in Gastrointestinal Stromal Tumors
Heinrich, M. C., Corless, C. L., Duensing, A., McGreevey, L., Chen, C.-J., Joseph, N., Singer, S., Griffith, D. J., Haley, A., Town, A., et al. (2003) · Science · doi:10.1126/science.1079666 · Cited by 2,301
Analysis of lung tumor initiation and progression using conditional expression of oncogenic K-ras
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Gefitinib-Sensitizing EGFR Mutations in Lung Cancer Activate Anti-Apoptotic Pathways
Sordella, R., Bell, D. W., Haber, D. A., & Settleman, J. (2004) · Science · doi:10.1126/science.1101637 · Cited by 1,606
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Herbst, R. S., Heymach, J. V., & Lippman, S. M. (2008) · New England Journal of Medicine · doi:10.1056/nejmra0802714 · Cited by 2,389
Co-occurring genomic alterations in non-small-cell lung cancer biology and therapy
Skoulidis, F., & Heymach, J. V. (2019) · Nature Reviews Cancer · doi:10.1038/s41568-019-0179-8 · Cited by 1,019
New driver mutations in non-small-cell lung cancer
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Metadata
- Authors
- Kong-Beltran, M., Seshagiri, S., Zha, J., Zhu, W., Bhawe, K., Mendoza, N., Holcomb, T., Pujara, K., Stinson, J., Fu, L., Severin, C., Rangell, L., Schwall, R., Amler, L., Wickramasinghe, D., & Yauch, R.
- Venue
- Cancer Research
- Published
- 2006-01-01
- Volume
- 66
- Issue
- 1
- Pages
- 283-289
- ISSN
- 0008-5472 (ISSN-L)
- 1538-7445
- OpenAlex
- W2121262970
- Cited by
- 490
- References
- 48
- FWCI
- 11.00
- Type
- journal article
- Language
- en
- Open access
- closed
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- Kong-Beltran, M., Seshagiri, S., Zha, J., Zhu, W., Bhawe, K., Mendoza, N., Holcomb, T., Pujara, K., Stinson, J., Fu, L., Severin, C., Rangell, L., Schwall, R., Amler, L., Wickramasinghe, D., & Yauch, R. (2006). Somatic Mutations Lead to an Oncogenic Deletion of Met in Lung Cancer. Cancer Research. https://doi.org/10.1158/0008-5472.can-05-2749
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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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