The DOI matches its Crossref record; 28 of the 28 references it cites were found in a registry or an index.
A mouse model for EML4-ALK -positive lung cancer
Open accessAbstract
EML4-ALK is a fusion-type protein tyrosine kinase that is generated in human non-small-cell lung cancer (NSCLC) as a result of a recurrent chromosome inversion, inv ( 2 )(p21p23). Although mouse 3T3 fibroblasts expressing human EML4-ALK form transformed foci in culture and s.c. tumors in nude mice, it has remained unclear whether this fusion protein plays an essential role in the carcinogenesis of NSCLC. To address this issue, we have now established transgenic mouse lines that express EML4-ALK specifically in lung alveolar epithelial cells. All of the transgenic mice examined developed hundreds of adenocarcinoma nodules in both lungs within a few weeks after birth, confirming the potent oncogenic activity of the fusion kinase. Although such tumors underwent progressive enlargement in control animals, oral administration of a small-molecule inhibitor of the kinase activity of ALK resulted in their rapid disappearance. Similarly, whereas i.v. injection of 3T3 cells expressing EML4-ALK induced lethal respiratory failure in recipient nude mice, administration of the ALK inhibitor effectively cleared the tumor burden and improved the survival of such animals. These data together reinforce the pivotal role of EML4-ALK in the pathogenesis of NSCLC in humans, and they provide experimental support for the treatment of this intractable cancer with ALK inhibitors.
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Identification of the transforming EML4–ALK fusion gene in non-small-cell lung cancer
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New driver mutations in non-small-cell lung cancer
Tanoue, L. T. (2012) · Yearbook of Pulmonary Disease · doi:10.1016/j.ypdi.2012.01.036 · Cited by 831
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In vivo engineering of oncogenic chromosomal rearrangements with the CRISPR/Cas9 system
Maddalo, D., Manchado, E., Concepcion, C. P., Bonetti, C., Vidigal, J. A., Han, Y.-C., Ogrodowski, P., Crippa, A., Rekhtman, N., de Stanchina, E., et al. (2014) · Nature · doi:10.1038/nature13902 · Cited by 640
Metadata
- Authors
- Soda, M., Takada, S., Takeuchi, K., Choi, Y. L., Enomoto, M., Ueno, T., Haruta, H., Hamada, T., Yamashita, Y., Ishikawa, Y., Sugiyama, Y., & Mano, H.
- Venue
- Proceedings of the National Academy of Sciences
- Published
- 2008-12-16
- Volume
- 105
- Issue
- 50
- Pages
- 19893-19897
- ISSN
- 0027-8424 (ISSN-L)
- 1091-6490
- OpenAlex
- W2136549983
- Cited by
- 512
- References
- 28
- FWCI
- 31.72
- Type
- journal article
- Language
- en
- Open access
- green
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- Soda, M., Takada, S., Takeuchi, K., Choi, Y. L., Enomoto, M., Ueno, T., Haruta, H., Hamada, T., Yamashita, Y., Ishikawa, Y., Sugiyama, Y., & Mano, H. (2008). A mouse model for EML4-ALK -positive lung cancer. Proceedings of the National Academy of Sciences. https://doi.org/10.1073/pnas.0805381105
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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.
