The DOI matches its Crossref record; 7 of the 7 references it cites were found in a registry or an index.
Inhibition of ALK, PI3K/MEK, and HSP90 in Murine Lung Adenocarcinoma Induced by EML4-ALK Fusion Oncogene
Open accessAbstract
Genetic rearrangements of the anaplastic lymphoma kinase (ALK) kinase occur in 3% to 13% of non–small cell lung cancer patients and rarely coexist with KRASor EGFR mutations. To evaluate potential treatment strategies for lung cancers driven by an activated EML4-ALK chimeric oncogene, we generated a genetically engineered mouse model that phenocopies the human disease where this rearranged gene arises. In this model, the ALK kinase inhibitor TAE684 produced greater tumor regression and improved overall survival compared with carboplatin and paclitaxel, representing clinical standard of care. 18F-FDG-PET-CT scans revealed almost complete inhibition of tumor metabolic activity within 24 hours of TAE684 exposure. In contrast, combined inhibition of the PI3K/AKT and MEK/ERK1/2 pathways did not result in significant tumor regression. We identified EML4-ALK in complex with multiple cellular chaperones including HSP90. In support of a functional reliance, treatment with geldanamycin-based HSP90 inhibitors resulted in rapid degradation of EML4-ALK in vitro and substantial, albeit transient, tumor regression in vivo. Taken together, our findings define a murine model that offers a reliable platform for the preclinical comparison of combinatorial treatment approaches for lung cancer characterized by ALK rearrangement.Cancer Res; 70(23); 9827–36. ©2010 AACR.
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Subramanian, A., Tamayo, P., Mootha, V. K., Mukherjee, S., Ebert, B. L., Gillette, M. A., Paulovich, A., Pomeroy, S. L., Golub, T. R., Lander, E. S., et al. (2005) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0506580102 · Cited by 53,625
Gefitinib or Carboplatin–Paclitaxel in Pulmonary Adenocarcinoma
Mok, T. S., Wu, Y.-L., Thongprasert, S., Yang, C.-H., Chu, D.-T., Saijo, N., Sunpaweravong, P., Han, B., Margono, B., Ichinose, Y., et al. (2009) · New England Journal of Medicine · doi:10.1056/nejmoa0810699 · Cited by 8,261
Identification of the transforming EML4–ALK fusion gene in non-small-cell lung cancer
Soda, M., Choi, Y. L., Enomoto, M., Takada, S., Yamashita, Y., Ishikawa, S., Fujiwara, S.-I., Watanabe, H., Kurashina, K., Hatanaka, H., et al. (2007) · Nature · doi:10.1038/nature05945 · Cited by 5,439
MET Amplification Leads to Gefitinib Resistance in Lung Cancer by Activating ERBB3 Signaling
Engelman, J. A., Zejnullahu, K., Mitsudomi, T., Song, Y., Hyland, C., Park, J. O., Lindeman, N., Gale, C.-M., Zhao, X., Christensen, J., et al. (2007) · Science · doi:10.1126/science.1141478 · Cited by 4,496
Self-citationClinical Resistance to STI-571 Cancer Therapy Caused by BCR-ABL Gene Mutation or Amplification
Gorre, M. E., Mohammed, M., Ellwood, K., Hsu, N., Paquette, R., Rao, P. N., & Sawyers, C. L. (2001) · Science · doi:10.1126/science.1062538 · Cited by 3,104
Novel mutant-selective EGFR kinase inhibitors against EGFR T790M
Zhou, W., Ercan, D., Chen, L., Yun, C.-H., Li, D., Capelletti, M., Cortot, A. B., Chirieac, L., Iacob, R. E., Padera, R., et al. (2009) · Nature · doi:10.1038/nature08622 · Cited by 1,013
Self-citationAn oncogenic KRAS2 expression signature identified by cross-species gene-expression analysis.
Sweet-Cordero, A., Mukherjee, S., Subramanian, A., You, H., Roix, J. J., Ladd-Acosta, C., Mesirov, J., Golub, T. R., & Jacks, T. (2005) · Nature Genetics · doi:10.1038/ng1490 · Cited by 414
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Mechanisms of Acquired Crizotinib Resistance in ALK-Rearranged Lung Cancers
Katayama, R., Shaw, A. T., Khan, T. M., Mino-Kenudson, M., Solomon, B. J., Halmos, B., Jessop, N. A., Wain, J. C., Yeo, A. T., Benes, C., et al. (2012) · Science Translational Medicine · doi:10.1126/scitranslmed.3003316 · Cited by 1,309
Kinase inhibitors: the road ahead
Ferguson, F. M., & Gray, N. S. (2018) · Nature Reviews Drug Discovery · doi:10.1038/nrd.2018.21 · Cited by 1,009
Self-citationTargeted therapy for non-small cell lung cancer: current standards and the promise of the future.
(2015) · Europe PMC (PubMed Central) · doi:10.3978/j.issn.2218-6751.2014.05.01 · Cited by 716
The role of the ALK receptor in cancer biology
Hallberg, B., & Palmer, R. H. (2016) · Annals of Oncology · doi:10.1093/annonc/mdw301 · Cited by 377
Emerging Paradigms in the Development of Resistance to Tyrosine Kinase Inhibitors in Lung Cancer
Gainor, J. F., & Shaw, A. T. (2013) · Journal of Clinical Oncology · doi:10.1200/jco.2012.45.2029 · Cited by 346
Metadata
- Authors
- Chen, Z., Sasaki, T., Tan, X., Carretero, J., Shimamura, T., Li, D., Xu, C., Wang, Y., Adelmant, G. O., Capelletti, M., Lee, H. J., Rodig, S. J., Borgman, C., Park, S.-I., Kim, H. R., Padera, R., Marto, J. A., Gray, N. S., Kung, A. L., Shapiro, G. I., Jänne, P. A., & Wong, K.-K.
- Venue
- Cancer Research
- Published
- 2010-12-01
- Volume
- 70
- Issue
- 23
- Pages
- 9827-9836
- ISSN
- 0008-5472 (ISSN-L)
- 1538-7445
- OpenAlex
- W2111361612
- Cited by
- 191
- References
- 7
- FWCI
- 17.96
- Type
- journal article
- Language
- en
- Open access
- green
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- CoChat. (2026). Citation check: Inhibition of ALK, PI3K/MEK, and HSP90 in Murine Lung Adenocarcinoma Induced by EML4-ALK Fusion Oncogene. https://app.cochat.ai/papers/10.1158/0008-5472.can-10-1671
- The paper
- Chen, Z., Sasaki, T., Tan, X., Carretero, J., Shimamura, T., Li, D., Xu, C., Wang, Y., Adelmant, G. O., Capelletti, M., Lee, H. J., Rodig, S. J., Borgman, C., Park, S.-I., Kim, H. R., Padera, R., Marto, J. A., Gray, N. S., Kung, A. L., . . . Wong, K.-K. (2010). Inhibition of ALK, PI3K/MEK, and HSP90 in Murine Lung Adenocarcinoma Induced by EML4-ALK Fusion Oncogene. Cancer Research. https://doi.org/10.1158/0008-5472.can-10-1671
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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.
