The DOI matches its Crossref record; 9 of the 9 references it cites were found in a registry or an index.
Phase I/II Study of the Src Inhibitor Dasatinib in Combination With Erlotinib in Advanced Non–Small-Cell Lung Cancer
Open accessAbstract
Purpose: Src family kinase (SFK) proteins are frequently activated in cancer and can coordinate tumor cell growth, survival, invasion, and angiogenesis. Given the importance of SFK signaling in cancer, known cooperation between SFK and epidermal growth factor receptor (EGFR) signaling, and efficacy of EGFR inhibitors, we performed a phase I trial combining dasatinib, an SFK and multikinase inhibitor, with erlotinib, an EGFR inhibitor, in patients with advanced non–small-cell lung cancer. Patients and Methods: Patients received erlotinib for 1 week before addition of dasatinib; pharmacokinetics were performed after weeks 1 and 2. Four cohorts were examined, including twice-daily and daily dasatinib dosing. Responses were assessed after 8 weeks. Plasma levels of angiogenic markers (vascular endothelial growth factor [VEGF], interleukin-8, and basic fibroblast growth factor [bFGF]) were determined before and during treatment. Results: Thirty-four patients were enrolled. The average duration of treatment was 73 days. The main adverse events include GI (diarrhea, anorexia, and nausea), skin rash, cytopenias, pleural effusions, and fatigue. No effect of escalating doses of dasatinib was observed on erlotinib pharmacokinetics. Two partial responses and one bone response were observed, and the disease control rate was 63%. Reductions in plasma VEGF and bFGF were observed, and reductions in VEGF correlated with disease control. Conclusion: The combination of erlotinib and dasatinib is tolerable, with adverse effects consistent with the two agents. Disease control and inhibition of plasma angiogenesis markers were observed. Personalized strategies for deployment of SFK should receive further attention.
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EGFR Mutations in Lung Cancer: Correlation with Clinical Response to Gefitinib Therapy
Paez, J. G., Jänne, P. A., Lee, J. C., Tracy, S., Greulich, H., Gabriel, S., Herman, P., Kaye, F. J., Lindeman, N., Boggon, T. J., et al. (2004) · Science · doi:10.1126/science.1099314 · Cited by 9,368
Erlotinib in Previously Treated Non–Small-Cell Lung Cancer
Shepherd, F. A., Rodrigues Pereira, J., Ciuleanu, T., Tan, E. H., Hirsh, V., Thongprasert, S., Campos, D., Maoleekoonpiroj, S., Smylie, M., Martins, R., et al. (2005) · New England Journal of Medicine · doi:10.1056/nejmoa050753 · Cited by 5,419
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
Yeatman, T. J. (2004) · Nature Reviews Cancer · doi:10.1038/nrc1366 · Cited by 1,113
c-Src and cooperating partners in human cancer
Ishizawar, R., & Parsons, S. J. (2004) · Cancer Cell · doi:10.1016/j.ccr.2004.09.001 · Cited by 617 · cited 1×
“SFKs cooperate with multiple receptor tyrosine kinases, such as the epidermal growth factor receptor (EGFR), to modulate signaling, transform cells, and promote tumor growth.(1-7) SFKs activate downstream signaling pathways, such as Ras/Raf/MAPK, PI3K/Akt, and STATs, that control tumor growth.”
BackgroundMaa, M. C., Leu, T. H., McCarley, D. J., Schatzman, R. C., & Parsons, S. J. (1995) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.92.15.6981 · Cited by 330
The Lipid Raft-Anchored Adaptor Protein Cbp Controls the Oncogenic Potential of c-Src
Oneyama, C., Hikita, T., Enya, K., Dobenecker, M.-W., Saito, K., Nada, S., Tarakhovsky, A., & Okada, M. (2008) · Molecular Cell · doi:10.1016/j.molcel.2008.03.026 · Cited by 116
Christopher, L. J., Cui, D., Li, W., Barros, A., Arora, V. K., Zhang, H., Wang, L., Zhang, D., Manning, J. A., He, K., et al. (2008) · Drug Metabolism and Disposition · doi:10.1124/dmd.107.018234 · Cited by 40
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Mutations in the DDR2 Kinase Gene Identify a Novel Therapeutic Target in Squamous Cell Lung Cancer
Hammerman, P. S., Sos, M. L., Ramos, A. H., Xu, C., Dutt, A., Zhou, W., Brace, L. E., Woods, B. A., Lin, W., Zhang, J., et al. (2011) · Cancer Discovery · doi:10.1158/2159-8274.cd-11-0005 · Cited by 482
Self-citationNew Targetable Oncogenes in Non–Small-Cell Lung Cancer
Oxnard, G. R., Binder, A., & Jänne, P. A. (2013) · Journal of Clinical Oncology · doi:10.1200/jco.2012.42.9829 · Cited by 299
Montero, J. C., Seoane, S., Ocaña, A., & Pandiella, A. (2011) · Clinical Cancer Research · doi:10.1158/1078-0432.ccr-10-2616 · Cited by 298
El‐Kenawi, A. E., & El‐Remessy, A. B. (2013) · British Journal of Pharmacology · doi:10.1111/bph.12344 · Cited by 253
Current status of SRC inhibitors in solid tumor malignancies
Puls, L. N., Eadens, M., & Messersmith, W. (2011) · The Oncologist · doi:10.1634/theoncologist.2010-0408 · Cited by 158
Metadata
- Authors
- Haura, E. B., Tanvetyanon, T., Chiappori, A., Williams, C., Simon, G., Antonia, S., Gray, J., Litschauer, S., Tetteh, L., Neuger, A., Song, L., Rawal, B., Schell, M. J., & Bepler, G.
- Venue
- Journal of Clinical Oncology
- Published
- 2010-03-10
- Volume
- 28
- Issue
- 8
- Pages
- 1387-1394
- ISSN
- 0732-183X (ISSN-L)
- 1527-7755
- OpenAlex
- W2114255370
- Cited by
- 194
- References
- 9
- FWCI
- 19.19
- Type
- journal article
- Language
- en
- Open access
- bronze
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- Haura, E. B., Tanvetyanon, T., Chiappori, A., Williams, C., Simon, G., Antonia, S., Gray, J., Litschauer, S., Tetteh, L., Neuger, A., Song, L., Rawal, B., Schell, M. J., & Bepler, G. (2010). Phase I/II Study of the Src Inhibitor Dasatinib in Combination With Erlotinib in Advanced Non–Small-Cell Lung Cancer. Journal of Clinical Oncology. https://doi.org/10.1200/jco.2009.25.4029
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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.
