The DOI matches its Crossref record; 27 of the 27 references it cites were found in a registry or an index.
Imatinib for Melanomas Harboring Mutationally Activated or Amplified KIT Arising on Mucosal, Acral, and Chronically Sun-Damaged Skin
Open accessAbstract
Purpose: Amplifications and mutations in the KIT proto-oncogene in subsets of melanomas provide therapeutic opportunities. Patients and Methods: We conducted a multicenter phase II trial of imatinib in metastatic mucosal, acral, or chronically sun-damaged (CSD) melanoma with KIT amplifications and/or mutations. Patients received imatinib 400 mg once per day or 400 mg twice per day if there was no initial response. Dose reductions were permitted for treatment-related toxicities. Additional oncogene mutation screening was performed by mass spectroscopy. Results: Twenty-five patients were enrolled (24 evaluable). Eight patients (33%) had tumors with KIT mutations, 11 (46%) with KIT amplifications, and five (21%) with both. Median follow-up was 10.6 months (range, 3.7 to 27.1 months). Best overall response rate (BORR) was 29% (21% excluding nonconfirmed responses) with a two-stage 95% CI of 13% to 51%. BORR was significantly greater than the hypothesized null of 5% and statistically significantly different by mutation status (7 of 13 or 54% KIT mutated v 0% KIT amplified only). There were no statistical differences in rates of progression or survival by mutation status or by melanoma site. The overall disease control rate was 50% but varied significantly by KIT mutation status (77% mutated v 18% amplified). Four patients harbored pretreatment NRAS mutations, and one patient acquired increased KIT amplification after treatment. Conclusion: Melanomas that arise on mucosal, acral, or CSD skin should be assessed for KIT mutations. Imatinib can be effective when tumors harbor KIT mutations, but not if KIT is amplified only. NRAS mutations and KIT copy number gain may be mechanisms of therapeutic resistance to imatinib.
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Mutations of the BRAF gene in human cancer
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Efficacy and safety of imatinib mesylate in advanced gastrointestinal stromal tumors
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Self-citationDistinct Sets of Genetic Alterations in Melanoma
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Kinase Mutations and Imatinib Response in Patients With Metastatic Gastrointestinal Stromal Tumor
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Self-citationFrequent somatic mutations of GNAQ in uveal melanoma and blue naevi
Van Raamsdonk, C. D., Bezrookove, V., Green, G., Bauer, J., Gaugler, L., O’Brien, J. M., Simpson, E. M., Barsh, G. S., & Bastian, B. C. (2009) · Nature · doi:10.1038/nature07586 · Cited by 1,623
Somatic Activation of KIT in Distinct Subtypes of Melanoma
Curtin, J. A., Busam, K., Pinkel, D., & Bastian, B. C. (2006) · Journal of Clinical Oncology · doi:10.1200/jco.2006.06.2984 · Cited by 1,616
KIT as a Therapeutic Target in Metastatic Melanoma
Carvajal, R. D. (2011) · JAMA · doi:10.1001/jama.2011.746 · Cited by 888
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Self-citationKIT Gene Mutations and Copy Number in Melanoma Subtypes
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Self-citationShi, H., Moriceau, G., Kong, X., Lee, M.-K., Lee, H., Koya, R. C., Ng, C., Chodon, T., Scolyer, R. A., Dahlman, K. B., et al. (2012) · Nature Communications · doi:10.1038/ncomms1727 · Cited by 640
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Sheng, X., Yan, X., Chi, Z., Si, L., Cui, C., Tang, B., Li, S., Mao, L., Lian, B., Wang, X., et al. (2019) · Journal of Clinical Oncology · doi:10.1200/jco.19.00210 · Cited by 175
Self-citationBasurto‐Lozada, P., Molina‐Aguilar, C., Castaneda‐Garcia, C., Vázquez‐Cruz, M. E., Garcia‐Salinas, O. I., Álvarez‐Cano, A., Martínez‐Said, H., Roldán‐Marín, R., Adams, D. J., Possik, P. A., et al. (2021) · Pigment Cell & Melanoma Research · doi:10.1111/pcmr.12885 · Cited by 154
Cancer Therapy Guided by Mutation Tests: Current Status and Perspectives
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Metadata
- Authors
- Hodi, F. S., Corless, C. L., Giobbie-Hurder, A., Fletcher, J. A., Zhu, M., Marino-Enriquez, A., Friedlander, P., Gonzalez, R., Weber, J. S., Gajewski, T. F., O'Day, S. J., Kim, K. B., Lawrence, D., Flaherty, K. T., Luke, J. J., Collichio, F. A., Ernstoff, M. S., Heinrich, M. C., Beadling, C., Zukotynski, K. A., Yap, J. T., Van den Abbeele, A. D., Demetri, G. D., & Fisher, D. E.
- Venue
- Journal of Clinical Oncology
- Published
- 2013-09-10
- Volume
- 31
- Issue
- 26
- Pages
- 3182-3190
- ISSN
- 0732-183X (ISSN-L)
- 1527-7755
- OpenAlex
- W2103152130
- Cited by
- 608
- References
- 27
- FWCI
- 21.52
- Type
- journal article
- Language
- en
- Open access
- bronze
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- Hodi, F. S., Corless, C. L., Giobbie-Hurder, A., Fletcher, J. A., Zhu, M., Marino-Enriquez, A., Friedlander, P., Gonzalez, R., Weber, J. S., Gajewski, T. F., O'Day, S. J., Kim, K. B., Lawrence, D., Flaherty, K. T., Luke, J. J., Collichio, F. A., Ernstoff, M. S., Heinrich, M. C., Beadling, C., . . . Fisher, D. E. (2013). Imatinib for Melanomas Harboring Mutationally Activated or Amplified KIT Arising on Mucosal, Acral, and Chronically Sun-Damaged Skin. Journal of Clinical Oncology. https://doi.org/10.1200/jco.2012.47.7836
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Bibliographic data: Semantic Scholar, OpenAlex, Crossref.
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.
