Bibliography
- Barouch-Bentov R, Sauer K. Mechanisms of dug-resistance in kinases. Expert Opin Investig Drugs 2011;20(2):153-208
- Flaherty KT, Puzanov I, Kim KB, Inhibition of mutated, activated BRAF in metastatic melanoma. N Engl J Med 2010;363(9):809-19
- Smalley KSM, Sondak VK. Melanoma – an unlikely poster child for targeted therapy. N Engl J Med 2010;363:876-78
- Nazarian R, Shi H, Wang Q, Melanomas acquire resistance to B-RAF(V600E) inhibition by RTK or N-RAS upregulation. Nature 2010 Nov 24. [Epub ahead of print]
- Villanueva J, Vultur A, Lee JT, Acquired resistance to BRAF inhibitors mediated by a RAF kinase switch in melanoma can be overcome by cotargeting MEK and IGF-1R/PI3K. Cancer Cell 2010;18(6):683-95
- Paraiso KH, Fedorenko IV, Cantini LP, Recovery of phospho-ERK activity allows melanoma cells to escape from BRAF inhibitor therapy. Br J Cancer 2010;102(12):1724-30
- Emery CM, Vijayendran KG, Zipser MC, MEK1 mutations confer resistance to MEK and B-RAF inhibition. Proc Natl Acad Sci USA 2009;106(48):20411-16
- Jiang CC, Lai F, Thorne RF, MEK-independent survival of B-RAFV600E melanoma cells selected for resistance to apoptosis induced by the RAF inhibitor PLX4720. Clin Cancer Res 2010 Nov 18. [Epub ahead of print]
- Johannessen CM, Boehm JS, Kim SY, COT drives resistance to RAF inhibition through MAP kinase pathway reactivation. Nature 2010 Nov 24. [Epub ahead of print]
- Corcoran RB, Dias-Santagata D, Bergethon K, BRAF gene amplification can promote acquired resistance to MEK inhibitors in cancer cells harboring the BRAF V600E mutation. Sci Signal 2010;3(149):ra84
- Stommel JM, Kimmelman AC, Ying H, Coactivation of receptor tyrosine kinases affects the response of tumor cells to targeted therapies. Science 2007;318(5848):287-90
- Sensi M, Nicolini G, Petti C, Mutually exclusive NRASQ61R and BRAFV600E mutations at the single-cell level in the same human melanoma. Oncogene 2006;25(24):3357-64
- Jovanovic B, Egyhazi S, Eskandarpour M, Coexisting NRAS and BRAF mutations in primary familial melanomas with specific CDKN2A germline alterations. J Invest Dermatol 2010;130(2):618-20
- Poulikakos PI, Zhang C, Bollag G, RAF inhibitors transactivate RAF dimers and ERK signalling in cells with wild-type BRAF. Nature 2010;464(7287):427-30
- Kaplan FM, Shao Y, Mayberry MM, Aplin AE. Hyperactivation of MEK-ERK1/2 signaling and resistance to apoptosis induced by the ongenic B-RAF inhibitor, PLX4720, in mutant N-Ras melanoma cell lines. Oncogene 2010 Sep 6. [Epub ahead of print]
- Roesch A, Fukunaga-Kalabis M, Schmidt EC, A temporarily distinct subpopulation of slow-cycling melanoma cells is required for continuous tumor growth. Cell 2010;141(4):583-94
- Sharma SV, Lee DY, Li B, A chromatin-mediated reversible drug-tolerant state in cancer cell subpopulations. Cell 2010;141(1):69-80
- Smalley KS, Nathanson KL, Flaherty KT. Genetic subgrouping of melanoma reveals new opportunities for targeted therapy. Cancer Res 2009;69(8):3241-4
- Smalley KS, Haass NK, Brafford PA, Multiple signaling pathways must be targeted to overcome drug resistance in cell lines derived from melanoma metastases. Mol Cancer Ther 2006;5(5):1136-44