Selumetinib (AZD6244; ARRY-142886) in the treatment of metastatic melanoma

Bibliography

• Siegel R, Ward E, Brawley O, Jemal A. Cancer statistics, 2011: the impact of eliminating socioeconomic and racial disparities on premature cancer deaths. CA Cancer J Clin 2011;61(4):212-36
   PubMed Web of Science ®Google Scholar
• Howlader N, Noone AM, Krapcho M, SEER Cancer Statistics Review 2011 1975-2008 Bethesda, MD: National Cancer Institute. Available from: http://seer.cancer.gov/csr/1975_2008/; based on November 2010 SEER data submission, posted to the SEER web site
   Google Scholar
• Tsao H, Atkins MB, Sober AJ. Management of cutaneous melanoma. N Engl J Med 2004;351(10):998-1012
   PubMed Web of Science ®Google Scholar
• Hodi FS, O'Day SJ, McDermott DF, Improved survival with ipilimumab in patients with metastatic melanoma. N Engl J Med 2010;363(8):711-23
   PubMed Web of Science ®Google Scholar
• Chapman PB, Hauschild A, Robert C, Improved survival with vemurafenib in melanoma with BRAF V600E mutation. N Engl J Med 2011;364(26):2507-16
   PubMed Web of Science ®Google Scholar
• Davies H, Bignell GR, Cox C, Mutations of the BRAF gene in human cancer. Nature 2002;417(6892):949-54
   PubMed Web of Science ®Google Scholar
• Curtin JA, Fridlyand J, Kageshita T, Distinct sets of genetic alterations in melanoma. N Engl J Med 2005;353(20):2135-47
   PubMed Web of Science ®Google Scholar
• Ribas A, Kim KB, Schuchter LM, BRIM-2: An open-label, multicenter phase II study of vemurafenib in previously treated patients with BRAF V600E mutation-positive metastatic melanoma. J Clin Oncol 2011;29(Suppl):abstract 8509
   Google Scholar
• Smalley KS. A pivotal role for ERK in the oncogenic behaviour of malignant melanoma? Int J Cancer 2003;104(5):527-32
   PubMed Web of Science ®Google Scholar
• Goydos JS, Mann B, Kim HJ, Detection of B-RAF and N-RAS mutations in human melanoma. J Am Coll Surg 2005;200(3):362-70
   PubMed Web of Science ®Google Scholar
• Goel VK, Lazar AJ, Warneke CL, Examination of mutations in BRAF, NRAS, and PTEN in primary cutaneous melanoma. J Invest Dermatol 2006;126(1):154-60
   PubMed Web of Science ®Google Scholar
• Gysin S, Salt M, Young A, McCormick F. Therapeutic strategies for targeting ras proteins. Genes Cancer 2011;2(3):359-72
   PubMedGoogle Scholar
• Solit DB, Garraway LA, Pratilas CA, BRAF mutation predicts sensitivity to MEK inhibition. Nature 2006;439(7074):358-62
   PubMed Web of Science ®Google Scholar
• Sebolt-Leopold JS, Dudley DT, Herrera R, Blockade of the MAP kinase pathway suppresses growth of colon tumors in vivo. Nat Med 1999;5(7):810-16
   PubMed Web of Science ®Google Scholar
• Yeh TC, Marsh V, Bernat BA, Biological characterization of ARRY-142886 (AZD6244), a potent, highly selective mitogen-activated protein kinase kinase 1/2 inhibitor. Clin Cancer Res 2007;13(5):1576-83
   PubMed Web of Science ®Google Scholar
• Haass NK, Sproesser K, Nguyen TK, The mitogen-activated protein/extracellular signal-regulated kinase kinase inhibitor AZD6244 (ARRY-142886) induces growth arrest in melanoma cells and tumor regression when combined with docetaxel. Clin Cancer Res 2008;14(1):230-9
   PubMed Web of Science ®Google Scholar
• Gopal YN, Deng W, Woodman SE, Basal and treatment-induced activation of AKT mediates resistance to cell death by AZD6244 (ARRY-142886) in Braf-mutant human cutaneous melanoma cells. Cancer Res 2010;70(21):8736-47
   PubMed Web of Science ®Google Scholar
• Van Raamsdonk CD, Bezrookove V, Green G, Frequent somatic mutations of GNAQ in uveal melanoma and blue naevi. Nature 2009;457(7229):599-602
   PubMed Web of Science ®Google Scholar
• Van Raamsdonk CD, Griewank KG, Crosby MB, Mutations in GNA11 in uveal melanoma. N Engl J Med 2010;363(23):2191-9
   PubMed Web of Science ®Google Scholar
• Mitsiades N, Chew SA, He B, Genotype-dependent sensitivity of uveal melanoma cell lines to inhibition of B-Raf, MEK, and Akt kinases: rationale for personalized therapy. Invest Ophthalmol Vis Sci 2011;52(10):7248-55
   PubMed Web of Science ®Google Scholar
• Prickett TD, Wei X, Cardenas-Navia I, Exon capture analysis of G protein-coupled receptors identifies activating mutations in GRM3 in melanoma. Nat Genet 2011;43(11):1119-26
   PubMed Web of Science ®Google Scholar
• Adjei AA, Cohen RB, Franklin W, Phase I pharmacokinetic and pharmacodynamic study of the oral, small-molecule mitogen-activated protein kinase kinase 1/2 inhibitor AZD6244 (ARRY-142886) in patients with advanced cancers. J Clin Oncol 2008;26(13):2139-46
   PubMed Web of Science ®Google Scholar
• Banerji U, Camidge DR, Verheul HM, The first-in-human study of the hydrogen sulfate (Hyd-sulfate) capsule of the MEK1/2 inhibitor AZD6244 (ARRY-142886): a phase I open-label multicenter trial in patients with advanced cancer. Clin Cancer Res 2010;16(5):1613-23
   PubMed Web of Science ®Google Scholar
• Leijen S, Soetekouw PM, Jeffry Evans TR, A phase I, open-label, randomized crossover study to assess the effect of dosing of the MEK 1/2 inhibitor Selumetinib (AZD6244; ARRY-142866) in the presence and absence of food in patients with advanced solid tumors. Cancer Chemother Pharmacol 2011;68(6):1619-28
   PubMed Web of Science ®Google Scholar
• Kim KB, Infante JR, Burris H, A Phase I dose-escalation study of selumetinib in combination with chemotherapies in patients with advanced solid tumors [abstract #B255. Proc AACR-NCI-EORTC International Conference; 2011
   Google Scholar
• Kirkwood JM, Bastholt L, Robert C, Phase II, open-label, randomized trial of the MEK1/2 inhibitor Selumetinib as monotherapy versus temozolomide in patients with advanced melanoma. Clin Cancer Res 2012;18(2):555-67
   PubMed Web of Science ®Google Scholar
• Patel SP, Lazar AJ, Mahoney S, Clinical responses to AZD6244 (ARRY-142886)-based combination therapy stratified by gene mutations in patients with metastatic melanoma. J Clin Oncol 2010;28(Suppl):abstract 8501
   Google Scholar
• Schad K, Baumann Conzett K, Zipser MC, Mitogen-activated protein/extracellular signal-regulated kinase kinase inhibition results in biphasic alteration of epidermal homeostasis with keratinocytic apoptosis and pigmentation disorders. Clin Cancer Res 2010;16(3):1058-64
   PubMed Web of Science ®Google Scholar
• Dai B, Meng J, Peyton M, STAT3 mediates resistance to MEK inhibitor through microRNA miR-17. Cancer Res 2011;71(10):3658-68
   PubMed Web of Science ®Google Scholar
• Meng J, Peng H, Dai B, High level of AKT activity is associated with resistance to MEK inhibitor AZD6244 (ARRY-142886). Cancer Biol Ther 2009;8(21):2073-80
   PubMed Web of Science ®Google Scholar
• Aziz SA, Jilaveanu LB, Zito C, Vertical targeting of the phosphatidylinositol-3 kinase pathway as a strategy for treating melanoma. Clin Cancer Res 2010;16(24):6029-39
   PubMed Web of Science ®Google Scholar
• 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
   PubMed Web of Science ®Google Scholar
• Zipser MC, Eichhoff OM, Widmer DS, A proliferative melanoma cell phenotype is responsive to RAF/MEK inhibition independent of BRAF mutation status. Pigment cell Melanoma Res 2011;24(2):326-33
   PubMed Web of Science ®Google Scholar
• Flaherty KT, Schiller J, Schuchter LM, A phase I trial of the oral, multikinase inhibitor sorafenib in combination with carboplatin and paclitaxel. Clin Cancer Res 2008;14(15):4836-42
   PubMed Web of Science ®Google Scholar
• Hauschild A, Agarwala SS, Trefzer U, Results of a phase III, randomized, placebo-controlled study of sorafenib in combination with carboplatin and paclitaxel as second-line treatment in patients with unresectable stage III or stage IV melanoma. J Clin Oncol 2009;27(17):2823-30
   PubMed Web of Science ®Google Scholar
• Flaherty KT, Lee SJ, Schuchter LM, Final results of E2603: a double-blind, randomized phase III trial comparing carboplatin (C)/paclitaxel (P) with or without sorafenib (S) in metastatic melanoma. J Clin Oncol 2010;28(Suppl):abstract 8511
   Google Scholar
• Kim KB, Davies MA, Papadopoulos NE, Phase I/II study of the combination of sorafenib and temsirolimus in patients with metastatic melanoma. J Clin Oncol 2009;27(Suppl):abstract 9026
   Google Scholar
• Nazarian R, Shi H, Wang Q, Melanomas acquire resistance to B-RAF(V600E) inhibition by RTK or N-RAS upregulation. Nature 2010;468(7326):973-7
   PubMed Web of Science ®Google Scholar
• Montagut C, Sharma SV, Shioda T, Elevated CRAF as a potential mechanism of acquired resistance to BRAF inhibition in melanoma. Cancer Res 2008;68(12):4853-61
   PubMed Web of Science ®Google Scholar
• Hatzivassiliou G, Song K, Yen I, RAF inhibitors prime wild-type RAF to activate the MAPK pathway and enhance growth. Nature 2010;464(7287):431-5
   PubMed Web of Science ®Google Scholar
• 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
   PubMed Web of Science ®Google Scholar
• Johannessen CM, Boehm JS, Kim SY, COT drives resistance to RAF inhibition through MAP kinase pathway reactivation. Nature 2010;468(7326):968-72
   PubMed Web of Science ®Google Scholar
• 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
   PubMed Web of Science ®Google Scholar
• 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
   PubMed Web of Science ®Google Scholar
• Poulikakos PI, Persaud Y, Janakiraman M, RAF inhibitor resistance is mediated by dimerization of aberrantly spliced BRAF(V600E). Nature 2011;480(7377):387-90
   PubMed Web of Science ®Google Scholar
• McArthur GA, Ribas A, Chapman PB, Molecular analyses from a phase I trial of vemurafenib to study mechanism of action (MOA) and resistance in repeated biopsies from BRAF mutation-positive metastatic melanoma patients (pts). J Clin Oncol 2011;29(Suppl):abstract 8502
   Google Scholar