References
- Stephen AG, Esposito D, Bagni RK, et al. Dragging ras back in the ring. Cancer Cell 2014; 25: 272–281.
- Chng WJ, Gonzalez-Paz N, Price-Troska T, et al. Clinical and biological significance of RAS mutations in multiple myeloma. Leukemia 2008; 22: 2280–2284.
- Mulligan G, Lichter DI, Di Bacco A, et al. Mutation of NRAS but not KRAS significantly reduces myeloma sensitivity to single-agent bortezomib therapy. Blood 2014; 123: 632–639.
- Rasmussen T, Kuehl M, Lodahl M, et al. Possible roles for activating RAS mutations in the MGUS to MM transition and in the intramedullary to extramedullary transition in some plasma cell tumors. Blood 2005; 105: 317–323.
- Smith D, Armenteros E, Percy L, et al. RAS mutation status and bortezomib therapy for relapsed multiple myeloma. Br J Haematol 2015; 169: 905–908.
- Colicelli J. Human RAS superfamily proteins and related GTPases. Sci STKE 2004; 2004: RE13.
- Cox AD, Fesik SW, Kimmelman AC, et al. Drugging the undruggable RAS: mission possible? Nat Rev Drug Discov 2014; 13: 828–851.
- Samatar AA, Poulikakos PI. Targeting RAS-ERK signalling in cancer: promises and challenges. Nat Rev Drug Discov 2014; 13: 928–942.
- Chapman MA, Lawrence MS, Keats JJ, et al. Initial genome sequencing and analysis of multiple myeloma. Nature 2011; 471: 467–472.
- Steinbrunn T, Stuhmer T, Gattenlohner S, et al. Mutated RAS and constitutively activated Akt delineate distinct oncogenic pathways, which independently contribute to multiple myeloma cell survival. Blood 2011; 117: 1998–2004.
- Leich E, Weißbach S, Klein HU, et al. Multiple myeloma is affected by multiple and heterogeneous somatic mutations in adhesion- and receptor tyrosine kinase signaling molecules. Blood Cancer J 2013; 3: e102.
- Zingone A, Kuehl WM. Pathogenesis of monoclonal gammopathy of undetermined significance and progression to multiple myeloma. Semin Hematol 2011; 48: 4–12.
- Liu P, Leong T, Quam L, et al. Activating mutations of N- and K-ras in multiple myeloma show different clinical associations: analysis of the Eastern Cooperative Oncology Group Phase III Trial. Blood 1996; 88: 2699–2706.
- Corradini P, Ladetto M, Voena C, et al. Mutational activation of N- and K-ras oncogenes in plasma cell dyscrasias. Blood 1993; 81: 2708–2713.
- Ostrem JM, Peters U, Sos ML, et al. K-Ras(G12C) inhibitors allosterically control GTP affinity and effector interactions. Nature 2013; 503: 548–551.
- Downward J. RAS synthetic lethal screens revisited: still seeking the elusive prize? Clin Cancer Res 2015; 21: 1802–1809.
- Gebauer N, Biersack H, Czerwinska AC, et al. Favourable prognostic impact of RAS mutation status in multiple myeloma treated with High-Dose Melphalan and Autologous Stem Cell Support in the era of novel agents – a single centre perspective. Leuk Lymphoma 2016; 57: 226–229. doi: 10.3109/10428194.2015.1046863.