Page 99 - 2021_03-Haematologica-web

Alternative splicing in multiple myeloma
normal physiology and cancer. Semin Cell
Dev Biol. 2014;28:49-56.
28. Lewis AM, Varghese S, Xu H, Alexander
HR. Interleukin-1 and cancer progression: the emerging role of interleukin-1 receptor antagonist as a novel therapeutic agent in cancer treatment. J Transl Med. 2006;4:48.
29. Huang M-Y, Xuan F, Liu W, Cui H-J. MINA controls proliferation and tumorigenesis of glioblastoma by epigenetically regulating cyclins and CDKs via H3K9me3 demethy- lation. Oncogene. 2017;36(3):387-396.
30. Chen Y-IG, Moore RE, Ge HY, Young MK, Lee TD, Stevens SW. Proteomic analysis of in vivo-assembled pre-mRNA splicing com- plexes expands the catalog of participating factors. Nucleic Acids Res. 2007;35(12): 3928-3944.
31. Hagiwara M. Alternative splicing: A new drug target of the post-genome era. Biochim Biophys Acta. 2005;1754(1-2):324-331.
32. Chan CC, Dostie J, Diem MD, et al. eIF4A3 is a novel component of the exon junction complex. RNA. 2004;10(2):200-209.
33. Liberzon A, Birger C, Thorvaldsdóttir H, Ghandi M, Mesirov JP, Tamayo P. The Molecular Signatures Database Hallmark Gene Set Collection. Cell Syst. 2015; 1(6):417-425.
34. Walker BA, Mavrommatis K, Wardell CP, et al. A high-risk, double-Hit, group of newly diagnosed myeloma identified by genomic analysis. Leukemia. 2019;33(1):159-170.
35. Pellagatti A, Armstrong RN, Steeples V, et al. Impact of spliceosome mutations on RNA splicing in myelodysplasia: dysregulated genes/pathways and clinical associations. Blood. 2018;132(12):1225-1240.
36. Yoshida K, Sanada M, Shiraishi Y, et al. Frequent pathway mutations of splicing machinery in myelodysplasia. Nature. 2011;478(7367):64-69.
37. Flach H, Rosenbaum M, Duchniewicz M, et al. Mzb1 protein regulates calcium home- ostasis, antibody secretion, and integrin acti- vation in innate-like B cells. Immunity. 2010; 33(5):723-735.
38. Rosenbaum M, Andreani V, Kapoor T, et al. MZB1 is a GRP94 cochaperone that enables proper immunoglobulin heavy chain biosynthesis upon ER stress. Genes Dev. 2014;28(11):1165-1178.
39. Herold T, Mulaw MA, Jurinovic V, et al. High expression of MZB1 predicts adverse prognosis in chronic lymphocytic leukemia, follicular lymphoma and diffuse large B-cell lymphoma and is associated with a unique gene expression signature. Leuk Lymphoma.
2013;54(8):1652-1657.
40. Walter P, Ron D. The unfolded protein
response: from stress pathway to homeosta- tic regulation. Science. 2011;334(6059):1081- 1086.
41.Lin JH, Li H, Yasumura D, et al. IRE1 Signaling affects cell fate during the unfold- ed protein response. Science. 2007; 318(5852):944-949.
42. Walker BA, Mavrommatis K, Wardell CP, et al. Identification of novel mutational drivers reveals oncogene dependencies in multiple myeloma. Blood. 2018;132(6):587-597.
43. Obeng EA, Chappell RJ, Seiler M, et al. Physiologic expression of Sf3b1K700E caus- es impaired erythropoiesis, aberrant splic- ing, and sensitivity to therapeutic spliceo- some modulation. Cancer Cell. 2016; 30(3):404-417.
44. Seiler M, Yoshimi A, Darman R, et al. H3B- 8800, an orally available small-molecule splicing modulator, induces lethality in spliceosome-mutant cancers. Nat Med. 2018;24(4):497-504.
45. Huang HH-L, Ferguson ID, Thornton AM, et al. Proteasome inhibitor-induced modula- tion reveals the spliceosome as a specific therapeutic vulnerability in multiple myelo- ma. bioRxiv. 2018;508549.
haematologica | 2021; 106(3)
745