Selinexor for the treatment of multiple myeloma

References

• Gravina GL, Senapedis W, McCauley D, et al. Nucleo-cytoplasmic transport as a therapeutic target of cancer. J Hematol Oncol. 2014;7:85.
   PubMed Web of Science ®Google Scholar
• Culjkovic-Kraljacic B, Baguet A, Volpon L, et al. The oncogene eIF4E reprograms the nuclear pore complex to promote mRNA export and oncogenic transformation. Cell Rep. 2012;2:207–215.
   PubMed Web of Science ®Google Scholar
• Conforti F, Wang Y, Rodriguez JA, et al. molecular pathways: anticancer activity by inhibition of nucleocytoplasmic shuttling. Clin Cancer Res. 2015;21:4508–4513.
   PubMed Web of Science ®Google Scholar
• Das A, Wei G, Parikh K, et al. Selective inhibitors of nuclear export (SINE) in hematological malignancies. Exp Hematol Oncol. 2015;4:7.
   PubMedGoogle Scholar
• Hutten S, Kehlenbach RH. CRM1-mediated nuclear export: to the pore and beyond. Trends Cell Biol. 2007;17:193–201.
   PubMed Web of Science ®Google Scholar
• Topisirovic I, Siddiqui N, Borden KLB. The eukaryotic translation initiation factor 4E (eIF4E) and HuR RNA operons collaboratively regulate the expression of survival and proliferative genes. Cell Cycle. 2009;8:960–961.
   PubMed Web of Science ®Google Scholar
• Turner JG, Dawson J, Cubitt CL, et al. Inhibition of CRM1-dependent nuclear export sensitizes malignant cells to cytotoxic and targeted agents. Semin Cancer Biol. 2014;27:62–73.
   PubMed Web of Science ®Google Scholar
• Gaubatz S, Lees JA, Lindeman GJ, et al. E2F4 is exported from the nucleus in a CRM1-dependent manner. Mol Cell Biol. 2001;21:1384–1392.
   PubMed Web of Science ®Google Scholar
• Hill R, Cautain B, de Pedro N, et al. Targeting nucleocytoplasmic transport in cancer therapy. Oncotarget. 2014;5:11–28.
   PubMedGoogle Scholar
• Tan DSP, Bedard PL, Kuruvilla J, et al. Promising SINEs for embargoing nuclear-cytoplasmic export as an anticancer strategy. Cancer Discov. 2014;4:527–537.
   PubMed Web of Science ®Google Scholar
• Balatti V, Bottoni A, Palamarchuk A, et al. NOTCH1 mutations in CLL associated with trisomy 12. Blood. 2012;119:329–331.
   PubMed Web of Science ®Google Scholar
• Puente XS, Pinyol M, Quesada V, et al. Whole-genome sequencing identifies recurrent mutations in chronic lymphocytic leukaemia. Nature. 2011;475:101–105.
   PubMed Web of Science ®Google Scholar
• Lapalombella R, Sun Q, Williams K, et al. Selective inhibitors of nuclear export show that CRM1/XPO1 is a target in chronic lymphocytic leukemia. Blood. 2012;120:4621–4634.
   PubMed Web of Science ®Google Scholar
• Noske A, Weichert W, Niesporek S, et al. Expression of the nuclear export protein chromosomal region maintenance/exportin 1/Xpo1 is a prognostic factor in human ovarian cancer. Cancer. 2008;112:1733–1743.
   PubMed Web of Science ®Google Scholar
• Kuruvilla J, Savona M, Baz R, et al. Selective inhibition of nuclear export with selinexor in patients with non-Hodgkin lymphoma. Blood. 2017;129:3175–3183.
   PubMed Web of Science ®Google Scholar
• Huang W, Yue L, Qiu W, et al. Prognostic value of CRM1 in pancreas cancer. Clin Invest Med. 2009;32:E315.
   PubMed Web of Science ®Google Scholar
• Shen A, Wang Y, Zhao Y, et al. Expression of CRM1 in human gliomas and its significance in p27 expression in clinical prognosis. Neurosurgery. 2009;65:153–160.
   PubMed Web of Science ®Google Scholar
• Yao Y, Dong Y, Lin F, et al. The expression of CRM1 is associated with prognosis in human osteosarcoma. Oncol Rep. 2009;21:229–235.
   PubMed Web of Science ®Google Scholar
• Kojima K, Kornblau SM, Ruvolo V, et al. Prognostic impact and targeting of CRM1 in acute myeloid leukemia. Blood. 2013;121:4166–4174.
   PubMed Web of Science ®Google Scholar
• Nair JS, Musi E, Schwartz GK. Selinexor (KPT-330) induces tumor suppression through nuclear sequestration of IκB and downregulation of survivin. Clin Cancer Res. 2017;23:4301–4311.
   PubMed Web of Science ®Google Scholar
• Mutka SC, Yang WQ, Dong SD, et al. Identification of nuclear export inhibitors with potent anticancer activity in vivo. Cancer Res. 2009;69:510–517.
   PubMed Web of Science ®Google Scholar
• Gravina GL, Tortoreto M, Mancini A, et al. XPO1/CRM1-selective inhibitors of nuclear export (SINE) reduce tumor spreading and improve overall survival in preclinical models of prostate cancer (PCa). J Hematol Oncol. 2014;7:46.
   PubMed Web of Science ®Google Scholar
• Parikh K, Cang S, Sekhri A, et al. Selective inhibitors of nuclear export (SINE)–a novel class of anti-cancer agents. J Hematol Oncol. 2014;7:78.
   PubMed Web of Science ®Google Scholar
• Senapedis WT, Baloglu E, Landesman Y. Clinical translation of nuclear export inhibitors in cancer. Semin Cancer Biol. 2014;27:74–86.
   PubMed Web of Science ®Google Scholar
• Turner JG, Marchion DC, Dawson JL, et al. Human multiple myeloma cells are sensitized to topoisomerase ii inhibitors by CRM1 inhibition. Cancer Res. 2009;69:6899–6905.
   PubMed Web of Science ®Google Scholar
• Sakakibara K, Saito N, Sato T, et al. CBS9106 is a novel reversible oral CRM1 inhibitor with CRM1 degrading activity. Blood. 2011;118:3922–3931.
   PubMed Web of Science ®Google Scholar
• Schmidt J, Braggio E, Kortuem KM, et al. Genome-wide studies in multiple myeloma identify XPO1/CRM1 as a critical target validated using the selective nuclear export inhibitor KPT-276. Leukemia. 2013;27:2357–2365.
   PubMed Web of Science ®Google Scholar
• Tai Y-T, Landesman Y, Acharya C, et al. CRM1 inhibition induces tumor cell cytotoxicity and impairs osteoclastogenesis in multiple myeloma: molecular mechanisms and therapeutic implications. Leukemia. 2014;28:155–165.
   PubMed Web of Science ®Google Scholar
• Kumar SK, Lee JH, Lahuerta JJ, et al. Risk of progression and survival in multiple myeloma relapsing after therapy with IMiDs and bortezomib: A multicenter international myeloma working group study. Leukemia. 2012;26:149–157.
   PubMed Web of Science ®Google Scholar
• Kumar SK, Dimopoulos MA, Kastritis E, et al. Natural history of relapsed myeloma, refractory to immunomodulatory drugs and proteasome inhibitors: a multicenter IMWG study. Leukemia. 2017;31:2443–2448.
   PubMed Web of Science ®Google Scholar
• Pick M, Vainstein V, Goldschmidt N, et al. Daratumumab resistance is frequent in advanced-stage multiple myeloma patients irrespective of CD38 expression and is related to dismal prognosis. Eur J Haematol. 2018;100:494–501.
   PubMed Web of Science ®Google Scholar
• Neggers JE, Vercruysse T, Jacquemyn M, et al. Identifying drug-target selectivity of small-molecule CRM1/XPO1 inhibitors by CRISPR/Cas9 genome editing. Chem Biol. 2015;22:107–116.
   PubMedGoogle Scholar
• Sun Q, Carrasco YP, Hu Y, et al. Nuclear export inhibition through covalent conjugation and hydrolysis of Leptomycin B by CRM1. Proc Natl Acad Sci U S A. 2013;110:1303–1308.
   PubMed Web of Science ®Google Scholar
• Jardin F, Pujals A, Pelletier L, et al. Recurrent mutations of the exportin 1 gene (XPO1) and their impact on selective inhibitor of nuclear export compounds sensitivity in primary mediastinal B-cell lymphoma. Am J Hematol. 2016;91:923–930.
   PubMed Web of Science ®Google Scholar
• Wang AY, Weiner H, Green M, et al. A phase I study of selinexor in combination with high-dose cytarabine and mitoxantrone for remission induction in patients with acute myeloid leukemia. J Hematol Oncol. 2018;11:4.
   PubMed Web of Science ®Google Scholar
• Wei XX, Siegel AP, Aggarwal R, et al. A Phase II trial of selinexor, an oral selective inhibitor of nuclear export compound, in abiraterone- and/or enzalutamide-refractory metastatic castration-resistant prostate cancer. Oncologist. 2018;23:656–e64.
   PubMed Web of Science ®Google Scholar
• Shafique M, Ismail-Khan R, Extermann M, et al. A phase II trial of selinexor (KPT-330) for metastatic triple-negative breast cancer. Oncologist. 2019;24:887–e416.
   PubMed Web of Science ®Google Scholar
• Bhatnagar B, Zhao Q, Mims AS, et al. Selinexor in combination with decitabine in patients with acute myeloid leukemia: results from a phase 1 study. Leuk Lymphoma. 2019;1–10. [Epub ahead of print]
   PubMed Web of Science ®Google Scholar
• Mendonca J, Sharma A, Kim H-S, et al. Selective inhibitors of nuclear export (SINE) as novel therapeutics for prostate cancer. Oncotarget. 2014;5:6102–6112.
   PubMedGoogle Scholar
• Cheng Y, Holloway MP, Nguyen K, et al. XPO1 (CRM1) inhibition represses STAT3 activation to drive a survivin-dependent oncogenic switch in triple-negative breast cancer. Mol Cancer Ther. 2014;13:675–686.
   PubMed Web of Science ®Google Scholar
• Salas Fragomeni RA, Chung HW, Landesman Y, et al. CRM1 and BRAF inhibition synergize and induce tumor regression in BRAF-mutant melanoma. Mol Cancer Ther. 2013;12:1171–1179.
   PubMed Web of Science ®Google Scholar
• Etchin J, Sanda T, Mansour MR, et al. KPT-330 inhibitor of CRM1 (XPO1)-mediated nuclear export has selective anti-leukaemic activity in preclinical models of T-cell acute lymphoblastic leukaemia and acute myeloid leukaemia. Br J Haematol. 2013;161:117–127.
   PubMed Web of Science ®Google Scholar
• Yan D, Pomicter AD, Tantravahi S, et al. Nuclear–cytoplasmic Transport Is a Therapeutic Target in Myelofibrosis. Clin Cancer Res. 2019;25:2323–2335.
   PubMed Web of Science ®Google Scholar
• Baek HB, Lombard AP, Libertini SJ, et al. XPO1 inhibition by selinexor induces potent cytotoxicity against high grade bladder malignancies. Oncotarget. 2018;9:34567–34581.
   PubMedGoogle Scholar
• Subhash VV, Yeo MS, Wang L, et al. Anti-tumor efficacy of Selinexor (KPT-330) in gastric cancer is dependent on nuclear accumulation of p53 tumor suppressor. Sci Rep. 2018;8:12248.
   PubMed Web of Science ®Google Scholar
• Nie D, Huang K, Yin S, et al. KPT-330 inhibition of chromosome region maintenance 1 is cytotoxic and sensitizes chronic myeloid leukemia to Imatinib. Cell Death Discov. 2018;4:48.
   PubMed Web of Science ®Google Scholar
• Body S, Esteve-Arenys A, Miloudi H, et al. Cytoplasmic cyclin D1 controls the migration and invasiveness of mantle lymphoma cells. Sci Rep. 2017;7:13946.
   PubMed Web of Science ®Google Scholar
• Garg M, Kanojia D, Mayakonda A, et al. Selinexor (KPT-330) has antitumor activity against anaplastic thyroid carcinoma in vitro and in vivo and enhances sensitivity to doxorubicin. Sci Rep. 2017;7:9749.
   PubMed Web of Science ®Google Scholar
• Chen Y, Camacho SC, Silvers TR, et al. Inhibition of the nuclear export receptor XPO1 as a therapeutic target for platinum-resistant ovarian cancer. Clin Cancer Res. 2017;23:1552–1563.
   PubMed Web of Science ®Google Scholar
• Sun H, Lin D-C, Cao Q, et al. CRM1 inhibition promotes cytotoxicity in Ewing sarcoma cells by repressing EWS-FLI1-dependent IGF-1 signaling. Cancer Res. 2016;76:2687–2697.
   PubMed Web of Science ®Google Scholar
• Walker CJ, Oaks JJ, Santhanam R, et al. Preclinical and clinical efficacy of XPO1/CRM1 inhibition by the karyopherin inhibitor KPT-330 in Ph+ leukemias. Blood. 2013;122:3034–3044.
   PubMed Web of Science ®Google Scholar
• Sun H, Hattori N, Chien W, et al. KPT-330 has antitumour activity against non-small cell lung cancer. Br J Cancer. 2014;111:281–291.
   PubMed Web of Science ®Google Scholar
• Abdul Razak AR, Mau-Soerensen M, Gabrail NY, et al. First-in-class, first-in-human phase I study of selinexor, a selective inhibitor of nuclear export, in patients with advanced solid tumors. J Clin Oncol. 2016;34:4142–4150.
   PubMed Web of Science ®Google Scholar
• Garzon R, Savona M, Baz R, et al. A phase 1 clinical trial of single-agent selinexor in acute myeloid leukemia. Blood. 2017;129:3165–3174.
   PubMed Web of Science ®Google Scholar
• Gounder MM, Zer A, Tap WD, et al. Phase IB study of selinexor, a first-in-class inhibitor of nuclear export, in patients with advanced refractory bone or soft tissue sarcoma. J Clin Oncol. 2016;34:3166–3174.
   PubMed Web of Science ®Google Scholar
• Alexander TB, Lacayo NJ, Choi JK, et al. Phase I study of selinexor, a selective inhibitor of nuclear export, in combination with fludarabine and cytarabine, in pediatric relapsed or refractory acute leukemia. J Clin Oncol. 2016;34:4094–4101.
   PubMed Web of Science ®Google Scholar
• Conforti F, Zhang X, Rao G, et al. Therapeutic effects of XPO1 inhibition in thymic epithelial tumors. Cancer Res. 2017;77:5614–5627.
   PubMed Web of Science ®Google Scholar
• Tiedemann RE, Zhu YX, Schmidt J, et al. Identification of molecular vulnerabilities in human multiple myeloma cells by RNA interference lethality screening of the druggable genome. Cancer Res. 2012;72:757–768.
   PubMed Web of Science ®Google Scholar
• Kashyap T, Argueta C, Aboukameel A, et al. Selinexor, a Selective Inhibitor of Nuclear Export (SINE) compound, acts through NF-kB deactivation and combines with proteasome inhibitors to synergistically induce tumor cell death. Oncotarget. 2016;7:78883–78895.
   PubMedGoogle Scholar
• Chesi M, Matthews GM, Garbitt VM, et al. Drug response in a genetically engineered mouse model of multiple myeloma is predictive of clinical efficacy. Blood. 2012;120:376–385.
   PubMed Web of Science ®Google Scholar
• Chen C, Garzon R, Gutierrez M, et al. Safety, efficacy, and determination of the recommended phase 2 dose for the oral selective inhibitor of nuclear export (SINE) selinexor (KPT-330). Blood. 2015;126:258.
   Web of Science ®Google Scholar
• Turner JG, Dawson JL, Grant S, et al. Treatment of acquired drug resistance in multiple myeloma by combination therapy with XPO1 and topoisomerase II inhibitors. J Hematol Oncol. 2016;9:73.
   PubMed Web of Science ®Google Scholar
• Argueta C, Kashyap T, Klebanov B, et al. Selinexor synergizes with dexamethasone to repress mTORC1 signaling and induce multiple myeloma cell death. Oncotarget. 2018;9:25529–25544.
   PubMedGoogle Scholar
• Rosebeck S, Alonge MM, Kandarpa M, et al. Synergistic myeloma cell death via novel intracellular activation of caspase-10-dependent apoptosis by carfilzomib and selinexor. Mol Cancer Ther. 2016;15:60–71.
   PubMed Web of Science ®Google Scholar
• Turner JG, Kashyap T, Dawson JL, et al. XPO1 inhibitor combination therapy with bortezomib or carfilzomib induces nuclear localization of IκBα and overcomes acquired proteasome inhibitor resistance in human multiple myeloma. Oncotarget. 2016;7:78896–78909.
   PubMedGoogle Scholar
• Chen C, Siegel D, Gutierrez M, et al. Safety and efficacy of selinexor in relapsed or refractory multiple myeloma and Waldenstrom macroglobulinemia. Blood. 2018;131:855–863.
   PubMed Web of Science ®Google Scholar
• Vogl DT, Dingli D, Cornell RF, et al. Selective inhibition of nuclear export with oral selinexor for treatment of relapsed or refractory multiple myeloma. J Clin Onco. 2018;36:859–866.
   PubMed Web of Science ®Google Scholar
• Nooka AK, Yee AJ, Huff CA, et al. Influence of cytogenetics in patients with relapsed refractory multiple myeloma treated with oral selinexor and dexamethasone: A post-hoc analysis of the STORM study. Blood. 2019;134:1872.
   Google Scholar
• Richardson PG, Oriol A, Beksac M, et al. Pomalidomide, bortezomib, and dexamethasone for patients with relapsed or refractory multiple myeloma previously treated with lenalidomide (OPTIMISMM): a randomised, open-label, phase 3 trial. Lancet Oncol. 2019;20:781–794.
   PubMed Web of Science ®Google Scholar
• Lonial S, Weiss BM, Usmani SZ, et al. Daratumumab monotherapy in patients with treatment-refractory multiple myeloma (SIRIUS): an open-label, randomised, phase 2 trial. Lancet. 2016;387:1551–1560.
   PubMed Web of Science ®Google Scholar
• Chari A, Vogl DT, Gavriatopoulou M, et al. Oral selinexor-dexamethasone for triple-class refractory multiple myeloma. N Engl J Med. 2019;381:727–738.
   PubMed Web of Science ®Google Scholar
• Yee AJ, Huff CA, Chari A, et al. Response to therapy and the effectiveness of treatment with selinexor and dexamethasone in patients with penta-exposed triple-class refractory myeloma who had plasmacytomas. Blood. 2019;134:3140.
   Google Scholar
• Gasparetto C, Lentzsch S, Schiller G, et al. Safety and efficacy of combination of selinexor, daratumumab, and dexamethasone (SDd) in patients with multiple myeloma (MM) previously exposed to proteasome inhibitors and immunomodulatory drugs. HemaSphere. 2019;3:740.
   Google Scholar
• Cornell R, Parameswaran H, Tang S, et al. Real world vs. clinical trial outcomes of triple class refractory penta-exposed multiple myeloma (MM). 17th Int. Myeloma Work. 2019;179–181 (FP-106).
   Google Scholar
• Costa LJ, Hari P, Kumar SK, et al. Overall survival of triple class refractory, penta-exposed multiple myeloma (MM) patients treated with selinexor plus dexamethasone or conventional care: a combined analysis of the STORM and Mammoth studies. Blood. 2019;134:3125.
   Google Scholar
• Richardson PG, Jagannath S, Chari A, et al. Overall survival (OS) with oral selinexor plus low dose dexamethasone (Sd) in patients with triple class refractory-multiple myeloma (TCR-MM). J Clin Oncol. 2019;37:8014.
   Web of Science ®Google Scholar
• Gavriatopoulou M, Vogl DT, Nooka A, et al. Effect of age on the safety and efficacy of selinexor in patients with relapsed refractory multiple myeloma: a post-hoc analysis of the STORM study. 17th Int Myeloma Work. 2019;183–184:FP–110.
   Google Scholar
• Vogl DT, Nooka A, Gavriatopoulou M, et al. Improvements in renal function with selinexor in relapsed/refractory multiple myeloma: post-hoc analyses from the STORM study. 17th Int Myeloma Work. 2019;184–186:FP–111.
   Google Scholar
• Chen C, Gasparetto C, White D, et al. Selinexor, pomalidomide, and dexamethasone (SPd) in patients with relapsed or refractory multiple myeloma. EHA Libr. 2019;266386:PF587.
   Google Scholar
• Chen CI, Bahlis N, Gasparetto C, et al. Selinexor, pomalidomide, and dexamethasone (SPd) in patients with relapsed or refractory multiple myeloma. Blood. 2019;134:141.
   Web of Science ®Google Scholar
• White D, LeBlanc R, Venner C, et al. Safety and efficacy of the combination of selinexor, lenalidomide and dexamethasone (SRd) in patients with relapsed/refractory multiple myeloma (RRMM). 17th Int. Myeloma Work. 2019; 84–86 (OAB-083).
   Google Scholar
• Bahlis NJ, Sutherland H, White D, et al. Selinexor plus low-dose bortezomib and dexamethasone for patients with relapsed or refractory multiple myeloma. Blood. 2018;132:2546–2554.
   PubMed Web of Science ®Google Scholar
• Knopf KB, Duh MS, Lafeuille M-H, et al. Meta-analysis of the efficacy and safety of bortezomib re-treatment in patients with multiple myeloma. Clin Lymphoma Myeloma Leuk. 2014;14:380–388.
   PubMed Web of Science ®Google Scholar
• Jakubowiak AJ, Jasielec JK, Rosenbaum CA, et al. Phase 1 study of selinexor plus carfilzomib and dexamethasone for the treatment of relapsed/refractory multiple myeloma. Br J Haematol. 2019;186:549–560.
   PubMed Web of Science ®Google Scholar
• Gasparetto C, Lentzsch S, Schiller G, et al. A phase 1b/2 study of selinexor, carfilzomib, and dexamethasone (SKd) in relapsed/refractory multiple myeloma (RRMM). HemaSphere. 2019;3:650.
   Google Scholar
• Gasparetto C, Schiller GJ, Callander NS, et al. A Phase 1b/2 Study of selinexor, carfilzomib, and dexamethasone (SKd) in relapsed/refractory multiple myeloma (RRMM). Blood. 2019;134:3157.
   Web of Science ®Google Scholar
• Gasparetto C, Lentzsch S, Schiller G, et al. A phase 1b study using the combination of selinexor, daratumumab, and dexamethasone in multiple myeloma patients previously exposed to proteasome inhibitors and immunomodulatory drugs. EHA Libr. 2018;215629:PS1329.
   Google Scholar
• Lokhorst HM, Plesner T, Laubach JP, et al. Targeting CD38 with daratumumab monotherapy in multiple myeloma. N Engl J Med. 2015;373:1207–1219.
   PubMed Web of Science ®Google Scholar
• Broiji A, Asselsberg E, Minnema M, et al. A phase II study of selinexor (KPT-330) combined with bortezomib and dexamethasone (SVd) for induction and consolidation for patients with progressive or refractory multiple myeloma: the SELVEDEX trial. HemaSphere. 2018;2(Suppl.):611–612.
   Google Scholar
• Chari A, Vogl DT, Jagannath S, et al. Selinexor-containing regimens for the treatment of patients with multiple myeloma refractory to chimeric antigen receptor T-cell (CAR-T) therapy. Blood. 2019;134:1854.
   Google Scholar
• White DJ, Lentzsch S, Gasparetto C, et al. Safety and efficacy of the combination of selinexor, lenalidomide and dexamethasone (SRd) in patients with newly diagnosed multiple myeloma. Blood. 2019;134:3165.
   Google Scholar
• Nishihori T, Alsina M, Ochoa J, et al. The result of a phase 1 study of selinexor in combination with high-dose melphalan and autologous hematopoietic cell transplantation for multiple myeloma. Blood. 2019;134:3314.
   Google Scholar
• Machlus KR, Wu SK, Vijey P, et al. Selinexor-induced thrombocytopenia results from inhibition of thrombopoietin signaling in early megakaryopoiesis. Blood. 2017;130:1132–1143.
   PubMed Web of Science ®Google Scholar
• Etchin J, Berezovskaya A, Conway AS, et al. KPT-8602, a second-generation inhibitor of XPO1-mediated nuclear export, is well tolerated and highly active against AML blasts and leukemia-initiating cells. Leukemia. 2017;31:143–150.
   PubMed Web of Science ®Google Scholar
• Hing ZA, Fung HYJ, Ranganathan P, et al. Next-generation XPO1 inhibitor shows improved efficacy and in vivo tolerability in hematological malignancies. Leukemia. 2016;30:2364–2372.
   PubMed Web of Science ®Google Scholar
• Vercruysse T, De Bie J, Neggers JE, et al. The second-generation exportin-1 inhibitor KPT-8602 demonstrates potent activity against acute lymphoblastic leukemia. Clin Cancer Res. 2017;23:2528–2541.
   PubMed Web of Science ®Google Scholar
• Serafimova IM, Pufall MA, Krishnan S, et al. Reversible targeting of noncatalytic cysteines with chemically tuned electrophiles. Nat Chem Biol. 2012;8:471–476.
   PubMed Web of Science ®Google Scholar
• Neggers JE, Vanstreels E, Baloglu E, et al. Heterozygous mutation of cysteine528 in XPO1 is sufficient for resistance to selective inhibitors of nuclear export. Oncotarget. 2016;7:68842–68850.
   PubMedGoogle Scholar