JLE

Innovations & Thérapeutiques en Oncologie

MENU

Anomalies de l’exportine 1 dans les hémopathies malignes : des mutations au ciblage thérapeutique Volume 4, numéro 2, Mars-Avril 2018

  • [1] Huang W., Yue L., Qiu W., Wang L.W., Zhou X., Sun Y. Prognostic value of CRM1 in pancreas cancer. Clin Invest Med. 2009;32:E315.
  • [2] Jain P., Kanagal-Shamanna R., Wierda W. Clinical and molecular characteristics of XPO1 mutations in patients with chronic lymphocytic leukemia. Am J Hematol. 2016;91:E478-E479.
  • [3] Kim J., McMillan E., Kim H.S. XPO1-dependent nuclear export is a druggable vulnerability in KRAS-mutant lung cancer. Nature. 2016;538:114-117.
  • [4] Liu X., Chong Y., Tu Y. CRM1/XPO1 is associated with clinical outcome in glioma and represents a therapeutic target by perturbing multiple core pathways. J Hematol Oncol. 2016;9:108.
  • [5] Noske A., Weichert W., Niesporek S. 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.
  • [6] van der Watt P.J., Zemanay W., Govender D., Hendricks D.T., Parker M.I., Leaner V.D. Elevated expression of the nuclear export protein, Crm1 (exportin 1), associates with human oesophageal squamous cell carcinoma. Oncol Rep. 2014;32:730-738.
  • [7] Yao Y., Dong Y., Lin F. The expression of CRM1 is associated with prognosis in human osteosarcoma. Oncol Rep. 2009;21:229-235.
  • [8] Abdul Razak A.R., Mau-Soerensen M., Gabrail N.Y. 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.
  • [9] Van Neck T., Pannecouque C., Vanstreels E., Stevens M., Dehaen W., Daelemans D. Inhibition of the CRM1-mediated nucleocytoplasmic transport by N-azolylacrylates: structure-activity relationship and mechanism of action. Bioorg Med Chem. 2008;16:9487-9497.
  • [10] Etchin J., Sun Q., Kentsis A. Antileukemic activity of nuclear export inhibitors that spare normal hematopoietic cells. Leukemia. 2013;27:66-74.
  • [11] Kashyap T., Argueta C., Aboukameel A. Selinexor, a selective inhibitor of nuclear export (SINE) compound, acts through NF-κB deactivation and combines with proteasome inhibitors to synergistically induce tumor cell death. Oncotarget. 2016;7:78883-78895.
  • [12] Muqbil I., Aboukameel A., Elloul S. Anti-tumor activity of selective inhibitor of nuclear export (SINE) compounds, is enhanced in non-Hodgkin's lymphoma through combination with mTOR inhibitor and dexamethasone. Cancer Lett. 2016;383:309-317.
  • [13] Jardin F., Pujals A., Pelletier L. 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.
  • [14] Camus V., Stamatoullas A., Mareschal S. Detection and prognostic value of recurrent exportin 1 mutations in tumor and cell-free circulating DNA of patients with classical Hodgkin's lymphoma. Haematologica. 2016;101:1094-1101.
  • [15] Bond J., Bergon A., Durand A. Cryptic XPO1-MLLT10 translocation is associated with HOXA locus deregulation in T-ALL. Blood. 2014;124:3023-3025.
  • [16] Jeromin S., Weissmann S., Haferlach C. SF3B1 mutations correlated to cytogenetics and mutations in NOTCH1, FBXW7, MYD88, XPO1 and TP53 in 1160 untreated CLL patients. Leukemia. 2014;28:108-117.
  • [17] Lin D.C., Hao J.J., Nagata Y. Genomic and molecular characterization of oesophageal squamous cell carcinoma. Nat Genet. 2014;46:467-473.
  • [18] Adachi Y., Yanajida M. Higher order chromosome structure is affected by cold-sensitive mutations in a Schizosaccharomyces pombe gene crm1+ which encodes a 115-kD protein preferentially localized in the nucleus and its periphery. J Cell Biol. 1989;108:1195-1207.
  • [19] Fornerod M., Ohno M., Yoshida M., Mattaj I.W. CRM1 is an export receptor for leucine-rich nuclear export signals. Cell. 1997;90:1051-1060.
  • [20] Fukuda M., Asano S., Nakamura T., Adachi M., Yoshida M., Nishida E. CRM1 is responsible for intracellular transport mediated by the nuclear export signal. Nature. 1997;390:308-311.
  • [21] Ossareh-Nazari B., Bachelerie F., Dargemont C. Evidence for a role of CRM1 in signal-mediated nuclear protein export. Science. 1997;278:141-144.
  • [22] Dong X., Biswas A., Süel K.E. Structural basis for leucine-rich nuclear export signal recognition by CRM1. Nature. 2009;458:1136-1141.
  • [23] Monecke T., Güttler T., Neumann P., Dickmanns A., Gorlich D., Ficner R. Crystal structure of the nuclear export receptor CRM1 in complex with snurportin1 and RanGTP. Science. 2009;324:1087-1091.
  • [24] Güttler T., Madl T., Neumann P. NES consensus redefined by structures of PKI-type and Rev-type nuclear export signals bound to CRM1. Nat Struct Mol Biol. 2010;17:1367-1376.
  • [25] Dong X., Biswas A., Chook Y.M. Structural basis for assembly and disassembly of the CRM1 nuclear export complex. Nat Struct Mol Biol. 2009;16:558-560.
  • [26] Saito N., Matsuura Y. A 2.1-Å-resolution crystal structure of unliganded CRM1 reveals the mechanism of autoinhibition. J Mol Biol. 2013;425:350-364.
  • [27] Koyama M., Matsuura Y. An allosteric mechanism to displace nuclear export cargo from CRM1 and RanGTP by RanBP1. EMBO J. 2010;29:2002-2013.
  • [28] Ishizawa J., Kojima K., Hail N. Jr., Tabe Y., Andreeff M. Expression, function and targeting of the nuclear exporter chromosome region maintenance 1 (CRM1) protein. Pharmacol Ther. 2015;153:25-35.
  • [29] Fox A.M., Ciziene D., McLaughlin S.H., Stewart M. Electrostatic interactions involving the extreme C terminus of nuclear export factor CRM1 modulate Its affinity for cargo. J Biol Chem. 2011;286:29325-29335.
  • [30] García-Santisteban I., Arregi I., Alonso-Mariño M. A cellular reporter to evaluate CRM1 nuclear export activity: functional analysis of the cancer-related mutant E571K. Cell Mol Life Sci. 2016;73:4685-4699.
  • [31] Xu D., Grishin N.V., Chook Y.M. NESdb: a database of NES-containing CRM1 cargoes. Mol Biol Cell. 2012;23:3673-3676.
  • [32] Xu D., Farmer A., Collett G., Grishin N.V., Chook Y.M. Sequence and structural analyses of nuclear export signals in the NESdb database. Mol Biol Cell. 2012;23:3677-3693.
  • [33] Okamura M., Inose H., Masuda S. RNA export through the NPC in eukaryotes. Genes. 2015;6:124-149.
  • [34] Dubois S., Viailly P.J., Mareschal S. Next-generation sequencing in diffuse large B-cell lymphoma highlights molecular divergence and therapeutic opportunities: a LYSA study. Clin Cancer Res. 2016;22:2919-2928.
  • [35] Chiu E., Gold T., Fettig V., LeVasseur M.T., Cressman D.E. Identification of a nuclear export sequence in the MHC CIITA. J Immunol. 2015;194:6102-6111.
  • [36] Hao Y., Chapuy B., Monti S., Sun H.H., Rodig S.J., Shipp M.A. Selective JAK2 inhibition specifically decreases Hodgkin's lymphoma and mediastinal large B-cell lymphoma growth and . Clin Cancer Res. 2014;20:2674-2683. in vitroin vivo
  • [37] Xie L., Ushmorov A., Leithauser F. FOXO1 is a tumor suppressor in classical Hodgkin's lymphoma. Blood. 2012;119:3503-3511.
  • [38] Traverse-Glehen A., Pittaluga S., Gaulard P. Mediastinal gray zone lymphoma: the missing link between classic Hodgkin's lymphoma and mediastinal large B-cell lymphoma. Am J Surg Pathol. 2005;29:1411-1421.
  • [39] Dunleavy K., Wilson W.H. Primary mediastinal B-cell lymphoma and mediastinal gray zone lymphoma: do they require a unique therapeutic approach? Blood. 2015;125:33-39.
  • [40] Dunleavy K., Grant C., Eberle F.C., Pittaluga S., Jaffe E.S., Wilson W.H. Gray zone lymphoma: better treated like Hodgkin's lymphoma or mediastinal large B-cell lymphoma? Curr Hematol Malig Rep. 2012;7:241-247.
  • [41] Puente X.S., Pinyol M., Quesada V. Whole-genome sequencing identifies recurrent mutations in chronic lymphocytic leukaemia. Nature. 2011;475:101-105.
  • [42] Reichel J., Chadburn A., Rubinstein P.G. Flow sorting and exome sequencing reveal the oncogenome of primary Hodgkin and Reed-Sternberg cells. Blood. 2015;125:1061-1072.
  • [43] Zhang K., Wang M., Tamayo A.T. Novel selective inhibitors of nuclear export CRM1 antagonists for therapy in mantle cell lymphoma. Exp Hematol. 2013;41:e4.
  • [44] Yoshimura M., Ishizawa J., Ruvolo V. Induction of p53-mediated transcription and apoptosis by exportin-1 (XPO1) inhibition in mantle cell lymphoma. Cancer Sci. 2014;105:795-801.
  • [45] Benzeno S., Diehl J.A. C-terminal sequences direct cyclin D1-CRM1 binding. J Biol Chem. 2004;279:56061-56066.
  • [46] Tabe Y., Kojima K., Yamamoto S. Ribosomal biogenesis and translational flux inhibition by the selective inhibitor of nuclear export (SINE) XPO1 antagonist KPT-185. PLoS One. 2015;10:e0137210.
  • [47] Lenz G., Wright G.W., Emre N.C.T. Molecular subtypes of diffuse large B-cell lymphoma arise by distinct genetic pathways. Proc Natl Acad Sci U S A. 2008;105:13520-13525.
  • [48] Weniger M.A., Gesk S., Ehrlich S. Gains of REL in primary mediastinal B-cell lymphoma coincide with nuclear accumulation of REL protein. Genes Chromosomes Cancer. 2007;46:406-415.
  • [49] Diaz L.A., Bardelli A. Liquid biopsies: genotyping circulating tumor DNA. J Clin Oncol. 2014;32:579-586.
  • [50] Bohers E., Viailly P.J., Dubois S. Somatic mutations of cell-free circulating DNA detected by next-generation sequencing reflect the genetic changes in both germinal center B-cell-like and activated B-cell-like diffuse large B-cell lymphomas at the time of diagnosis. Haematologica. 2015;100:e280-e284.
  • [51] Frattini M., Gallino G., Signoroni S. Quantitative analysis of plasma DNA in colorectal cancer patients: a novel prognostic tool. Ann N Y Acad Sci. 2006;1075:185-190.
  • [52] Jung K., Stephan C., Lewandowski M. Increased cell-free DNA in plasma of patients with metastatic spread in prostate cancer. Cancer Lett. 2004;205:173-180.
  • [53] Leon S.A., Shapiro B., Sklaroff D.M., Yaros M.J. Free DNA in the serum of cancer patients and the effect of therapy. Cancer Res. 1977;37:646-650.
  • [54] Sozzi G., Conte D., Leon M. Quantification of free circulating DNA as a diagnostic marker in lung cancer. J Clin Oncol. 2003;21:3902-3908.
  • [55] Kurtz D.M., Green M.R., Bratman S.V. Noninvasive monitoring of diffuse large B-cell lymphoma by immunoglobulin high-throughput sequencing. Blood. 2015;125:3679-3687.
  • [56] Roschewski M., Dunleavy K., Pittaluga S. Circulating tumour DNA and CT monitoring in patients with untreated diffuse large B-cell lymphoma: a correlative biomarker study. Lancet Oncol. 2015;16:541-549.
  • [57] Leithäuser F., Bäuerle M., Huynh M.Q., Möller P. Isotype-switched immunoglobulin genes with a high load of somatic hypermutation and lack of ongoing mutational activity are prevalent in mediastinal B-cell lymphoma. Blood. 2001;98:2762-2770.
  • [58] Camus V., Sarafan-Vasseur N., Bohers E. Digital PCR for quantification of recurrent and potentially actionable somatic mutations in circulating free DNA from patients with diffuse large B-cell lymphoma. Leuk Lymphoma. 2016;57:2171-2179.
  • [59] Kojima K., Kornblau S.M., Ruvolo V. Prognostic impact and targeting of CRM1 in acute myeloid leukemia. Blood. 2013;121:4166-4174.
  • [60] Schmidt J., Braggio E., Kortuem K.M. 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.
  • [61] Tai Y.T., Landesman Y., Acharya C. CRM1 inhibition induces tumor cell cytotoxicity and impairs osteoclastogenesis in multiple myeloma: molecular mechanisms and therapeutic implications. Leukemia. 2014;28:155-165.
  • [62] Kudo N., Matsumori N., Taoka H. Leptomycin B inactivates CRM1/exportin 1 by covalent modification at a cysteine residue in the central conserved region. Proc Natl Acad Sci U S A. 1999;96:9112-9117.
  • [63] Parikh K., Cang S., Sekhri A., Liu D. Selective inhibitors of nuclear export (SINE) – a novel class of anti-cancer agents. J Hematol Oncol. 2014;7:78.
  • [64] Lapalombella R., Sun Q., Williams K. Selective inhibitors of nuclear export show that CRM1/XPO1 is a target in chronic lymphocytic leukemia. Blood. 2012;120:4621-4634.
  • [65] Neggers J.E., Vercruysse T., Jacquemyn M. Identifying drug-target selectivity of small-molecule CRM1/XPO1 inhibitors by CRISPR/Cas9 genome editing. Chem Biol. 2015;22:101-116.
  • [66] Ranganathan P., Kashyap T., Yu X. XPO1 inhibition using Selinexor synergizes with chemotherapy in acute myeloid leukemia (AML) by targeting DNA repair and restoring topoisomease IIα in the nucleus. Clin Cancer Res. 2016;22:6142-6152.
  • [67] Blum W., Garzon R., Klisovic R.B. Clinical response and predictive significance in older AML patients treated with a 10-day schedule of decitabine. Proc Natl Acad Sci U S A. 2010;107:7473-7478. miR-29b
  • [68] Ranganathan P., Yu X., Santhanam R. Decitabine priming enhances the antileukemic effects of exportin 1 (XPO1) selective inhibitor selinexor in acute myeloid leukemia. Blood. 2015;125:2689-2692.
  • [69] Hing Z.A., Mantel R., Beckwith K.A. Selinexor is effective in acquired resistance to ibrutinib and synergizes with ibrutinib in chronic lymphocytic leukemia. Blood. 2015;125:3128-3132.
  • [70] Chen Y., Camacho C., Silvers T.R. Inhibition of the nuclear export receptor XPO1 as a therapeutic target for platinium resistant ovarian cancer. Clin Cancer Res. 2017;23:1552-1563.
  • [71] Kazim S., Malafa M.P., Coppola D. Selective nuclear export inhibitor KPT-330 enhances the antitumor activity of gemcitabine in human pancreatic cancer. Mol Cancer Ther. 2015;14:1570-1581.
  • [72] Ferreiro-Neira I., Torres N.E., Liesenfeld L.F. XPO1 inhibition enhances radiation response in preclinical models of rectal cancer. Clin Cancer Res. 2016;22:1663-1673.
  • [73] Farren M.R., Shakya R., Hennessey R. Selinexor, a selective inhibitor of nuclear export (SINE), shows enhanced activity in combination with PD-1/PD-L1 blockade in syngeneic murine models of colon cancer and melanoma. J Immunother Cancer. 2015;3:P355.
  • [74] Hing Z.A., Fung H.Y.J., Ranganathan P. Next-generation XPO1 inhibitor shows improved efficacy and tolerability in hematological malignancies. Leukemia. 2016;30:2364-2372. in vivo
  • [75] Etchin J., Berezoskaya A., Conway A.S. 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.
  • [76] Gutierrez M., Goy A., Byrd J.C. A phase 1 dose-escalation study of the oral selective inhibitor of nuclear export (SINE) KPT-330 (selinexor) in patients (pts) with heavily pretreated non-Hodgkin's lymphoma (NHL). J Clin Oncol. 2014;32:5s. (abstr 8518)
  • [77] Alexander T.B., Lacayo N.J., Choi J.K., Ribeiro R.C., Pui C.H., Rubnitz J.E. Phase I study of selinexor, a selective inhibitor of nuclear export, in combination with fludarabine and cytarabine, in pediatric relapsed of refractory acute leukemia. J Clin Oncol. 2016;34:4094-4101.
  • [78] Gounder M.M., Zer A., Tap W.D. 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.
  • [79] Sun Q., Carrasco Y.P., Hu Y. Nuclear export inhibition through covalent conjugation and hydrolysis of Leptomycin B by CRM1. Proc Natl Acad Sci U S A. 2013;110:1303-1308.
  • [80] Etchin J., Sanda T., Mansour M.R. 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.
  • [81] Azmi A.S., Al-Katib A., Aboukameel A. Selective inhibitors of nuclear export for the treatment of non-Hodgkin's lymphomas. Haematologica. 2013;98:1098-1106.
  • [82] Walker B.A., Wardell C.P., Melchor L. Intraclonal heterogeneity is a critical early event in the development of myeloma and precedes the development of clinical symptoms. Leukemia. 2014;28:384-390.
  • [83] Zhong Y., El-Gamal D., Dubovsky J.A. Selinexor suppresses downstream effectors of B-cell activation, proliferation and migration in chronic lymphocytic leukemia cells. Leukemia. 2014;28:1158-1163.