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Whole exome sequencing has identified hot-spot somatic\n                      <jats:italic>XPO1<\/jats:italic>\n                      point mutations which we found to disrupt highly conserved biophysical interactions in the NES-binding groove, conferring novel cargo-binding abilities and forcing cellular mis-localization of critical regulators. However, the pathogenic role played by change-in-function\n                      <jats:italic>XPO1<\/jats:italic>\n                      mutations in CLL is not fully understood.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      We performed a large, multi-center retrospective analysis of CLL cases (\n                      <jats:italic>N<\/jats:italic>\n                      \u2009=\u20091286) to correlate nonsynonymous mutations in\n                      <jats:italic>XPO1<\/jats:italic>\n                      (predominantly E571K or E571G;\n                      <jats:italic>n<\/jats:italic>\n                      \u2009=\u200972) with genetic and epigenetic features contributing to the overall outcomes in these patients. We then established a mouse model with over-expression of wildtype (wt) or mutant (E571K or E571G)\n                      <jats:italic>XPO1<\/jats:italic>\n                      restricted to the B cell compartment (E\u00b5-XPO1). E\u00b5-XPO1 mice were then crossed with the E\u00b5-TCL1 CLL mouse model. Lastly, we determined crystal structures of XPO1 (wt or E571K) bound to several selective inhibitors of nuclear export (SINE) molecules (KPT-185, KPT-330\/Selinexor, and KPT-8602\/Eltanexor).\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      We report that nonsynonymous mutations in XPO1 associate with high risk genetic and epigenetic features and accelerated CLL progression. Using the newly-generated E\u00b5-XPO1 mouse model, we found that constitutive B-cell over-expression of wt or mutant\n                      <jats:italic>XPO1<\/jats:italic>\n                      could affect development of a CLL-like disease in aged mice. Furthermore, concurrent B-cell expression of\n                      <jats:italic>XPO1<\/jats:italic>\n                      with E571K or E571G mutations and\n                      <jats:italic>TCL1<\/jats:italic>\n                      accelerated the rate of leukemogenesis relative to that of E\u00b5-TCL1 mice. Lastly, crystal structures of E571 or E571K-XPO1 bound to SINEs, including Selinexor, are highly similar, suggesting that the activity of this class of compounds will not be affected by\n                      <jats:italic>XPO1<\/jats:italic>\n                      mutations at E571 in patients with CLL.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>\n                      These findings indicate that mutations in\n                      <jats:italic>XPO1<\/jats:italic>\n                      at E571 can drive leukemogenesis by priming the pre-neoplastic lymphocytes for acquisition of additional genetic and epigenetic abnormalities that collectively result in neoplastic transformation.\n                    <\/jats:p>\n                  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All CLL patient data was obtained after patients provided informed consent and approved by the institutional review board (IRB) from each respective institution. Blood from newly diagnosed untreated CLL patients were obtained from the Ohio State University Leukemia Tissue Bank after obtaining informed consent approved by the cancer institution review board. All mouse protocols were reviewed and approved by The Ohio State University Institutional Animal Care and Use Committee (IACUC).","order":1,"name":"Ethics","group":{"name":"EthicsHeading","label":"Ethics approval and consent to participate"}},{"value":"Not applicable.","order":2,"name":"Ethics","group":{"name":"EthicsHeading","label":"Consent for publication"}},{"value":"SS is employed by and is a stockholder of Karyopharm Therapeutics Inc. SS holds Patents (8999996, 9079865, 9714226, PCT\/US12\/048319, and I574957) on hydrazide containing nuclear transport modulators and uses, and pending Patents (PCT\/US12\/048319, 499\/2012, PI20102724, and 2012000928) on hydrazide-containing nuclear transport modulators and uses. All other authors declare no competing interests.","order":3,"name":"Ethics","group":{"name":"EthicsHeading","label":"Competing interests"}}],"article-number":"17"}}