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As microtubule inhibitors could represent a therapeutic strategy for <jats:styled-content style=\"fixed-case\">CLL<\/jats:styled-content>, this study investigated the capability of nocodazole, a synthetic depolymerizing agent, to kill <jats:styled-content style=\"fixed-case\">CLL<\/jats:styled-content> leukaemic cells. We demonstrated that nocodazole was highly specific for the <jats:italic>in vitro<\/jats:italic> induction of apoptosis in leukaemic cells from 90 <jats:styled-content style=\"fixed-case\">CLL<\/jats:styled-content> patients, without affecting the viability of T\u2010cells and\/or mesenchymal stromal cells (<jats:styled-content style=\"fixed-case\">MSC<\/jats:styled-content>s) recovered from the same patients. Nocodazole was observed to overcome the pro\u2010survival signals provided by <jats:styled-content style=\"fixed-case\">MSC<\/jats:styled-content>s. Competing with <jats:styled-content style=\"fixed-case\">ATP<\/jats:styled-content> for the nucleotide\u2010binding site, nocodazole has been observed to turn off the high basal tyrosine phosphorylation of leukaemic cells mediated by the Src\u2010kinase Lyn. Considering that most anti\u2010microtubule drugs have limited clinical use because of their strong toxic effects, the high selectivity of nocodazole for leukaemic cells in <jats:styled-content style=\"fixed-case\">CLL<\/jats:styled-content> and its capability to bypass microenvironmental pro\u2010survival stimuli, suggests the use of this inhibitor for designing new therapeutic strategies in <jats:styled-content style=\"fixed-case\">CLL<\/jats:styled-content> treatment.<\/jats:p>","DOI":"10.1111\/bjh.12815","type":"journal-article","created":{"date-parts":[[2014,3,7]],"date-time":"2014-03-07T13:17:24Z","timestamp":1394198244000},"page":"659-672","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":22,"title":["Leukaemic cells from chronic lymphocytic leukaemia patients undergo apoptosis following microtubule depolymerization and <scp>L<\/scp>yn inhibition by nocodazole"],"prefix":"10.1111","volume":"165","author":[{"given":"Federica","family":"Frezzato","sequence":"first","affiliation":[{"name":"Venetian Institute of Molecular Medicine (VIMM) Centro di Eccellenza per la Ricerca Biomedica Padova Italy"},{"name":"Department of Medicine, Haematology and Clinical Immunology Branch Padova University School of Medicine Padova Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Valentina","family":"Trimarco","sequence":"additional","affiliation":[{"name":"Venetian Institute of Molecular Medicine (VIMM) Centro di Eccellenza per la Ricerca Biomedica Padova Italy"},{"name":"Department of Medicine, Haematology and Clinical Immunology Branch Padova University School of Medicine Padova Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Veronica","family":"Martini","sequence":"additional","affiliation":[{"name":"Venetian Institute of Molecular Medicine (VIMM) Centro di Eccellenza per la Ricerca Biomedica Padova 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