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Previously, we identified the farnesyl transferase inhibitor\n                    <jats:styled-content style=\"fixed-case\">BMS<\/jats:styled-content>\n                    \u2010214662 as a selective inducer of apoptosis in\n                    <jats:styled-content style=\"fixed-case\">LSC<\/jats:styled-content>\n                    s of\n                    <jats:styled-content style=\"fixed-case\">CML<\/jats:styled-content>\n                    patients relative to normal controls; however, the mechanism underlying\n                    <jats:styled-content style=\"fixed-case\">LSC<\/jats:styled-content>\n                    \u2010specific apoptosis remains unclear. To identify pathways involved in the favourable effects of\n                    <jats:styled-content style=\"fixed-case\">BMS<\/jats:styled-content>\n                    \u2010214662 in\n                    <jats:styled-content style=\"fixed-case\">CML<\/jats:styled-content>\n                    , we employed a proteomic approach (based on iTRAQ) to analyse changes in protein expression in response to drug treatment in the nuclear and cytoplasmic fractions of\n                    <jats:styled-content style=\"fixed-case\">CD<\/jats:styled-content>\n                    34\n                    <jats:sup>+<\/jats:sup>\n                    <jats:styled-content style=\"fixed-case\">CML<\/jats:styled-content>\n                    cells. The study identified 88 proteins as altered after drug treatment, which included proteins known to be involved in nucleic acid metabolism, oncogenesis, developmental processes and intracellular protein trafficking. We found that expression of\n                    <jats:styled-content style=\"fixed-case\">E<\/jats:styled-content>\n                    bp1, a negative regulator of proliferation, was upregulated in the nucleus of\n                    <jats:styled-content style=\"fixed-case\">BMS<\/jats:styled-content>\n                    \u2010214662\u2010treated cells. Furthermore, proteins showing altered levels in the cytosol, such as histones, were predominantly derived from the nucleus and\n                    <jats:styled-content style=\"fixed-case\">BMS<\/jats:styled-content>\n                    \u2010214662 affected expression levels of nuclear pore complex proteins. Validation of key facets of these observations suggests that drug\u2010induced alterations in protein localisation, potentially via loss of nuclear membrane integrity, contributes to the\n                    <jats:styled-content style=\"fixed-case\">LSC<\/jats:styled-content>\n                    specificity of\n                    <jats:styled-content style=\"fixed-case\">BMS<\/jats:styled-content>\n                    \u2010214662, possibly via\n                    <jats:styled-content style=\"fixed-case\">R<\/jats:styled-content>\n                    an proteins as targets.\n                  <\/jats:p>","DOI":"10.1002\/pmic.201200022","type":"journal-article","created":{"date-parts":[[2012,11,26]],"date-time":"2012-11-26T14:18:49Z","timestamp":1353939529000},"page":"153-168","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":4,"title":["Quantitative proteomics analysis of\n                    <scp>BMS<\/scp>\n                    \u2010214662 effects on\n                    <scp>CD<\/scp>\n                    34 positive cells from chronic myeloid leukaemia patients"],"prefix":"10.1002","volume":"13","author":[{"given":"Stefan","family":"Balabanov","sequence":"first","affiliation":[{"name":"Institute of Cancer Sciences University of Glasgow  Glasgow UK"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Caroline A.","family":"Evans","sequence":"additional","affiliation":[{"name":"Stem Cell and Leukaemia Proteomics Laboratory Manchester Academic Health Sciences Centre University of Manchester  Manchester UK"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Sheela A.","family":"Abraham","sequence":"additional","affiliation":[{"name":"Institute of Cancer Sciences University of Glasgow  Glasgow UK"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Francesca","family":"Pellicano","sequence":"additional","affiliation":[{"name":"Institute of Cancer Sciences University of Glasgow  Glasgow UK"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Mhairi","family":"Copland","sequence":"additional","affiliation":[{"name":"Institute of Cancer Sciences University of Glasgow  Glasgow UK"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Michael J.","family":"Walker","sequence":"additional","affiliation":[{"name":"Stem Cell and Leukaemia Proteomics Laboratory Manchester Academic Health Sciences Centre University of Manchester  Manchester UK"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Anthony D.","family":"Whetton","sequence":"additional","affiliation":[{"name":"Stem Cell and Leukaemia Proteomics Laboratory Manchester Academic Health Sciences Centre University of Manchester  Manchester UK"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Tessa L.","family":"Holyoake","sequence":"additional","affiliation":[{"name":"Institute of Cancer Sciences University of Glasgow  Glasgow 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