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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Sustained deep molecular responses in patients switched to nilotinib due to persistent <italic>BCR-ABL1</italic> on imatinib: final ENESTcmr randomized trial results</title><author><name sortKey="Hughes, T P" sort="Hughes, T P" uniqKey="Hughes T" first="T P" last="Hughes">T P Hughes</name><affiliation><nlm:aff id="aff1"><institution>Division of Haematology, SA Pathology and South Australian Health and Medical Research Institute, University of Adelaide</institution>, Adelaide, South Australia,<country>Australia</country></nlm:aff></affiliation></author><author><name sortKey="Leber, B" sort="Leber, B" uniqKey="Leber B" first="B" last="Leber">B. Leber</name><affiliation><nlm:aff id="aff2"><institution>Clinical Pathology, McMaster University</institution>, Hamilton, Ontario,<country>Canada</country></nlm:aff></affiliation></author><author><name sortKey="Cervantes, F" sort="Cervantes, F" uniqKey="Cervantes F" first="F" last="Cervantes">F. Cervantes</name><affiliation><nlm:aff id="aff3"><institution>Department of Hematology, Hospital Clinic, IDIBAPS, University of Barcelona</institution>, Barcelona,<country>Spain</country></nlm:aff></affiliation></author><author><name sortKey="Spector, N" sort="Spector, N" uniqKey="Spector N" first="N" last="Spector">N. Spector</name><affiliation><nlm:aff id="aff4"><institution>Departamento de Clínica Médica/FM, Universidade Federal do Rio de Janeiro</institution>, Rio de Janeiro,<country>Brazil</country></nlm:aff></affiliation></author><author><name sortKey="Pasquini, R" sort="Pasquini, R" uniqKey="Pasquini R" first="R" last="Pasquini">R. Pasquini</name><affiliation><nlm:aff id="aff5"><institution>Division of Hematology and Medical Oncology, Federal University of Paraná</institution>, Curitiba,<country>Brazil</country></nlm:aff></affiliation></author><author><name sortKey="Clementino, N C D" sort="Clementino, N C D" uniqKey="Clementino N" first="N C D" last="Clementino">N C D. Clementino</name><affiliation><nlm:aff id="aff6"><institution>Hospital Das Clinicas da UFMG</institution>, Belo Horizonte,<country>Brazil</country></nlm:aff></affiliation></author><author><name sortKey="Schwarer, A P" sort="Schwarer, A P" uniqKey="Schwarer A" first="A P" last="Schwarer">A P Schwarer</name><affiliation><nlm:aff id="aff7"><institution>Department of Hematology, Alfred Hospital</institution>, Melbourne, Victoria,<country>Australia</country></nlm:aff></affiliation></author><author><name sortKey="Dorlhiac Llacer, P E" sort="Dorlhiac Llacer, P E" uniqKey="Dorlhiac Llacer P" first="P E" last="Dorlhiac-Llacer">P E Dorlhiac-Llacer</name><affiliation><nlm:aff id="aff8"><institution>Department of Hematology, Hospital das Clinicas FMUSP</institution>, São Paulo,<country>Brazil</country></nlm:aff></affiliation></author><author><name sortKey="Mahon, F X" sort="Mahon, F X" uniqKey="Mahon F" first="F-X" last="Mahon">F-X Mahon</name><affiliation><nlm:aff id="aff9"><institution>Laboratoire Hématopoïèse Leucémique et Cible Thérapeutique, Inserm U1035, Université Victor Ségalen</institution>, Bordeaux,<country>France</country></nlm:aff></affiliation></author><author><name sortKey="Rea, D" sort="Rea, D" uniqKey="Rea D" first="D" last="Rea">D. Rea</name><affiliation><nlm:aff id="aff10"><institution>Unité de Thérapie Cellulaire et Clinique Transfusionnelle, Service des Maladies du Sang et EA3518, Hôpital Saint-Louis</institution>, Paris,<country>France</country></nlm:aff></affiliation></author><author><name sortKey="Guerci Bresler, A" sort="Guerci Bresler, A" uniqKey="Guerci Bresler A" first="A" last="Guerci-Bresler">A. Guerci-Bresler</name><affiliation><nlm:aff id="aff11"><institution>Department of Hematology, Brabois Hospital, Vandoeuvre-lès-Nancy</institution>, Vandoeuvre,<country>France</country></nlm:aff></affiliation></author><author><name sortKey="Kamel Reid, S" sort="Kamel Reid, S" uniqKey="Kamel Reid S" first="S" last="Kamel-Reid">S. Kamel-Reid</name><affiliation><nlm:aff id="aff12"><institution>Clinical Laboratory Genetics, Genome Diagnostics, University Health Network, Toronto General Hospital</institution>, Toronto, Ontario,<country>Canada</country></nlm:aff></affiliation></author><author><name sortKey="Bendit, I" sort="Bendit, I" uniqKey="Bendit I" first="I" last="Bendit">I. Bendit</name><affiliation><nlm:aff id="aff13"><institution>Hematology Unit, Faculty of Medicine, University of São Paulo</institution>, São Paulo,<country>Brazil</country></nlm:aff></affiliation></author><author><name sortKey="Acharya, S" sort="Acharya, S" uniqKey="Acharya S" first="S" last="Acharya">S. Acharya</name><affiliation><nlm:aff id="aff14"><institution>Novartis Healthcare Pvt Ltd</institution>, Hyderabad,<country>India</country></nlm:aff></affiliation></author><author><name sortKey="Glynos, T" sort="Glynos, T" uniqKey="Glynos T" first="T" last="Glynos">T. Glynos</name><affiliation><nlm:aff id="aff15"><institution>Novartis Pharmaceuticals Corporation</institution>, East Hanover, NJ,<country>USA</country></nlm:aff></affiliation></author><author><name sortKey="Dalal, D" sort="Dalal, D" uniqKey="Dalal D" first="D" last="Dalal">D. Dalal</name><affiliation><nlm:aff id="aff15"><institution>Novartis Pharmaceuticals Corporation</institution>, East Hanover, NJ,<country>USA</country></nlm:aff></affiliation></author><author><name sortKey="Branford, S" sort="Branford, S" uniqKey="Branford S" first="S" last="Branford">S. Branford</name><affiliation><nlm:aff id="aff16"><institution>Leukaemia Unit, Centre for Cancer Biology, SA Pathology, University of South Australia and University of Adelaide</institution>, Adelaide, South Australia,<country>Australia</country></nlm:aff></affiliation></author><author><name sortKey="Lipton, J H" sort="Lipton, J H" uniqKey="Lipton J" first="J H" last="Lipton">J H Lipton</name><affiliation><nlm:aff id="aff17"><institution>Blood and Marrow Transplant Service, Princess Margaret Cancer Centre, University of Toronto</institution>, Toronto, Ontario,<country>Canada</country></nlm:aff></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PMC</idno><idno type="pmid">28862704</idno><idno type="pmc">5668492</idno><idno type="url">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5668492</idno><idno type="RBID">PMC:5668492</idno><idno type="doi">10.1038/leu.2017.247</idno><date when="2017">2017</date><idno type="wicri:Area/Pmc/Corpus">000678</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Corpus" wicri:corpus="PMC">000678</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">Sustained deep molecular responses in patients switched to nilotinib due to persistent <italic>BCR-ABL1</italic> on imatinib: final ENESTcmr randomized trial results</title><author><name sortKey="Hughes, T P" sort="Hughes, T P" uniqKey="Hughes T" first="T P" last="Hughes">T P Hughes</name><affiliation><nlm:aff id="aff1"><institution>Division of Haematology, SA Pathology and South Australian Health and Medical Research Institute, University of Adelaide</institution>, Adelaide, South Australia,<country>Australia</country></nlm:aff></affiliation></author><author><name sortKey="Leber, B" sort="Leber, B" uniqKey="Leber B" first="B" last="Leber">B. Leber</name><affiliation><nlm:aff id="aff2"><institution>Clinical Pathology, McMaster University</institution>, Hamilton, Ontario,<country>Canada</country></nlm:aff></affiliation></author><author><name sortKey="Cervantes, F" sort="Cervantes, F" uniqKey="Cervantes F" first="F" last="Cervantes">F. Cervantes</name><affiliation><nlm:aff id="aff3"><institution>Department of Hematology, Hospital Clinic, IDIBAPS, University of Barcelona</institution>, Barcelona,<country>Spain</country></nlm:aff></affiliation></author><author><name sortKey="Spector, N" sort="Spector, N" uniqKey="Spector N" first="N" last="Spector">N. Spector</name><affiliation><nlm:aff id="aff4"><institution>Departamento de Clínica Médica/FM, Universidade Federal do Rio de Janeiro</institution>, Rio de Janeiro,<country>Brazil</country></nlm:aff></affiliation></author><author><name sortKey="Pasquini, R" sort="Pasquini, R" uniqKey="Pasquini R" first="R" last="Pasquini">R. Pasquini</name><affiliation><nlm:aff id="aff5"><institution>Division of Hematology and Medical Oncology, Federal University of Paraná</institution>, Curitiba,<country>Brazil</country></nlm:aff></affiliation></author><author><name sortKey="Clementino, N C D" sort="Clementino, N C D" uniqKey="Clementino N" first="N C D" last="Clementino">N C D. Clementino</name><affiliation><nlm:aff id="aff6"><institution>Hospital Das Clinicas da UFMG</institution>, Belo Horizonte,<country>Brazil</country></nlm:aff></affiliation></author><author><name sortKey="Schwarer, A P" sort="Schwarer, A P" uniqKey="Schwarer A" first="A P" last="Schwarer">A P Schwarer</name><affiliation><nlm:aff id="aff7"><institution>Department of Hematology, Alfred Hospital</institution>, Melbourne, Victoria,<country>Australia</country></nlm:aff></affiliation></author><author><name sortKey="Dorlhiac Llacer, P E" sort="Dorlhiac Llacer, P E" uniqKey="Dorlhiac Llacer P" first="P E" last="Dorlhiac-Llacer">P E Dorlhiac-Llacer</name><affiliation><nlm:aff id="aff8"><institution>Department of Hematology, Hospital das Clinicas FMUSP</institution>, São Paulo,<country>Brazil</country></nlm:aff></affiliation></author><author><name sortKey="Mahon, F X" sort="Mahon, F X" uniqKey="Mahon F" first="F-X" last="Mahon">F-X Mahon</name><affiliation><nlm:aff id="aff9"><institution>Laboratoire Hématopoïèse Leucémique et Cible Thérapeutique, Inserm U1035, Université Victor Ségalen</institution>, Bordeaux,<country>France</country></nlm:aff></affiliation></author><author><name sortKey="Rea, D" sort="Rea, D" uniqKey="Rea D" first="D" last="Rea">D. Rea</name><affiliation><nlm:aff id="aff10"><institution>Unité de Thérapie Cellulaire et Clinique Transfusionnelle, Service des Maladies du Sang et EA3518, Hôpital Saint-Louis</institution>, Paris,<country>France</country></nlm:aff></affiliation></author><author><name sortKey="Guerci Bresler, A" sort="Guerci Bresler, A" uniqKey="Guerci Bresler A" first="A" last="Guerci-Bresler">A. Guerci-Bresler</name><affiliation><nlm:aff id="aff11"><institution>Department of Hematology, Brabois Hospital, Vandoeuvre-lès-Nancy</institution>, Vandoeuvre,<country>France</country></nlm:aff></affiliation></author><author><name sortKey="Kamel Reid, S" sort="Kamel Reid, S" uniqKey="Kamel Reid S" first="S" last="Kamel-Reid">S. Kamel-Reid</name><affiliation><nlm:aff id="aff12"><institution>Clinical Laboratory Genetics, Genome Diagnostics, University Health Network, Toronto General Hospital</institution>, Toronto, Ontario,<country>Canada</country></nlm:aff></affiliation></author><author><name sortKey="Bendit, I" sort="Bendit, I" uniqKey="Bendit I" first="I" last="Bendit">I. Bendit</name><affiliation><nlm:aff id="aff13"><institution>Hematology Unit, Faculty of Medicine, University of São Paulo</institution>, São Paulo,<country>Brazil</country></nlm:aff></affiliation></author><author><name sortKey="Acharya, S" sort="Acharya, S" uniqKey="Acharya S" first="S" last="Acharya">S. Acharya</name><affiliation><nlm:aff id="aff14"><institution>Novartis Healthcare Pvt Ltd</institution>, Hyderabad,<country>India</country></nlm:aff></affiliation></author><author><name sortKey="Glynos, T" sort="Glynos, T" uniqKey="Glynos T" first="T" last="Glynos">T. Glynos</name><affiliation><nlm:aff id="aff15"><institution>Novartis Pharmaceuticals Corporation</institution>, East Hanover, NJ,<country>USA</country></nlm:aff></affiliation></author><author><name sortKey="Dalal, D" sort="Dalal, D" uniqKey="Dalal D" first="D" last="Dalal">D. Dalal</name><affiliation><nlm:aff id="aff15"><institution>Novartis Pharmaceuticals Corporation</institution>, East Hanover, NJ,<country>USA</country></nlm:aff></affiliation></author><author><name sortKey="Branford, S" sort="Branford, S" uniqKey="Branford S" first="S" last="Branford">S. Branford</name><affiliation><nlm:aff id="aff16"><institution>Leukaemia Unit, Centre for Cancer Biology, SA Pathology, University of South Australia and University of Adelaide</institution>, Adelaide, South Australia,<country>Australia</country></nlm:aff></affiliation></author><author><name sortKey="Lipton, J H" sort="Lipton, J H" uniqKey="Lipton J" first="J H" last="Lipton">J H Lipton</name><affiliation><nlm:aff id="aff17"><institution>Blood and Marrow Transplant Service, Princess Margaret Cancer Centre, University of Toronto</institution>, Toronto, Ontario,<country>Canada</country></nlm:aff></affiliation></author></analytic><series><title level="j">Leukemia</title><idno type="ISSN">0887-6924</idno><idno type="eISSN">1476-5551</idno><imprint><date when="2017">2017</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><back><div1 type="bibliography"><listBibl><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct></listBibl></div1></back></TEI><pmc article-type="letter"><pmc-dir>properties open_access</pmc-dir>
<front><journal-meta><journal-id journal-id-type="nlm-ta">Leukemia</journal-id><journal-id journal-id-type="iso-abbrev">Leukemia</journal-id><journal-title-group><journal-title>Leukemia</journal-title></journal-title-group><issn pub-type="ppub">0887-6924</issn><issn pub-type="epub">1476-5551</issn><publisher><publisher-name>Nature Publishing Group</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="pmid">28862704</article-id><article-id pub-id-type="pmc">5668492</article-id><article-id pub-id-type="pii">leu2017247</article-id><article-id pub-id-type="doi">10.1038/leu.2017.247</article-id><article-categories><subj-group subj-group-type="heading"><subject>Letter to the Editor</subject></subj-group></article-categories><title-group><article-title>Sustained deep molecular responses in patients switched to nilotinib due to persistent <italic>BCR-ABL1</italic> on imatinib: final ENESTcmr randomized trial results</article-title><alt-title alt-title-type="running">Letter to the Editor</alt-title></title-group><contrib-group><contrib contrib-type="author"><name><surname>Hughes</surname><given-names>T P</given-names></name><xref ref-type="aff" rid="aff1">1</xref><xref ref-type="corresp" rid="caf1">*</xref></contrib><contrib contrib-type="author"><name><surname>Leber</surname><given-names>B</given-names></name><xref ref-type="aff" rid="aff2">2</xref></contrib><contrib contrib-type="author"><name><surname>Cervantes</surname><given-names>F</given-names></name><xref ref-type="aff" rid="aff3">3</xref></contrib><contrib contrib-type="author"><name><surname>Spector</surname><given-names>N</given-names></name><xref ref-type="aff" rid="aff4">4</xref></contrib><contrib contrib-type="author"><name><surname>Pasquini</surname><given-names>R</given-names></name><xref ref-type="aff" rid="aff5">5</xref></contrib><contrib contrib-type="author"><name><surname>Clementino</surname><given-names>N C D</given-names></name><xref ref-type="aff" rid="aff6">6</xref></contrib><contrib contrib-type="author"><name><surname>Schwarer</surname><given-names>A P</given-names></name><xref ref-type="aff" rid="aff7">7</xref></contrib><contrib contrib-type="author"><name><surname>Dorlhiac-Llacer</surname><given-names>P E</given-names></name><xref ref-type="aff" rid="aff8">8</xref></contrib><contrib contrib-type="author"><name><surname>Mahon</surname><given-names>F-X</given-names></name><xref ref-type="aff" rid="aff9">9</xref></contrib><contrib contrib-type="author"><name><surname>Rea</surname><given-names>D</given-names></name><xref ref-type="aff" rid="aff10">10</xref></contrib><contrib contrib-type="author"><name><surname>Guerci-Bresler</surname><given-names>A</given-names></name><xref ref-type="aff" rid="aff11">11</xref></contrib><contrib contrib-type="author"><name><surname>Kamel-Reid</surname><given-names>S</given-names></name><xref ref-type="aff" rid="aff12">12</xref></contrib><contrib contrib-type="author"><name><surname>Bendit</surname><given-names>I</given-names></name><xref ref-type="aff" rid="aff13">13</xref></contrib><contrib contrib-type="author"><name><surname>Acharya</surname><given-names>S</given-names></name><xref ref-type="aff" rid="aff14">14</xref></contrib><contrib contrib-type="author"><name><surname>Glynos</surname><given-names>T</given-names></name><xref ref-type="aff" rid="aff15">15</xref></contrib><contrib contrib-type="author"><name><surname>Dalal</surname><given-names>D</given-names></name><xref ref-type="aff" rid="aff15">15</xref></contrib><contrib contrib-type="author"><name><surname>Branford</surname><given-names>S</given-names></name><xref ref-type="aff" rid="aff16">16</xref></contrib><contrib contrib-type="author"><name><surname>Lipton</surname><given-names>J H</given-names></name><xref ref-type="aff" rid="aff17">17</xref></contrib><aff id="aff1"><label>1</label><institution>Division of Haematology, SA Pathology and South Australian Health and Medical Research Institute, University of Adelaide</institution>, Adelaide, South Australia,<country>Australia</country></aff><aff id="aff2"><label>2</label><institution>Clinical Pathology, McMaster University</institution>, Hamilton, Ontario,<country>Canada</country></aff><aff id="aff3"><label>3</label><institution>Department of Hematology, Hospital Clinic, IDIBAPS, University of Barcelona</institution>, Barcelona,<country>Spain</country></aff><aff id="aff4"><label>4</label><institution>Departamento de Clínica Médica/FM, Universidade Federal do Rio de Janeiro</institution>, Rio de Janeiro,<country>Brazil</country></aff><aff id="aff5"><label>5</label><institution>Division of Hematology and Medical Oncology, Federal University of Paraná</institution>, Curitiba,<country>Brazil</country></aff><aff id="aff6"><label>6</label><institution>Hospital Das Clinicas da UFMG</institution>, Belo Horizonte,<country>Brazil</country></aff><aff id="aff7"><label>7</label><institution>Department of Hematology, Alfred Hospital</institution>, Melbourne, Victoria,<country>Australia</country></aff><aff id="aff8"><label>8</label><institution>Department of Hematology, Hospital das Clinicas FMUSP</institution>, São Paulo,<country>Brazil</country></aff><aff id="aff9"><label>9</label><institution>Laboratoire Hématopoïèse Leucémique et Cible Thérapeutique, Inserm U1035, Université Victor Ségalen</institution>, Bordeaux,<country>France</country></aff><aff id="aff10"><label>10</label><institution>Unité de Thérapie Cellulaire et Clinique Transfusionnelle, Service des Maladies du Sang et EA3518, Hôpital Saint-Louis</institution>, Paris,<country>France</country></aff><aff id="aff11"><label>11</label><institution>Department of Hematology, Brabois Hospital, Vandoeuvre-lès-Nancy</institution>, Vandoeuvre,<country>France</country></aff><aff id="aff12"><label>12</label><institution>Clinical Laboratory Genetics, Genome Diagnostics, University Health Network, Toronto General Hospital</institution>, Toronto, Ontario,<country>Canada</country></aff><aff id="aff13"><label>13</label><institution>Hematology Unit, Faculty of Medicine, University of São Paulo</institution>, São Paulo,<country>Brazil</country></aff><aff id="aff14"><label>14</label><institution>Novartis Healthcare Pvt Ltd</institution>, Hyderabad,<country>India</country></aff><aff id="aff15"><label>15</label><institution>Novartis Pharmaceuticals Corporation</institution>, East Hanover, NJ,<country>USA</country></aff><aff id="aff16"><label>16</label><institution>Leukaemia Unit, Centre for Cancer Biology, SA Pathology, University of South Australia and University of Adelaide</institution>, Adelaide, South Australia,<country>Australia</country></aff><aff id="aff17"><label>17</label><institution>Blood and Marrow Transplant Service, Princess Margaret Cancer Centre, University of Toronto</institution>, Toronto, Ontario,<country>Canada</country></aff></contrib-group><author-notes><corresp id="caf1"><label>*</label><email>tim.hughes@sahmri.com</email></corresp></author-notes><pub-date pub-type="ppub"><month>11</month><year>2017</year></pub-date><pub-date pub-type="epreprint"><day>03</day><month>08</month><year>2017</year></pub-date><pub-date pub-type="epub"><day>01</day><month>09</month><year>2017</year></pub-date><volume>31</volume><issue>11</issue><fpage>2529</fpage><lpage>2531</lpage><permissions><copyright-statement>Copyright © 2017 The Author(s)</copyright-statement><copyright-year>2017</copyright-year><copyright-holder>The Author(s)</copyright-holder><license license-type="open-access" xlink:href="http://creativecommons.org/licenses/by/4.0/"><pmc-comment>author-paid</pmc-comment>
<license-p>This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit <ext-link ext-link-type="uri" xlink:href="http://creativecommons.org/licenses/by/4.0/">http://creativecommons.org/licenses/by/4.0/</ext-link></license-p></license></permissions></article-meta></front><body><p>For patients with chronic myeloid leukemia in chronic phase (CML-CP), treatment with a BCR-ABL1 tyrosine kinase inhibitor (TKI), such as imatinib or nilotinib, can result in high response rates and near-normal life expectancies.<sup><xref ref-type="bibr" rid="bib1">1</xref>, <xref ref-type="bibr" rid="bib2">2</xref>, <xref ref-type="bibr" rid="bib3">3</xref></sup> Although most patients treated with imatinib achieve a complete cytogenetic response (CCyR) and many achieve a major molecular response (MMR; <italic>BCR-ABL1</italic>⩽0.1% on the International Scale (<italic>BCR-ABL1</italic><sup>IS</sup>)), MR<sup><xref ref-type="bibr" rid="bib4">4</xref></sup> (<italic>BCR-ABL1</italic><sup>IS</sup>⩽0.01%), or MR<sup>4.5</sup> (<italic>BCR-ABL1</italic><sup>IS</sup>⩽0.0032%),<sup><xref ref-type="bibr" rid="bib4">4</xref>, <xref ref-type="bibr" rid="bib5">5</xref>, <xref ref-type="bibr" rid="bib6">6</xref>, <xref ref-type="bibr" rid="bib7">7</xref>, <xref ref-type="bibr" rid="bib8">8</xref>, <xref ref-type="bibr" rid="bib9">9</xref>, <xref ref-type="bibr" rid="bib10">10</xref></sup> results from the Evaluating Nilotinib Efficacy and Safety in Clinical Trials–Newly Diagnosed Patients (ENESTnd) study showed that frontline nilotinib therapy results in higher response rates than frontline imatinib therapy.<sup><xref ref-type="bibr" rid="bib9">9</xref>, <xref ref-type="bibr" rid="bib10">10</xref></sup></p><p>ENEST–Complete Molecular Remission (ENESTcmr) was a 48-month, open-label, randomized, phase 3 study designed to investigate whether patients with CCyR but persistent minimal residual disease (MRD) on long-term imatinib could achieve deeper molecular responses by switching to nilotinib 400 mg twice daily vs remaining on imatinib. The study design and methods were previously described in detail<sup><xref ref-type="bibr" rid="bib11">11</xref></sup> and are summarized in the Supplemental Methods. The study was conducted in accordance with the Declaration of Helsinki. An independent ethics committee or institutional review board at each center approved the protocol. All patients provided written informed consent before randomization. The trial was registered at <ext-link ext-link-type="uri" xlink:href="http://www.ClinicalTrials.gov">www.ClinicalTrials.gov</ext-link> (NCT00760877).</p><p>Results from the first 24 months of follow-up were previously reported and showed that patients randomized to nilotinib achieved higher rates of MMR and deeper molecular responses than did patients randomized to continue imatinib.<sup><xref ref-type="bibr" rid="bib11">11</xref></sup> Per the study protocol, patients in the imatinib arm with detectable <italic>BCR-ABL1</italic> at 24 months were allowed to cross over to nilotinib. Here we report updated results from ENESTcmr based on 48 months of treatment for patients who completed the study, including an evaluation of the impact of crossover on patients’ molecular responses.</p><p>Of 104 patients randomized to nilotinib 400 mg twice daily, 59 (56.7%) completed 48 months of nilotinib treatment on study and 45 (43.3%) discontinued early (<xref ref-type="supplementary-material" rid="sup1">Supplementary Figure 1</xref>). Of 103 patients randomized to imatinib, 41 (39.8%) completed 48 months of imatinib treatment on study, 16 (15.5%) discontinued without crossing over to nilotinib, and 46 (44.7%) crossed over to nilotinib (due to detectable <italic>BCR-ABL1</italic> after 24 months of study treatment <italic>(n</italic>=41), imatinib failure <italic>(n</italic>=3), or loss of undetectable <italic>BCR-ABL1</italic><italic>(n</italic>=2)); after crossing over, 36 patients completed the study on nilotinib and 10 discontinued early. The most common reason for early discontinuation of study treatment in both arms was adverse events (AEs; nilotinib, <italic>n</italic>=19; imatinib, <italic>n</italic>=12 (5 prior to crossover and 7 after crossover); <xref ref-type="supplementary-material" rid="sup1">Supplementary Figure 2</xref>).</p><p>Overall, 56 of 104 patients (53.8%) in the nilotinib arm achieved MR<sup>4.5</sup> by 48 months; among patients in the imatinib arm, 46 of 103 (44.7%) achieved MR<sup>4.5</sup> by 48 months, but 13 of these patients achieved MR<sup>4.5</sup> only after crossover to nilotinib. The Kaplan–Meier–estimated median time to MR<sup>4.5</sup> was 24 (95% CI, 14.8–47.5) months in the nilotinib arm and was not reached by 48 months in the imatinib arm (<xref ref-type="fig" rid="fig1">Figure 1</xref>). Among patients without MR<sup>4.5</sup> at baseline, 51 of 98 (52.0%) in the nilotinib arm and 40 of 96 (41.7%) in the imatinib arm achieved MR<sup>4.5</sup> by 48 months (<xref ref-type="supplementary-material" rid="sup1">Supplementary Figure 3</xref>). Thirty-eight of 46 patients who crossed over from imatinib to nilotinib had not achieved MR<sup>4.5</sup> on imatinib prior to crossover; of these, 13 achieved a first MR<sup>4.5</sup> on nilotinib. Of the eight patients who achieved MR<sup>4.5</sup> prior to crossover (including 4 with MR<sup>4.5</sup> detected at the time of crossover), seven achieved or maintained MR<sup>4.5</sup> on nilotinib. Similarly, among the subsets of patients without MMR at baseline or with MMR but without MR<sup>4.5</sup> at baseline, more patients achieved MR<sup>4.5</sup> on study with nilotinib than with imatinib (<xref rid="tbl1" ref-type="table">Table 1</xref>).</p><p>Among patients who crossed over to nilotinib at 24 months and remained on nilotinib with an evaluable molecular assessment at 48 months, <italic>BCR-ABL1</italic><sup>IS</sup> levels decreased rapidly following crossover, despite having previously remained relatively stable during imatinib therapy (<xref ref-type="supplementary-material" rid="sup1">Supplementary Figure 4</xref>). Median (25th–75th percentile) <italic>BCR-ABL1</italic><sup>IS</sup> levels decreased from 0.0205% (0.0074–0.1841%) at 24 months to 0.0086% (0.0012–0.0266%) at 48 months in patients who were eligible to cross over at 24 months, crossed over and remained on nilotinib at 48 months. In contrast, <italic>BCR-ABL1</italic><sup>IS</sup> levels in patients who remained on imatinib through month 48 despite being eligible to cross over at 24 months were relatively stable; the median (25th–75th percentile) <italic>BCR-ABL1</italic><sup>IS</sup> level in these patients was 0.0086% (0.0055–0.0247%) at 24 months and 0.0075% (0.0028–0.0159%) at 48 months.</p><p>No patient in either arm progressed to accelerated phase/blast crisis by 48 months. Three patients in each arm died (none due to CML). In the nilotinib arm, two patients discontinued study treatment due to death (one each due to myocardial infarction (on study day 178) and cardiopulmonary failure (day 780)), and one patient died >28 days after study drug discontinuation (due to liver failure (day 1439, ≈8 months after discontinuation)). In the imatinib arm, one patient discontinued study treatment due to death (due to peritoneal carcinomatosis (day 1334)), and two patients died >28 days after study drug discontinuation (one each due to prostate cancer (day 736, ≈18 months after discontinuation) and metastatic non-small cell lung cancer (day 1127, ≈2 months after discontinuation)). No patient who crossed over from imatinib to nilotinib died on study treatment or after study drug discontinuation. The estimated rate of overall survival at 48 months was 96.6% (95% CI, 89.7–98.9%) in the nilotinib arm and 96.9% (95% CI, 90.6–99.0%) in the imatinib arm (regardless of crossover).</p><p>Safety results were consistent with the previous analysis.<sup><xref ref-type="bibr" rid="bib11">11</xref></sup> Additionally, with ≈2 years of nilotinib treatment after crossover, the safety profile of nilotinib 400 mg twice daily in patients who crossed over was comparable to that observed during the first 24 months of study treatment in patients randomized to the nilotinib arm (<xref ref-type="supplementary-material" rid="sup1">Supplementary Table 1</xref>). Cardiovascular events (CVEs, including ischemic heart disease (IHD), ischemic cerebrovascular events (ICVEs), and peripheral artery disease (PAD)) occurring during study treatment were reported in 13 patients in the nilotinib arm (12.9% (IHD, <italic>n</italic>=4; ICVE, <italic>n</italic>=4; PAD, <italic>n</italic>=7)), two patients in the imatinib arm prior to crossover (1.9% (IHD, <italic>n</italic>=1; ICVE, <italic>n</italic>=1)), and three patients after crossover to nilotinib (6.5% (IHD, <italic>n</italic>=1; ICVE, <italic>n</italic>=1; PAD, <italic>n</italic>=1)). Of the 18 patients in both arms with CVEs during study treatment, 13 had ⩾1 known preexisting cardiovascular risk factor (including age⩾65 years (<italic>n</italic>=9), history of hypertension <italic>(n</italic>=4, all receiving treatment), history of diabetes mellitus (<italic>n</italic>=2, both receiving treatment), and/or history of hypercholesterolemia (<italic>n</italic>=1, untreated)) and/or a prior CVE (<italic>n</italic>=3, including one patient with a history of transient ischemic attack; one patient with a history of thrombosis, deep vein thrombosis, peripheral vascular disorder and transient ischemic attack; and one patient with a history of Raynaud phenomenon) at enrollment. AEs of pancreatitis were reported in 3 (3.0%) and 0 patients in the nilotinib and imatinib arms, respectively; pancreatitis was not reported after crossover in any patient.</p><p>Although this study was not powered to evaluate differences in long-term outcomes between the study arms, the results reported here demonstrate that switching to nilotinib therapy may enable some patients with persistent MRD on long-term imatinib to achieve further reductions in <italic>BCR-ABL1</italic> levels, resulting in increased rates of deep molecular response. Moreover, as achievement of a sustained deep molecular response is a key eligibility criterion for attempting treatment-free remission (TFR),<sup><xref ref-type="bibr" rid="bib12">12</xref></sup> these results suggest that switch to nilotinib may enable some patients to become eligible for TFR and support further investigation of TFR following nilotinib therapy. Importantly, however, not all patients were able to achieve deep molecular responses after switching to nilotinib treatment, and some discontinued nilotinib due to AEs. Thus, both the potential for improved efficacy with nilotinib and the potential for new AEs, including CVEs, should be considered when evaluating whether to switch treatment for a patient. Nonetheless, the observed dynamics of changes in <italic>BCR-ABL1</italic> transcript levels after patients in the imatinib arm crossed over to nilotinib provide a further illustration of the benefits of switching to nilotinib. <italic>BCR-ABL1</italic> levels rapidly decreased following crossover to nilotinib, enabling many patients to achieve MR<sup>4.5</sup>, whereas patients who were eligible to cross over for persistent detectable MRD at 24 months (by which time such patients had received imatinib for a total duration of ⩾4–5 years, including treatment prior to study enrollment<sup><xref ref-type="bibr" rid="bib11">11</xref></sup>) but remained on imatinib had relatively stable transcript levels between 24 and 48 months. These results suggest that most patients have stable <italic>BCR-ABL1</italic> levels following long-term imatinib therapy and are unlikely to achieve further substantial reductions in transcript levels with continued imatinib therapy. Overall, results from ENESTcmr support switching to nilotinib for some patients with persistent MRD after long-term imatinib.</p></body><back><ack><p>The ENESTcmr study and the work presented here were sponsored and funded by Novartis Pharmaceuticals Corporation. Financial support for medical editorial assistance was provided by Novartis Pharmaceuticals Corporation. We thank Karen Kaluza, PhD, and Jonathan Morgan, PhD, of ArticulateScience LLC, for medical editorial assistance with this manuscript.</p><p><bold>Author contributions</bold></p><p>Study conception and design: TPH, BL, NS, SK-R, SA, JHL. Provision of study materials and patients: TPH, BL, FC, NS, RP, APS, NCDC, PED-L, F-XM, DR, AG-B, SK-R, IB, JHL. Data collection: TPH, RP, APS, AG-B, SK-R, DD, JHL. Data analysis and interpretation: TPH, APS, SA, DD, SB, JHL. All authors drafted, reviewed, and approved the manuscript.</p></ack><fn-group><fn><p><xref ref-type="supplementary-material" rid="sup1">Supplementary Information</xref> accompanies this paper on the <italic>Leukemia</italic> website (http://www.nature.com/leu)</p></fn><fn fn-type="COI-statement"><p>The authors declare the following relationships: TPH: Novartis (research funding, honoraria, board of directors or advisory board membership), Bristol-Myers Squibb (research funding, honoraria, board of directors or advisory board membership), Ariad (research funding, honoraria, board of directors or advisory board membership); BL: Novartis (consultancy, honoraria, speakers bureau, board of directors or advisory board membership); FC: Novartis (honoraria, speakers bureau), Ariad (speakers bureau), Bristol-Myers Squibb (speakers bureau); APS: Novartis (honoraria), Bristol-Myers Squibb (honoraria), Pfizer (honoraria), Celgene (honoraria); F-XM: Bristol-Myers Squibb (consultancy, honoraria), Novartis (consultancy, research funding, honoraria), Pfizer (honoraria), Ariad (honoraria); DR: Novartis (honoraria), Ariad (honoraria), Bristol-Myers Squibb (honoraria), Pfizer (honoraria); AG-B: Novartis (honoraria), Amgen (honoraria), Bristol-Myers Squibb (consultancy, honoraria), Pfizer (honoraria); SA: Novartis (employment); TG: Novartis (employment); DD: Novartis (employment); SB: Novartis (research funding, honoraria, speakers bureau, board of directors or advisory board membership), Qiagen (honoraria, board of directors or advisory board membership), Ariad (research funding); JHL: Novartis (consultancy, research funding, honoraria, board of directors or advisory board membership), Ariad (consultancy, research funding, honoraria, board of directors or advisory board membership), Bristol-Myers Squibb (consultancy, research funding, honoraria, board of directors or advisory board membership), Pfizer (consultancy, research funding, honoraria, board of directors or advisory board membership). 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<volume>124</volume>: <fpage>729</fpage>–736.<pub-id pub-id-type="pmid">24948656</pub-id></mixed-citation></ref><ref id="bib12"><mixed-citation publication-type="journal">Hughes TP, Ross DM. <article-title>Moving treatment-free remission into mainstream clinical practice in CML</article-title>. <source>Blood</source><year>2016</year>; <volume>128</volume>: <fpage>17</fpage>–23.<pub-id pub-id-type="pmid">27013442</pub-id></mixed-citation></ref></ref-list><sec sec-type="supplementary-material" id="sup1"><title>Supplementary Material</title><supplementary-material content-type="local-data" id="xob1"><label>Supplementary Information</label><media xlink:href="leu2017247x1.docx"><caption><p>Click here for additional data file.</p></caption></media></supplementary-material></sec></back><floats-group><fig id="fig1"><label>Figure 1</label><caption><p>Time to Achievement of First MR<sup>4.5</sup> (ITT population). ITT, intention-to-treat; MR<sup>4.5</sup>, <italic>BCR-ABL1</italic> ⩽0.0032% on the International Scale.</p></caption><graphic xlink:href="leu2017247f1"></graphic></fig><table-wrap id="tbl1"><label>Table 1</label><caption><title>Achievement of MR<sup>4.5</sup> according to response status at baseline and crossover</title></caption><table frame="hsides" rules="groups" border="1"><colgroup><col align="left"></col><col align="center"></col><col align="center"></col><col align="center"></col></colgroup><thead valign="bottom"><tr><th align="left" valign="top" charoff="50"> </th><th align="center" valign="top" charoff="50"><italic>Nilotinib arm</italic></th><th align="center" valign="top" charoff="50"><italic>Imatinib arm</italic></th><th align="center" valign="top" charoff="50">P-<italic>value</italic><xref ref-type="fn" rid="t1-fn2">a</xref></th></tr></thead><tbody valign="top"><tr><td align="left" valign="top" charoff="50"><italic>All patients</italic></td><td align="left" valign="top" charoff="50"><italic>n</italic>=104</td><td align="left" valign="top" charoff="50"><italic>n</italic>=103</td><td align="left" valign="top" charoff="50"> </td></tr><tr><td colspan="4" align="left" valign="top" charoff="50"> Achieved MR<sup>4.5</sup> by 48 months</td></tr><tr><td align="left" valign="top" charoff="50"> ITT, <italic>n</italic> (%)</td><td align="left" valign="top" charoff="50">56 (53.8)</td><td align="left" valign="top" charoff="50">46 (44.7)</td><td align="left" valign="top" charoff="50">0.1766</td></tr><tr><td align="left" valign="top" charoff="50"> Up to crossover, <italic>n</italic> (%)</td><td align="left" valign="top" charoff="50">56 (53.8)</td><td align="left" valign="top" charoff="50">33 (32.0)</td><td align="left" valign="top" charoff="50">0.0011</td></tr><tr><td align="left" valign="top" charoff="50"> After crossover, n/m (%)<xref ref-type="fn" rid="t1-fn3">b</xref></td><td align="center" valign="top" charoff="50">NA</td><td align="left" valign="top" charoff="50">20/46 (43.5)<xref ref-type="fn" rid="t1-fn4">c</xref></td><td align="center" valign="top" charoff="50">NA</td></tr><tr><td align="left" valign="top" charoff="50"> </td><td align="left" valign="top" charoff="50"> </td><td align="left" valign="top" charoff="50"> </td><td align="left" valign="top" charoff="50"> </td></tr><tr><td align="left" valign="top" charoff="50"><italic>Patients without MMR at baseline</italic></td><td align="left" valign="top" charoff="50"><italic>n</italic>=24</td><td align="left" valign="top" charoff="50"><italic>n</italic>=28</td><td align="left" valign="top" charoff="50"> </td></tr><tr><td colspan="4" align="left" valign="top" charoff="50"> Achieved MR<sup>4.5</sup> by 48 months</td></tr><tr><td align="left" valign="top" charoff="50"> ITT, <italic>n</italic> (%)</td><td align="left" valign="top" charoff="50">8 (33.3)</td><td align="left" valign="top" charoff="50">6 (21.4)</td><td align="left" valign="top" charoff="50">0.4279</td></tr><tr><td align="left" valign="top" charoff="50"> Up to crossover, <italic>n</italic> (%)</td><td align="left" valign="top" charoff="50">8 (33.3)</td><td align="left" valign="top" charoff="50">1 (3.6)</td><td align="left" valign="top" charoff="50">0.0055</td></tr><tr><td align="left" valign="top" charoff="50"> After crossover, n/m (%)<xref ref-type="fn" rid="t1-fn5">d</xref></td><td align="center" valign="top" charoff="50">NA</td><td align="left" valign="top" charoff="50">5/17 (29.4)<xref ref-type="fn" rid="t1-fn6">e</xref></td><td align="center" valign="top" charoff="50">NA</td></tr><tr><td align="left" valign="top" charoff="50"> </td><td align="left" valign="top" charoff="50"> </td><td align="left" valign="top" charoff="50"> </td><td align="left" valign="top" charoff="50"> </td></tr><tr><td align="left" valign="top" charoff="50"><italic>Patients with MMR but without MR</italic><sup>4.5</sup><italic>at baseline</italic></td><td align="left" valign="top" charoff="50"><italic>n</italic>=74</td><td align="left" valign="top" charoff="50"><italic>n</italic>=68</td><td align="left" valign="top" charoff="50"> </td></tr><tr><td colspan="4" align="left" valign="top" charoff="50"> Achieved MR<sup>4.5</sup> by 48 months</td></tr><tr><td align="left" valign="top" charoff="50"> ITT, <italic>n</italic> (%)</td><td align="left" valign="top" charoff="50">43 (58.1)</td><td align="left" valign="top" charoff="50">34 (50.0)</td><td align="left" valign="top" charoff="50">0.2273</td></tr><tr><td align="left" valign="top" charoff="50"> Up to crossover, <italic>n</italic> (%)</td><td align="left" valign="top" charoff="50">43 (58.1)</td><td align="left" valign="top" charoff="50">26 (38.2)</td><td align="left" valign="top" charoff="50">0.0084</td></tr><tr><td align="left" valign="top" charoff="50"> After crossover, n/m (%)<xref ref-type="fn" rid="t1-fn7">f</xref></td><td align="center" valign="top" charoff="50">NA</td><td align="left" valign="top" charoff="50">14/28 (50.0)<xref ref-type="fn" rid="t1-fn8">g</xref></td><td align="center" valign="top" charoff="50">NA</td></tr></tbody></table><table-wrap-foot><fn id="t1-fn1"><p>Abbreviations: ITT, intention-to-treat; MMR, major molecular response; MR<sup>4.5</sup>, <italic>BCR-ABL1</italic> ⩽0.0032% on the International Scale.</p></fn><fn id="t1-fn2"><label>a</label><p><italic>P</italic>-values are nominal. No multiplicity adjustments were made; therefore, statistical interpretation should be made with caution. <italic>P</italic>-values were obtained using the Cochran–Mantel–Haenszel test.</p></fn><fn id="t1-fn3"><label>b</label><p>Denominator is the number of patients who crossed over.</p></fn><fn id="t1-fn4"><label>c</label><p>A total of 20 patients achieved MR<sup>4.5</sup> after crossover, including 13 who achieved MR<sup>4.5</sup> for the first time on nilotinib, 4 who achieved MR<sup>4.5</sup> on imatinib and maintained the response on nilotinib and 3 who regained MR<sup>4.5</sup> on nilotinib after losing the response prior to crossover.</p></fn><fn id="t1-fn5"><label>d</label><p>Denominator is the number of patients without MMR at baseline who crossed over.</p></fn><fn id="t1-fn6"><label>e</label><p>Of the 11 patients without MMR at baseline who did not crossover, 1 achieved MR<sup>4.5</sup> on imatinib and was not eligible to crossover; the other 10 patients were eligible to crossover but did not, and none of these achieved MR<sup>4.5</sup>.</p></fn><fn id="t1-fn7"><label>f</label><p>Denominator is the number of patients with MMR but without MR<sup>4.5</sup> at baseline who crossed over.</p></fn><fn id="t1-fn8"><label>g</label><p>Of the 68 patients with MMR but without MR<sup>4.5</sup> at baseline, 28 crossed over and 40 did not crossover. Twenty of the 40 patients who did not crossover achieved MR<sup>4.5</sup> on imatinib by the end of the study. Fourteen of the 28 patients who crossed over achieved MR<sup>4.5</sup> by the end of the study, including 10 patients who achieved MR<sup>4.5</sup> for the first time after crossover and 4 patients who achieved MR<sup>4.5</sup> before and after crossover.</p></fn></table-wrap-foot></table-wrap></floats-group></pmc></record>Pour manipuler ce document sous Unix (Dilib)
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