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Overall survival with ponatinib versus allogeneic stem cell transplantation in Philadelphia chromosome-positive leukemias with the T315I mutation.

Identifieur interne : 000843 ( PubMed/Corpus ); précédent : 000842; suivant : 000844

Overall survival with ponatinib versus allogeneic stem cell transplantation in Philadelphia chromosome-positive leukemias with the T315I mutation.

Auteurs : Franck E. Nicolini ; Grzegorz W. Basak ; Dong-Wook Kim ; Eduardo Olavarria ; Javier Pinilla-Ibarz ; Jane F. Apperley ; Timothy Hughes ; Dietger Niederwieser ; Michael J. Mauro ; Charles Chuah ; Andreas Hochhaus ; Giovanni Martinelli ; Maral Dersarkissian ; Mei Sheng Duh ; Lisa J. Mcgarry ; Hagop M. Kantarjian ; Jorge E. Cortes

Source :

RBID : pubmed:28387926

English descriptors

Abstract

Effective treatment options for patients with chronic myeloid leukemia (CML) or Philadelphia-positive (Ph+) acute lymphoblastic leukemia (ALL) who have the threonine to isoleucine mutation at codon 315 (T315I) are few. The objective of this study was to compare overall survival (OS) between patients with CML and those with Ph+ ALL who received treatment with ponatinib versus allogeneic stem cell transplantation (allo-SCT).

DOI: 10.1002/cncr.30558
PubMed: 28387926

Links to Exploration step

pubmed:28387926

Le document en format XML

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<nlm:affiliation>Department of Haematology, Imperial College London, Hammersmith Hospital, London, United Kingdom.</nlm:affiliation>
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<name sortKey="Niederwieser, Dietger" sort="Niederwieser, Dietger" uniqKey="Niederwieser D" first="Dietger" last="Niederwieser">Dietger Niederwieser</name>
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<nlm:affiliation>Department of Leukemia, Memorial Sloan Kettering Cancer Center, New York, New York.</nlm:affiliation>
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<name sortKey="Chuah, Charles" sort="Chuah, Charles" uniqKey="Chuah C" first="Charles" last="Chuah">Charles Chuah</name>
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<nlm:affiliation>Department of Haematology, Singapore General Hospital, Duke-NUS Medical School, Singapore.</nlm:affiliation>
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<name sortKey="Hochhaus, Andreas" sort="Hochhaus, Andreas" uniqKey="Hochhaus A" first="Andreas" last="Hochhaus">Andreas Hochhaus</name>
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<name sortKey="Martinelli, Giovanni" sort="Martinelli, Giovanni" uniqKey="Martinelli G" first="Giovanni" last="Martinelli">Giovanni Martinelli</name>
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<nlm:affiliation>L. e A. Seragnoli Institute of Hematology, Bologna, Italy.</nlm:affiliation>
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<name sortKey="Dersarkissian, Maral" sort="Dersarkissian, Maral" uniqKey="Dersarkissian M" first="Maral" last="Dersarkissian">Maral Dersarkissian</name>
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<name sortKey="Mcgarry, Lisa J" sort="Mcgarry, Lisa J" uniqKey="Mcgarry L" first="Lisa J" last="Mcgarry">Lisa J. Mcgarry</name>
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<nlm:affiliation>ARIAD Pharmaceuticals, Inc, Cambridge, Massachusetts.</nlm:affiliation>
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<name sortKey="Kantarjian, Hagop M" sort="Kantarjian, Hagop M" uniqKey="Kantarjian H" first="Hagop M" last="Kantarjian">Hagop M. Kantarjian</name>
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<nlm:affiliation>Department of Leukemia, The University of Texas MD Anderson Cancer Center, Houston, Texas.</nlm:affiliation>
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<name sortKey="Cortes, Jorge E" sort="Cortes, Jorge E" uniqKey="Cortes J" first="Jorge E" last="Cortes">Jorge E. Cortes</name>
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<nlm:affiliation>Department of Leukemia, The University of Texas MD Anderson Cancer Center, Houston, Texas.</nlm:affiliation>
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<title level="j">Cancer</title>
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<term>Adult</term>
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<term>Antineoplastic Agents (therapeutic use)</term>
<term>Blast Crisis (genetics)</term>
<term>Blast Crisis (therapy)</term>
<term>Female</term>
<term>Humans</term>
<term>Imidazoles (therapeutic use)</term>
<term>Kaplan-Meier Estimate</term>
<term>Leukemia, Myelogenous, Chronic, BCR-ABL Positive (genetics)</term>
<term>Leukemia, Myelogenous, Chronic, BCR-ABL Positive (therapy)</term>
<term>Male</term>
<term>Middle Aged</term>
<term>Multivariate Analysis</term>
<term>Mutation</term>
<term>Philadelphia Chromosome</term>
<term>Precursor Cell Lymphoblastic Leukemia-Lymphoma (genetics)</term>
<term>Precursor Cell Lymphoblastic Leukemia-Lymphoma (therapy)</term>
<term>Proportional Hazards Models</term>
<term>Pyridazines (therapeutic use)</term>
<term>Retrospective Studies</term>
<term>Stem Cell Transplantation (methods)</term>
<term>Survival Rate</term>
<term>Transplantation, Homologous</term>
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<term>Antineoplastic Agents</term>
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<term>Blast Crisis</term>
<term>Leukemia, Myelogenous, Chronic, BCR-ABL Positive</term>
<term>Precursor Cell Lymphoblastic Leukemia-Lymphoma</term>
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<term>Stem Cell Transplantation</term>
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<term>Blast Crisis</term>
<term>Leukemia, Myelogenous, Chronic, BCR-ABL Positive</term>
<term>Precursor Cell Lymphoblastic Leukemia-Lymphoma</term>
</keywords>
<keywords scheme="MESH" xml:lang="en">
<term>Adult</term>
<term>Aged</term>
<term>Female</term>
<term>Humans</term>
<term>Kaplan-Meier Estimate</term>
<term>Male</term>
<term>Middle Aged</term>
<term>Multivariate Analysis</term>
<term>Mutation</term>
<term>Philadelphia Chromosome</term>
<term>Proportional Hazards Models</term>
<term>Retrospective Studies</term>
<term>Survival Rate</term>
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<front>
<div type="abstract" xml:lang="en">Effective treatment options for patients with chronic myeloid leukemia (CML) or Philadelphia-positive (Ph+) acute lymphoblastic leukemia (ALL) who have the threonine to isoleucine mutation at codon 315 (T315I) are few. The objective of this study was to compare overall survival (OS) between patients with CML and those with Ph+ ALL who received treatment with ponatinib versus allogeneic stem cell transplantation (allo-SCT).</div>
</front>
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<PMID Version="1">28387926</PMID>
<DateCreated>
<Year>2017</Year>
<Month>04</Month>
<Day>07</Day>
</DateCreated>
<DateCompleted>
<Year>2017</Year>
<Month>09</Month>
<Day>11</Day>
</DateCompleted>
<DateRevised>
<Year>2017</Year>
<Month>09</Month>
<Day>17</Day>
</DateRevised>
<Article PubModel="Print-Electronic">
<Journal>
<ISSN IssnType="Electronic">1097-0142</ISSN>
<JournalIssue CitedMedium="Internet">
<Volume>123</Volume>
<Issue>15</Issue>
<PubDate>
<Year>2017</Year>
<Month>Aug</Month>
<Day>01</Day>
</PubDate>
</JournalIssue>
<Title>Cancer</Title>
<ISOAbbreviation>Cancer</ISOAbbreviation>
</Journal>
<ArticleTitle>Overall survival with ponatinib versus allogeneic stem cell transplantation in Philadelphia chromosome-positive leukemias with the T315I mutation.</ArticleTitle>
<Pagination>
<MedlinePgn>2875-2880</MedlinePgn>
</Pagination>
<ELocationID EIdType="doi" ValidYN="Y">10.1002/cncr.30558</ELocationID>
<Abstract>
<AbstractText Label="BACKGROUND" NlmCategory="BACKGROUND">Effective treatment options for patients with chronic myeloid leukemia (CML) or Philadelphia-positive (Ph+) acute lymphoblastic leukemia (ALL) who have the threonine to isoleucine mutation at codon 315 (T315I) are few. The objective of this study was to compare overall survival (OS) between patients with CML and those with Ph+ ALL who received treatment with ponatinib versus allogeneic stem cell transplantation (allo-SCT).</AbstractText>
<AbstractText Label="METHODS" NlmCategory="METHODS">A post hoc, retrospective, indirect comparison of OS among patients who received single-agent ponatinib in the Ponatinib Ph+ ALL and CML Evaluation (PACE) trial with those who underwent allo-SCT as reported to the European Bone Marrow Transplant registry, stratified by CML disease phase and Ph+ ALL, was conducted. Kaplan-Meier survival curves and multivariate Cox proportional-hazards models were used to compare OS between intervention groups, adjusting for time from diagnosis to intervention, age, sex, and geographic region; 24-month and 48-month OS rates and median OS were reported.</AbstractText>
<AbstractText Label="RESULTS" NlmCategory="RESULTS">After adjustment for potential confounders, 24-month and 48-month OS rates were significantly higher in patients with chronic-phase CML (CP-CML) who received ponatinib compared with those who underwent allo-SCT (24 months: 84% vs 60.5%, respectively; P = .004; 48 months: 72.7% vs 55.8%, respectively; P = .013), with a hazard ratio (HR) of 0.37 (95% confidence interval [CI], 0.16-0.84; P = .017). In patients who had accelerated-phase CML, OS rates were not significantly different between the groups (HR, 0.90; 95% CI, 0.20-4.10; P = .889). In patients who had blast-crisis CML and those with Ph+ ALL, ponatinib was associated with shorter OS compared with allo-SCT (blast-crisis CML: HR, 2.29 [95% CI, 1.08-4.82; P = .030]; Ph+ ALL: HR, 2.77 [95% CI, 0.73-10.56; P = .146]).</AbstractText>
<AbstractText Label="CONCLUSIONS" NlmCategory="CONCLUSIONS">Although allo-SCT remains an important treatment option for patients with T315I-positive advanced CML and Ph+ ALL, ponatinib represents a valuable alternative for patients with T315I-positive CP-CML. Cancer 2017;123:2875-80. © 2017 American Cancer Society.</AbstractText>
<CopyrightInformation>© 2017 The Authors. Cancer published by Wiley Periodicals, Inc. on behalf of American Cancer Society.</CopyrightInformation>
</Abstract>
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<Author ValidYN="Y">
<LastName>Nicolini</LastName>
<ForeName>Franck E</ForeName>
<Initials>FE</Initials>
<AffiliationInfo>
<Affiliation>Hematology Department, Lyon South-Pierre-Bénite Hospital Center and Unit 1052, National Institute of Health and Medical Research Lyon Cancer Research Center/Léon Berard Center, Lyon, France.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y">
<LastName>Basak</LastName>
<ForeName>Grzegorz W</ForeName>
<Initials>GW</Initials>
<AffiliationInfo>
<Affiliation>Department of Hematology, Oncology and Internal Medicine, Medical University of Warsaw, Warsaw, Poland.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y">
<LastName>Kim</LastName>
<ForeName>Dong-Wook</ForeName>
<Initials>DW</Initials>
<AffiliationInfo>
<Affiliation>Leukemia Research Institute, Seoul St. Mary's Hospital, The Catholic University of Korea, Seoul, Korea.</Affiliation>
</AffiliationInfo>
</Author>
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<LastName>Olavarria</LastName>
<ForeName>Eduardo</ForeName>
<Initials>E</Initials>
<AffiliationInfo>
<Affiliation>Department of Haematology, Imperial College London, Hammersmith Hospital, London, United Kingdom.</Affiliation>
</AffiliationInfo>
</Author>
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<LastName>Pinilla-Ibarz</LastName>
<ForeName>Javier</ForeName>
<Initials>J</Initials>
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<Affiliation>H. Lee Moffitt Cancer Center and Research Institute, Tampa, Florida.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y">
<LastName>Apperley</LastName>
<ForeName>Jane F</ForeName>
<Initials>JF</Initials>
<AffiliationInfo>
<Affiliation>Department of Haematology, Imperial College London, Hammersmith Hospital, London, United Kingdom.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y">
<LastName>Hughes</LastName>
<ForeName>Timothy</ForeName>
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<AffiliationInfo>
<Affiliation>Department of Pathology, Royal Adelaide Hospital, Adelaide, South Australia, Australia.</Affiliation>
</AffiliationInfo>
</Author>
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<Affiliation>Department of Haematology and Medical Oncology, University of Leipzig, Leipzig, Germany.</Affiliation>
</AffiliationInfo>
</Author>
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<LastName>Mauro</LastName>
<ForeName>Michael J</ForeName>
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<Affiliation>Department of Leukemia, Memorial Sloan Kettering Cancer Center, New York, New York.</Affiliation>
</AffiliationInfo>
</Author>
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<LastName>Chuah</LastName>
<ForeName>Charles</ForeName>
<Initials>C</Initials>
<AffiliationInfo>
<Affiliation>Department of Haematology, Singapore General Hospital, Duke-NUS Medical School, Singapore.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y">
<LastName>Hochhaus</LastName>
<ForeName>Andreas</ForeName>
<Initials>A</Initials>
<AffiliationInfo>
<Affiliation>Clinic and Polyclinic for Internal Medicine II, Division of Hematology and Oncology, Jena University Hospital, Jena, Germany.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y">
<LastName>Martinelli</LastName>
<ForeName>Giovanni</ForeName>
<Initials>G</Initials>
<AffiliationInfo>
<Affiliation>L. e A. Seragnoli Institute of Hematology, Bologna, Italy.</Affiliation>
</AffiliationInfo>
</Author>
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<LastName>DerSarkissian</LastName>
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<Initials>M</Initials>
<AffiliationInfo>
<Affiliation>Analysis Group, Inc, Boston, Massachusetts.</Affiliation>
</AffiliationInfo>
</Author>
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<LastName>Duh</LastName>
<ForeName>Mei Sheng</ForeName>
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</AffiliationInfo>
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<LastName>McGarry</LastName>
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<LastName>Cortes</LastName>
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<RefSource>Biologics. 2014 Oct 20;8:243-54</RefSource>
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<CommentsCorrections RefType="Cites">
<RefSource>Cancer Res. 2005 Jun 1;65(11):4500-5</RefSource>
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<RefSource>Cancer. 2015 May 15;121(10):1637-44</RefSource>
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<CommentsCorrections RefType="Cites">
<RefSource>Blood. 2010 Nov 4;116(18):3409-17</RefSource>
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<RefSource>N Engl J Med. 2013 Nov 7;369(19):1783-96</RefSource>
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<RefSource>Haematologica. 2010 Jan;95(1):8-12</RefSource>
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<RefSource>Leukemia. 2016 Mar;30(3):562-9</RefSource>
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<RefSource>Blood. 2011 Nov 17;118(20):5697-700</RefSource>
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<RefSource>Lancet Oncol. 2015 Nov;16(15):1547-55</RefSource>
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<RefSource>Cancer Cell. 2009 Nov 6;16(5):401-12</RefSource>
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<RefSource>Comput Methods Programs Biomed. 2004 Jul;75(1):45-9</RefSource>
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<RefSource>Blood. 2009 Dec 17;114(26):5271-8</RefSource>
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<RefSource>Epidemiology. 2000 Sep;11(5):550-60</RefSource>
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<CommentsCorrections RefType="Cites">
<RefSource>Epidemiology. 2000 Sep;11(5):561-70</RefSource>
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<CommentsCorrections RefType="Cites">
<RefSource>Haematologica. 2013 Oct;98(10):1510-6</RefSource>
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<Keyword MajorTopicYN="N">allogeneic stem cell transplantation (allo-SCT)</Keyword>
<Keyword MajorTopicYN="N">chronic myeloid leukemia (CML)</Keyword>
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<Month>12</Month>
<Day>05</Day>
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