AustralieFrV1, PascalFrancis, Corpus, bibRecord, 003A17

Dasatinib or high-dose imatinib for chronic-phase chronic myeloid leukemia after failure of first-line imatinib : a randomized phase 2 trial. Commentary

Identifieur interne : 003A17 ( PascalFrancis/Corpus ); précédent : 003A16; suivant : 003A18

Dasatinib or high-dose imatinib for chronic-phase chronic myeloid leukemia after failure of first-line imatinib : a randomized phase 2 trial. Commentary

Auteurs : Charles A. Schiffer ; Hagop Kantarjian ; Ricardo Pasquini ; Nelson Hamerschlak ; Philippe Rousselot ; Jerzy Holowiecki ; Saengsuree Jootar ; Tadeusz Robak ; Nina Khoroshko ; Tamas Masszi ; Aleksander Skotnicki ; Andrzej Hellmann ; Andrey Zaritsky ; Anatoly Golenkov ; Jerald Radich ; Timothy Hughes ; Athena Countouriotis ; Neil Shah

Source :

Blood [ 0006-4971 ] ; 2007.

RBID : Pascal:07-0397572

Descripteurs français

Pascal (Inist)
- Imatinib, Anticancéreux, Dose forte, Protein-tyrosine kinase, Inhibiteur enzyme, Essai clinique phase II, Essai clinique, Randomisation, Hématologie, Dasatinib, Leucémie myéloïde chronique, Traitement première intention.

English descriptors

KwdEn :
- Antineoplastic agent, Chronic myelocytic leukemia, Clinical trial, Enzyme inhibitor, First line treatment, Hematology, High dose, Imatinib, Phase II trial, Protein-tyrosine kinase, Randomization.

Abstract

Therapeutic options for chronic myelogenous leukemia (CML) resistant to 400 to 600 mg imatinib are limited. Escalating imatinib doses may overcome resistance. Dasatinib, a significantly more potent inhibitor of BCR-ABL, is safe and effective in this population. Patients with imatinib-resistant chronic-phase (CP) CML were randomized 2:1 to 140 mg dasatinib (n = 101) or 800 mg imatinib (n = 49). With a median follow up of 15 months, complete hematologic responses were observed in 93% and 82% of patients receiving dasatinib and high-dose imatinib (P = .034), respectively. Dasatinib resulted in higher major cytogenetic response rates (52%) than high-dose imatinib (33%) (P = .023); this included complete cytogenetic response in 40% and 16% (P = .004). Major molecular responses were also more frequent with dasatinib (16% versus 4%; P = 0.038). Treatment failure (hazard ratio [HR], 0.16; P <.001) and progression-free survival (HR, 0.14; P <.001) both favored dasatinib. Superficial edema (42% versus 15%) and fluid retention (45% versus 30%) were more prevalent with imatinib; pleural effusion was more common with dasatinib (17% versus 0%). Grade 3 to 4 nonhematologic toxicity was minimal. Cytopenias were more frequent and severe with dasatinib. Dasatinib represents a safe and effective therapy for CP-CML resistant to conventional imatinib doses with improved cytogenetic and molecular response rates and progression-free survival relative to high-dose imatinib.

Notice en format standard (ISO 2709)

Pour connaître la documentation sur le format Inist Standard.

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C01	`01`		`ENG`	@0 Therapeutic options for chronic myelogenous leukemia (CML) resistant to 400 to 600 mg imatinib are limited. Escalating imatinib doses may overcome resistance. Dasatinib, a significantly more potent inhibitor of BCR-ABL, is safe and effective in this population. Patients with imatinib-resistant chronic-phase (CP) CML were randomized 2:1 to 140 mg dasatinib (n = 101) or 800 mg imatinib (n = 49). With a median follow up of 15 months, complete hematologic responses were observed in 93% and 82% of patients receiving dasatinib and high-dose imatinib (P = .034), respectively. Dasatinib resulted in higher major cytogenetic response rates (52%) than high-dose imatinib (33%) (P = .023); this included complete cytogenetic response in 40% and 16% (P = .004). Major molecular responses were also more frequent with dasatinib (16% versus 4%; P = 0.038). Treatment failure (hazard ratio [HR], 0.16; P <.001) and progression-free survival (HR, 0.14; P <.001) both favored dasatinib. Superficial edema (42% versus 15%) and fluid retention (45% versus 30%) were more prevalent with imatinib; pleural effusion was more common with dasatinib (17% versus 0%). Grade 3 to 4 nonhematologic toxicity was minimal. Cytopenias were more frequent and severe with dasatinib. Dasatinib represents a safe and effective therapy for CP-CML resistant to conventional imatinib doses with improved cytogenetic and molecular response rates and progression-free survival relative to high-dose imatinib.
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Format Inist (serveur)

NO :	PASCAL 07-0397572 INIST
ET :	Dasatinib or high-dose imatinib for chronic-phase chronic myeloid leukemia after failure of first-line imatinib : a randomized phase 2 trial. Commentary
AU :	SCHIFFER (Charles A.); KANTARJIAN (Hagop); PASQUINI (Ricardo); HAMERSCHLAK (Nelson); ROUSSELOT (Philippe); HOLOWIECKI (Jerzy); JOOTAR (Saengsuree); ROBAK (Tadeusz); KHOROSHKO (Nina); MASSZI (Tamas); SKOTNICKI (Aleksander); HELLMANN (Andrzej); ZARITSKY (Andrey); GOLENKOV (Anatoly); RADICH (Jerald); HUGHES (Timothy); COUNTOURIOTIS (Athena); SHAH (Neil)
AF :	KARMANOS CANCER INSTITUTE/Etats-Unis (1 aut.); M. D. Anderson Cancer Center/Houston, TX/Etats-Unis (2 aut.); Hospital De Clinicas De Curitiba/Curitiba, Parana/Brésil (3 aut.); Hospital Israelita Albert Einstein/Sao Paulo/Brésil (4 aut.); Hospital Saint Louis/Paris/France (5 aut.); Katedra I Klinika Hematologii I Transplantacji Szpiku/Katowice/Pologne (6 aut.); Ramathibodi Hospital/Bangkok/Thaïlande (7 aut.); Szpital Specjalistyczny Im. Kopernika Klinika Hematologii/Lodz/Pologne (8 aut.); National Research Hematology Center/Moscow/Russie (9 aut.); National Medical Center/Budapest/Hongrie (10 aut.); Collegium Medicum Uniwesytetu Jagiellonskiego/Krakow/Pologne (11 aut.); Klinika Hematologii, Akademia Medyczna/Gdansk/Pologne (12 aut.); St Petersburg State Medical University/St Petersburg/Russie (13 aut.); Moscow Region Research Clinical Institute/Moscow/Russie (14 aut.); Clinical Research Division, Fred Hutchinson Cancer Research Center/Seattle, WA/Etats-Unis (15 aut.); Division of Hematology, Institute of Medical and Veterinary Science/Adelaide/Australie (16 aut.); Bristol-Myers Squibb/Wallingford, CT/Etats-Unis (17 aut.); Division of Hematology and Oncology, University College of San Francisco School of Medicine/San Francisco, CA/Etats-Unis (18 aut.)
DT :	Publication en série; Article; Commentaire; Niveau analytique
SO :	Blood; ISSN 0006-4971; Etats-Unis; Da. 2007; Vol. 109; No. 12; 5068-5069, 5143-5150 [10 p.]; Bibl. 28 ref.
LA :	Anglais
EA :	Therapeutic options for chronic myelogenous leukemia (CML) resistant to 400 to 600 mg imatinib are limited. Escalating imatinib doses may overcome resistance. Dasatinib, a significantly more potent inhibitor of BCR-ABL, is safe and effective in this population. Patients with imatinib-resistant chronic-phase (CP) CML were randomized 2:1 to 140 mg dasatinib (n = 101) or 800 mg imatinib (n = 49). With a median follow up of 15 months, complete hematologic responses were observed in 93% and 82% of patients receiving dasatinib and high-dose imatinib (P = .034), respectively. Dasatinib resulted in higher major cytogenetic response rates (52%) than high-dose imatinib (33%) (P = .023); this included complete cytogenetic response in 40% and 16% (P = .004). Major molecular responses were also more frequent with dasatinib (16% versus 4%; P = 0.038). Treatment failure (hazard ratio [HR], 0.16; P <.001) and progression-free survival (HR, 0.14; P <.001) both favored dasatinib. Superficial edema (42% versus 15%) and fluid retention (45% versus 30%) were more prevalent with imatinib; pleural effusion was more common with dasatinib (17% versus 0%). Grade 3 to 4 nonhematologic toxicity was minimal. Cytopenias were more frequent and severe with dasatinib. Dasatinib represents a safe and effective therapy for CP-CML resistant to conventional imatinib doses with improved cytogenetic and molecular response rates and progression-free survival relative to high-dose imatinib.
CC :	002B19B
FD :	Imatinib; Anticancéreux; Dose forte; Protein-tyrosine kinase; Inhibiteur enzyme; Essai clinique phase II; Essai clinique; Randomisation; Hématologie; Dasatinib; Leucémie myéloïde chronique; Traitement première intention
FG :	Transferases; Enzyme; Hémopathie maligne; Myéloprolifératif syndrome; Inhibiteur de la tyrosine kinase; Inhibiteur multikinase
ED :	Imatinib; Antineoplastic agent; High dose; Protein-tyrosine kinase; Enzyme inhibitor; Phase II trial; Clinical trial; Randomization; Hematology; Chronic myelocytic leukemia; First line treatment
EG :	Transferases; Enzyme; Malignant hemopathy; Myeloproliferative syndrome
SD :	Imatinib; Anticanceroso; Dosis fuerte; Protein-tyrosine kinase; Inhibidor enzima; Ensayo clínico fase II; Ensayo clínico; Aleatorización; Hematología; Leucemia mieloidea; Tratamiento primer línea
LO :	INIST-3178.354000162838230090
ID :	07-0397572

Links to Exploration step

Pascal:07-0397572

Le document en format XML

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<author><name sortKey="Golenkov, Anatoly" sort="Golenkov, Anatoly" uniqKey="Golenkov A" first="Anatoly" last="Golenkov">Anatoly Golenkov</name>
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<author><name sortKey="Radich, Jerald" sort="Radich, Jerald" uniqKey="Radich J" first="Jerald" last="Radich">Jerald Radich</name>
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<author><name sortKey="Hughes, Timothy" sort="Hughes, Timothy" uniqKey="Hughes T" first="Timothy" last="Hughes">Timothy Hughes</name>
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<sZ>18 aut.</sZ>
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</affiliation>
</author>
</titleStmt>
<publicationStmt><idno type="wicri:source">INIST</idno>
<idno type="inist">07-0397572</idno>
<date when="2007">2007</date>
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<idno type="RBID">Pascal:07-0397572</idno>
<idno type="wicri:Area/PascalFrancis/Corpus">003A17</idno>
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<sourceDesc><biblStruct><analytic><title xml:lang="en" level="a">Dasatinib or high-dose imatinib for chronic-phase chronic myeloid leukemia after failure of first-line imatinib : a randomized phase 2 trial. Commentary</title>
<author><name sortKey="Schiffer, Charles A" sort="Schiffer, Charles A" uniqKey="Schiffer C" first="Charles A." last="Schiffer">Charles A. Schiffer</name>
<affiliation><inist:fA14 i1="01"><s1>KARMANOS CANCER INSTITUTE</s1>
<s3>USA</s3>
<sZ>1 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Kantarjian, Hagop" sort="Kantarjian, Hagop" uniqKey="Kantarjian H" first="Hagop" last="Kantarjian">Hagop Kantarjian</name>
<affiliation><inist:fA14 i1="02"><s1>M. D. Anderson Cancer Center</s1>
<s2>Houston, TX</s2>
<s3>USA</s3>
<sZ>2 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Pasquini, Ricardo" sort="Pasquini, Ricardo" uniqKey="Pasquini R" first="Ricardo" last="Pasquini">Ricardo Pasquini</name>
<affiliation><inist:fA14 i1="03"><s1>Hospital De Clinicas De Curitiba</s1>
<s2>Curitiba, Parana</s2>
<s3>BRA</s3>
<sZ>3 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Hamerschlak, Nelson" sort="Hamerschlak, Nelson" uniqKey="Hamerschlak N" first="Nelson" last="Hamerschlak">Nelson Hamerschlak</name>
<affiliation><inist:fA14 i1="04"><s1>Hospital Israelita Albert Einstein</s1>
<s2>Sao Paulo</s2>
<s3>BRA</s3>
<sZ>4 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Rousselot, Philippe" sort="Rousselot, Philippe" uniqKey="Rousselot P" first="Philippe" last="Rousselot">Philippe Rousselot</name>
<affiliation><inist:fA14 i1="05"><s1>Hospital Saint Louis</s1>
<s2>Paris</s2>
<s3>FRA</s3>
<sZ>5 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Holowiecki, Jerzy" sort="Holowiecki, Jerzy" uniqKey="Holowiecki J" first="Jerzy" last="Holowiecki">Jerzy Holowiecki</name>
<affiliation><inist:fA14 i1="06"><s1>Katedra I Klinika Hematologii I Transplantacji Szpiku</s1>
<s2>Katowice</s2>
<s3>POL</s3>
<sZ>6 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Jootar, Saengsuree" sort="Jootar, Saengsuree" uniqKey="Jootar S" first="Saengsuree" last="Jootar">Saengsuree Jootar</name>
<affiliation><inist:fA14 i1="07"><s1>Ramathibodi Hospital</s1>
<s2>Bangkok</s2>
<s3>THA</s3>
<sZ>7 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Robak, Tadeusz" sort="Robak, Tadeusz" uniqKey="Robak T" first="Tadeusz" last="Robak">Tadeusz Robak</name>
<affiliation><inist:fA14 i1="08"><s1>Szpital Specjalistyczny Im. Kopernika Klinika Hematologii</s1>
<s2>Lodz</s2>
<s3>POL</s3>
<sZ>8 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Khoroshko, Nina" sort="Khoroshko, Nina" uniqKey="Khoroshko N" first="Nina" last="Khoroshko">Nina Khoroshko</name>
<affiliation><inist:fA14 i1="09"><s1>National Research Hematology Center</s1>
<s2>Moscow</s2>
<s3>RUS</s3>
<sZ>9 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Masszi, Tamas" sort="Masszi, Tamas" uniqKey="Masszi T" first="Tamas" last="Masszi">Tamas Masszi</name>
<affiliation><inist:fA14 i1="10"><s1>National Medical Center</s1>
<s2>Budapest</s2>
<s3>HUN</s3>
<sZ>10 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Skotnicki, Aleksander" sort="Skotnicki, Aleksander" uniqKey="Skotnicki A" first="Aleksander" last="Skotnicki">Aleksander Skotnicki</name>
<affiliation><inist:fA14 i1="11"><s1>Collegium Medicum Uniwesytetu Jagiellonskiego</s1>
<s2>Krakow</s2>
<s3>POL</s3>
<sZ>11 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Hellmann, Andrzej" sort="Hellmann, Andrzej" uniqKey="Hellmann A" first="Andrzej" last="Hellmann">Andrzej Hellmann</name>
<affiliation><inist:fA14 i1="12"><s1>Klinika Hematologii, Akademia Medyczna</s1>
<s2>Gdansk</s2>
<s3>POL</s3>
<sZ>12 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Zaritsky, Andrey" sort="Zaritsky, Andrey" uniqKey="Zaritsky A" first="Andrey" last="Zaritsky">Andrey Zaritsky</name>
<affiliation><inist:fA14 i1="13"><s1>St Petersburg State Medical University</s1>
<s2>St Petersburg</s2>
<s3>RUS</s3>
<sZ>13 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Golenkov, Anatoly" sort="Golenkov, Anatoly" uniqKey="Golenkov A" first="Anatoly" last="Golenkov">Anatoly Golenkov</name>
<affiliation><inist:fA14 i1="14"><s1>Moscow Region Research Clinical Institute</s1>
<s2>Moscow</s2>
<s3>RUS</s3>
<sZ>14 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Radich, Jerald" sort="Radich, Jerald" uniqKey="Radich J" first="Jerald" last="Radich">Jerald Radich</name>
<affiliation><inist:fA14 i1="15"><s1>Clinical Research Division, Fred Hutchinson Cancer Research Center</s1>
<s2>Seattle, WA</s2>
<s3>USA</s3>
<sZ>15 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Hughes, Timothy" sort="Hughes, Timothy" uniqKey="Hughes T" first="Timothy" last="Hughes">Timothy Hughes</name>
<affiliation><inist:fA14 i1="16"><s1>Division of Hematology, Institute of Medical and Veterinary Science</s1>
<s2>Adelaide</s2>
<s3>AUS</s3>
<sZ>16 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Countouriotis, Athena" sort="Countouriotis, Athena" uniqKey="Countouriotis A" first="Athena" last="Countouriotis">Athena Countouriotis</name>
<affiliation><inist:fA14 i1="17"><s1>Bristol-Myers Squibb</s1>
<s2>Wallingford, CT</s2>
<s3>USA</s3>
<sZ>17 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Shah, Neil" sort="Shah, Neil" uniqKey="Shah N" first="Neil" last="Shah">Neil Shah</name>
<affiliation><inist:fA14 i1="18"><s1>Division of Hematology and Oncology, University College of San Francisco School of Medicine</s1>
<s2>San Francisco, CA</s2>
<s3>USA</s3>
<sZ>18 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
</analytic>
<series><title level="j" type="main">Blood</title>
<title level="j" type="abbreviated">Blood</title>
<idno type="ISSN">0006-4971</idno>
<imprint><date when="2007">2007</date>
</imprint>
</series>
</biblStruct>
</sourceDesc>
<seriesStmt><title level="j" type="main">Blood</title>
<title level="j" type="abbreviated">Blood</title>
<idno type="ISSN">0006-4971</idno>
</seriesStmt>
</fileDesc>
<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Antineoplastic agent</term>
<term>Chronic myelocytic leukemia</term>
<term>Clinical trial</term>
<term>Enzyme inhibitor</term>
<term>First line treatment</term>
<term>Hematology</term>
<term>High dose</term>
<term>Imatinib</term>
<term>Phase II trial</term>
<term>Protein-tyrosine kinase</term>
<term>Randomization</term>
</keywords>
<keywords scheme="Pascal" xml:lang="fr"><term>Imatinib</term>
<term>Anticancéreux</term>
<term>Dose forte</term>
<term>Protein-tyrosine kinase</term>
<term>Inhibiteur enzyme</term>
<term>Essai clinique phase II</term>
<term>Essai clinique</term>
<term>Randomisation</term>
<term>Hématologie</term>
<term>Dasatinib</term>
<term>Leucémie myéloïde chronique</term>
<term>Traitement première intention</term>
</keywords>
</textClass>
</profileDesc>
</teiHeader>
<front><div type="abstract" xml:lang="en">Therapeutic options for chronic myelogenous leukemia (CML) resistant to 400 to 600 mg imatinib are limited. Escalating imatinib doses may overcome resistance. Dasatinib, a significantly more potent inhibitor of BCR-ABL, is safe and effective in this population. Patients with imatinib-resistant chronic-phase (CP) CML were randomized 2:1 to 140 mg dasatinib (n = 101) or 800 mg imatinib (n = 49). With a median follow up of 15 months, complete hematologic responses were observed in 93% and 82% of patients receiving dasatinib and high-dose imatinib (P = .034), respectively. Dasatinib resulted in higher major cytogenetic response rates (52%) than high-dose imatinib (33%) (P = .023); this included complete cytogenetic response in 40% and 16% (P = .004). Major molecular responses were also more frequent with dasatinib (16% versus 4%; P = 0.038). Treatment failure (hazard ratio [HR], 0.16; P <.001) and progression-free survival (HR, 0.14; P <.001) both favored dasatinib. Superficial edema (42% versus 15%) and fluid retention (45% versus 30%) were more prevalent with imatinib; pleural effusion was more common with dasatinib (17% versus 0%). Grade 3 to 4 nonhematologic toxicity was minimal. Cytopenias were more frequent and severe with dasatinib. Dasatinib represents a safe and effective therapy for CP-CML resistant to conventional imatinib doses with improved cytogenetic and molecular response rates and progression-free survival relative to high-dose imatinib.</div>
</front>
</TEI>
<inist><standard h6="B"><pA><fA01 i1="01" i2="1"><s0>0006-4971</s0>
</fA01>
<fA03 i2="1"><s0>Blood</s0>
</fA03>
<fA05><s2>109</s2>
</fA05>
<fA06><s2>12</s2>
</fA06>
<fA08 i1="01" i2="1" l="ENG"><s1>Dasatinib or high-dose imatinib for chronic-phase chronic myeloid leukemia after failure of first-line imatinib : a randomized phase 2 trial. Commentary</s1>
</fA08>
<fA11 i1="01" i2="1"><s1>SCHIFFER (Charles A.)</s1>
<s9>comment.</s9>
</fA11>
<fA11 i1="02" i2="1"><s1>KANTARJIAN (Hagop)</s1>
</fA11>
<fA11 i1="03" i2="1"><s1>PASQUINI (Ricardo)</s1>
</fA11>
<fA11 i1="04" i2="1"><s1>HAMERSCHLAK (Nelson)</s1>
</fA11>
<fA11 i1="05" i2="1"><s1>ROUSSELOT (Philippe)</s1>
</fA11>
<fA11 i1="06" i2="1"><s1>HOLOWIECKI (Jerzy)</s1>
</fA11>
<fA11 i1="07" i2="1"><s1>JOOTAR (Saengsuree)</s1>
</fA11>
<fA11 i1="08" i2="1"><s1>ROBAK (Tadeusz)</s1>
</fA11>
<fA11 i1="09" i2="1"><s1>KHOROSHKO (Nina)</s1>
</fA11>
<fA11 i1="10" i2="1"><s1>MASSZI (Tamas)</s1>
</fA11>
<fA11 i1="11" i2="1"><s1>SKOTNICKI (Aleksander)</s1>
</fA11>
<fA11 i1="12" i2="1"><s1>HELLMANN (Andrzej)</s1>
</fA11>
<fA11 i1="13" i2="1"><s1>ZARITSKY (Andrey)</s1>
</fA11>
<fA11 i1="14" i2="1"><s1>GOLENKOV (Anatoly)</s1>
</fA11>
<fA11 i1="15" i2="1"><s1>RADICH (Jerald)</s1>
</fA11>
<fA11 i1="16" i2="1"><s1>HUGHES (Timothy)</s1>
</fA11>
<fA11 i1="17" i2="1"><s1>COUNTOURIOTIS (Athena)</s1>
</fA11>
<fA11 i1="18" i2="1"><s1>SHAH (Neil)</s1>
</fA11>
<fA14 i1="01"><s1>KARMANOS CANCER INSTITUTE</s1>
<s3>USA</s3>
<sZ>1 aut.</sZ>
</fA14>
<fA14 i1="02"><s1>M. D. Anderson Cancer Center</s1>
<s2>Houston, TX</s2>
<s3>USA</s3>
<sZ>2 aut.</sZ>
</fA14>
<fA14 i1="03"><s1>Hospital De Clinicas De Curitiba</s1>
<s2>Curitiba, Parana</s2>
<s3>BRA</s3>
<sZ>3 aut.</sZ>
</fA14>
<fA14 i1="04"><s1>Hospital Israelita Albert Einstein</s1>
<s2>Sao Paulo</s2>
<s3>BRA</s3>
<sZ>4 aut.</sZ>
</fA14>
<fA14 i1="05"><s1>Hospital Saint Louis</s1>
<s2>Paris</s2>
<s3>FRA</s3>
<sZ>5 aut.</sZ>
</fA14>
<fA14 i1="06"><s1>Katedra I Klinika Hematologii I Transplantacji Szpiku</s1>
<s2>Katowice</s2>
<s3>POL</s3>
<sZ>6 aut.</sZ>
</fA14>
<fA14 i1="07"><s1>Ramathibodi Hospital</s1>
<s2>Bangkok</s2>
<s3>THA</s3>
<sZ>7 aut.</sZ>
</fA14>
<fA14 i1="08"><s1>Szpital Specjalistyczny Im. Kopernika Klinika Hematologii</s1>
<s2>Lodz</s2>
<s3>POL</s3>
<sZ>8 aut.</sZ>
</fA14>
<fA14 i1="09"><s1>National Research Hematology Center</s1>
<s2>Moscow</s2>
<s3>RUS</s3>
<sZ>9 aut.</sZ>
</fA14>
<fA14 i1="10"><s1>National Medical Center</s1>
<s2>Budapest</s2>
<s3>HUN</s3>
<sZ>10 aut.</sZ>
</fA14>
<fA14 i1="11"><s1>Collegium Medicum Uniwesytetu Jagiellonskiego</s1>
<s2>Krakow</s2>
<s3>POL</s3>
<sZ>11 aut.</sZ>
</fA14>
<fA14 i1="12"><s1>Klinika Hematologii, Akademia Medyczna</s1>
<s2>Gdansk</s2>
<s3>POL</s3>
<sZ>12 aut.</sZ>
</fA14>
<fA14 i1="13"><s1>St Petersburg State Medical University</s1>
<s2>St Petersburg</s2>
<s3>RUS</s3>
<sZ>13 aut.</sZ>
</fA14>
<fA14 i1="14"><s1>Moscow Region Research Clinical Institute</s1>
<s2>Moscow</s2>
<s3>RUS</s3>
<sZ>14 aut.</sZ>
</fA14>
<fA14 i1="15"><s1>Clinical Research Division, Fred Hutchinson Cancer Research Center</s1>
<s2>Seattle, WA</s2>
<s3>USA</s3>
<sZ>15 aut.</sZ>
</fA14>
<fA14 i1="16"><s1>Division of Hematology, Institute of Medical and Veterinary Science</s1>
<s2>Adelaide</s2>
<s3>AUS</s3>
<sZ>16 aut.</sZ>
</fA14>
<fA14 i1="17"><s1>Bristol-Myers Squibb</s1>
<s2>Wallingford, CT</s2>
<s3>USA</s3>
<sZ>17 aut.</sZ>
</fA14>
<fA14 i1="18"><s1>Division of Hematology and Oncology, University College of San Francisco School of Medicine</s1>
<s2>San Francisco, CA</s2>
<s3>USA</s3>
<sZ>18 aut.</sZ>
</fA14>
<fA20><s2>5068-5069, 5143-5150 [10 p.]</s2>
</fA20>
<fA21><s1>2007</s1>
</fA21>
<fA23 i1="01"><s0>ENG</s0>
</fA23>
<fA43 i1="01"><s1>INIST</s1>
<s2>3178</s2>
<s5>354000162838230090</s5>
</fA43>
<fA44><s0>0000</s0>
<s1>© 2007 INIST-CNRS. All rights reserved.</s1>
</fA44>
<fA45><s0>28 ref.</s0>
</fA45>
<fA47 i1="01" i2="1"><s0>07-0397572</s0>
</fA47>
<fA60><s1>P</s1>
<s3>AR</s3>
<s3>CT</s3>
</fA60>
<fA61><s0>A</s0>
</fA61>
<fA64 i1="01" i2="1"><s0>Blood</s0>
</fA64>
<fA66 i1="01"><s0>USA</s0>
</fA66>
<fC01 i1="01" l="ENG"><s0>Therapeutic options for chronic myelogenous leukemia (CML) resistant to 400 to 600 mg imatinib are limited. Escalating imatinib doses may overcome resistance. Dasatinib, a significantly more potent inhibitor of BCR-ABL, is safe and effective in this population. Patients with imatinib-resistant chronic-phase (CP) CML were randomized 2:1 to 140 mg dasatinib (n = 101) or 800 mg imatinib (n = 49). With a median follow up of 15 months, complete hematologic responses were observed in 93% and 82% of patients receiving dasatinib and high-dose imatinib (P = .034), respectively. Dasatinib resulted in higher major cytogenetic response rates (52%) than high-dose imatinib (33%) (P = .023); this included complete cytogenetic response in 40% and 16% (P = .004). Major molecular responses were also more frequent with dasatinib (16% versus 4%; P = 0.038). Treatment failure (hazard ratio [HR], 0.16; P <.001) and progression-free survival (HR, 0.14; P <.001) both favored dasatinib. Superficial edema (42% versus 15%) and fluid retention (45% versus 30%) were more prevalent with imatinib; pleural effusion was more common with dasatinib (17% versus 0%). Grade 3 to 4 nonhematologic toxicity was minimal. Cytopenias were more frequent and severe with dasatinib. Dasatinib represents a safe and effective therapy for CP-CML resistant to conventional imatinib doses with improved cytogenetic and molecular response rates and progression-free survival relative to high-dose imatinib.</s0>
</fC01>
<fC02 i1="01" i2="X"><s0>002B19B</s0>
</fC02>
<fC03 i1="01" i2="X" l="FRE"><s0>Imatinib</s0>
<s2>FR</s2>
<s5>01</s5>
</fC03>
<fC03 i1="01" i2="X" l="ENG"><s0>Imatinib</s0>
<s2>FR</s2>
<s5>01</s5>
</fC03>
<fC03 i1="01" i2="X" l="SPA"><s0>Imatinib</s0>
<s2>FR</s2>
<s5>01</s5>
</fC03>
<fC03 i1="02" i2="X" l="FRE"><s0>Anticancéreux</s0>
<s5>02</s5>
</fC03>
<fC03 i1="02" i2="X" l="ENG"><s0>Antineoplastic agent</s0>
<s5>02</s5>
</fC03>
<fC03 i1="02" i2="X" l="SPA"><s0>Anticanceroso</s0>
<s5>02</s5>
</fC03>
<fC03 i1="03" i2="X" l="FRE"><s0>Dose forte</s0>
<s5>03</s5>
</fC03>
<fC03 i1="03" i2="X" l="ENG"><s0>High dose</s0>
<s5>03</s5>
</fC03>
<fC03 i1="03" i2="X" l="SPA"><s0>Dosis fuerte</s0>
<s5>03</s5>
</fC03>
<fC03 i1="04" i2="X" l="FRE"><s0>Protein-tyrosine kinase</s0>
<s2>FE</s2>
<s5>05</s5>
</fC03>
<fC03 i1="04" i2="X" l="ENG"><s0>Protein-tyrosine kinase</s0>
<s2>FE</s2>
<s5>05</s5>
</fC03>
<fC03 i1="04" i2="X" l="SPA"><s0>Protein-tyrosine kinase</s0>
<s2>FE</s2>
<s5>05</s5>
</fC03>
<fC03 i1="05" i2="X" l="FRE"><s0>Inhibiteur enzyme</s0>
<s5>06</s5>
</fC03>
<fC03 i1="05" i2="X" l="ENG"><s0>Enzyme inhibitor</s0>
<s5>06</s5>
</fC03>
<fC03 i1="05" i2="X" l="SPA"><s0>Inhibidor enzima</s0>
<s5>06</s5>
</fC03>
<fC03 i1="06" i2="X" l="FRE"><s0>Essai clinique phase II</s0>
<s5>07</s5>
</fC03>
<fC03 i1="06" i2="X" l="ENG"><s0>Phase II trial</s0>
<s5>07</s5>
</fC03>
<fC03 i1="06" i2="X" l="SPA"><s0>Ensayo clínico fase II</s0>
<s5>07</s5>
</fC03>
<fC03 i1="07" i2="X" l="FRE"><s0>Essai clinique</s0>
<s5>08</s5>
</fC03>
<fC03 i1="07" i2="X" l="ENG"><s0>Clinical trial</s0>
<s5>08</s5>
</fC03>
<fC03 i1="07" i2="X" l="SPA"><s0>Ensayo clínico</s0>
<s5>08</s5>
</fC03>
<fC03 i1="08" i2="X" l="FRE"><s0>Randomisation</s0>
<s5>09</s5>
</fC03>
<fC03 i1="08" i2="X" l="ENG"><s0>Randomization</s0>
<s5>09</s5>
</fC03>
<fC03 i1="08" i2="X" l="SPA"><s0>Aleatorización</s0>
<s5>09</s5>
</fC03>
<fC03 i1="09" i2="X" l="FRE"><s0>Hématologie</s0>
<s5>11</s5>
</fC03>
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<s5>11</s5>
</fC03>
<fC03 i1="09" i2="X" l="SPA"><s0>Hematología</s0>
<s5>11</s5>
</fC03>
<fC03 i1="10" i2="X" l="FRE"><s0>Dasatinib</s0>
<s4>INC</s4>
<s5>86</s5>
</fC03>
<fC03 i1="11" i2="X" l="FRE"><s0>Leucémie myéloïde chronique</s0>
<s4>CD</s4>
<s5>96</s5>
</fC03>
<fC03 i1="11" i2="X" l="ENG"><s0>Chronic myelocytic leukemia</s0>
<s4>CD</s4>
<s5>96</s5>
</fC03>
<fC03 i1="11" i2="X" l="SPA"><s0>Leucemia mieloidea</s0>
<s4>CD</s4>
<s5>96</s5>
</fC03>
<fC03 i1="12" i2="X" l="FRE"><s0>Traitement première intention</s0>
<s4>CD</s4>
<s5>97</s5>
</fC03>
<fC03 i1="12" i2="X" l="ENG"><s0>First line treatment</s0>
<s4>CD</s4>
<s5>97</s5>
</fC03>
<fC03 i1="12" i2="X" l="SPA"><s0>Tratamiento primer línea</s0>
<s4>CD</s4>
<s5>97</s5>
</fC03>
<fC07 i1="01" i2="X" l="FRE"><s0>Transferases</s0>
<s2>FE</s2>
</fC07>
<fC07 i1="01" i2="X" l="ENG"><s0>Transferases</s0>
<s2>FE</s2>
</fC07>
<fC07 i1="01" i2="X" l="SPA"><s0>Transferases</s0>
<s2>FE</s2>
</fC07>
<fC07 i1="02" i2="X" l="FRE"><s0>Enzyme</s0>
<s2>FE</s2>
</fC07>
<fC07 i1="02" i2="X" l="ENG"><s0>Enzyme</s0>
<s2>FE</s2>
</fC07>
<fC07 i1="02" i2="X" l="SPA"><s0>Enzima</s0>
<s2>FE</s2>
</fC07>
<fC07 i1="03" i2="X" l="FRE"><s0>Hémopathie maligne</s0>
<s5>37</s5>
</fC07>
<fC07 i1="03" i2="X" l="ENG"><s0>Malignant hemopathy</s0>
<s5>37</s5>
</fC07>
<fC07 i1="03" i2="X" l="SPA"><s0>Hemopatía maligna</s0>
<s5>37</s5>
</fC07>
<fC07 i1="04" i2="X" l="FRE"><s0>Myéloprolifératif syndrome</s0>
<s5>38</s5>
</fC07>
<fC07 i1="04" i2="X" l="ENG"><s0>Myeloproliferative syndrome</s0>
<s5>38</s5>
</fC07>
<fC07 i1="04" i2="X" l="SPA"><s0>Mieloproliferativo síndrome</s0>
<s5>38</s5>
</fC07>
<fC07 i1="05" i2="X" l="FRE"><s0>Inhibiteur de la tyrosine kinase</s0>
<s4>INC</s4>
<s5>87</s5>
</fC07>
<fC07 i1="06" i2="X" l="FRE"><s0>Inhibiteur multikinase</s0>
<s4>INC</s4>
<s5>88</s5>
</fC07>
<fN21><s1>260</s1>
</fN21>
<fN44 i1="01"><s1>OTO</s1>
</fN44>
<fN82><s1>OTO</s1>
</fN82>
</pA>
</standard>
<server><NO>PASCAL 07-0397572 INIST</NO>
<ET>Dasatinib or high-dose imatinib for chronic-phase chronic myeloid leukemia after failure of first-line imatinib : a randomized phase 2 trial. Commentary</ET>
<AU>SCHIFFER (Charles A.); KANTARJIAN (Hagop); PASQUINI (Ricardo); HAMERSCHLAK (Nelson); ROUSSELOT (Philippe); HOLOWIECKI (Jerzy); JOOTAR (Saengsuree); ROBAK (Tadeusz); KHOROSHKO (Nina); MASSZI (Tamas); SKOTNICKI (Aleksander); HELLMANN (Andrzej); ZARITSKY (Andrey); GOLENKOV (Anatoly); RADICH (Jerald); HUGHES (Timothy); COUNTOURIOTIS (Athena); SHAH (Neil)</AU>
<AF>KARMANOS CANCER INSTITUTE/Etats-Unis (1 aut.); M. D. Anderson Cancer Center/Houston, TX/Etats-Unis (2 aut.); Hospital De Clinicas De Curitiba/Curitiba, Parana/Brésil (3 aut.); Hospital Israelita Albert Einstein/Sao Paulo/Brésil (4 aut.); Hospital Saint Louis/Paris/France (5 aut.); Katedra I Klinika Hematologii I Transplantacji Szpiku/Katowice/Pologne (6 aut.); Ramathibodi Hospital/Bangkok/Thaïlande (7 aut.); Szpital Specjalistyczny Im. Kopernika Klinika Hematologii/Lodz/Pologne (8 aut.); National Research Hematology Center/Moscow/Russie (9 aut.); National Medical Center/Budapest/Hongrie (10 aut.); Collegium Medicum Uniwesytetu Jagiellonskiego/Krakow/Pologne (11 aut.); Klinika Hematologii, Akademia Medyczna/Gdansk/Pologne (12 aut.); St Petersburg State Medical University/St Petersburg/Russie (13 aut.); Moscow Region Research Clinical Institute/Moscow/Russie (14 aut.); Clinical Research Division, Fred Hutchinson Cancer Research Center/Seattle, WA/Etats-Unis (15 aut.); Division of Hematology, Institute of Medical and Veterinary Science/Adelaide/Australie (16 aut.); Bristol-Myers Squibb/Wallingford, CT/Etats-Unis (17 aut.); Division of Hematology and Oncology, University College of San Francisco School of Medicine/San Francisco, CA/Etats-Unis (18 aut.)</AF>
<DT>Publication en série; Article; Commentaire; Niveau analytique</DT>
<SO>Blood; ISSN 0006-4971; Etats-Unis; Da. 2007; Vol. 109; No. 12; 5068-5069, 5143-5150 [10 p.]; Bibl. 28 ref.</SO>
<LA>Anglais</LA>
<EA>Therapeutic options for chronic myelogenous leukemia (CML) resistant to 400 to 600 mg imatinib are limited. Escalating imatinib doses may overcome resistance. Dasatinib, a significantly more potent inhibitor of BCR-ABL, is safe and effective in this population. Patients with imatinib-resistant chronic-phase (CP) CML were randomized 2:1 to 140 mg dasatinib (n = 101) or 800 mg imatinib (n = 49). With a median follow up of 15 months, complete hematologic responses were observed in 93% and 82% of patients receiving dasatinib and high-dose imatinib (P = .034), respectively. Dasatinib resulted in higher major cytogenetic response rates (52%) than high-dose imatinib (33%) (P = .023); this included complete cytogenetic response in 40% and 16% (P = .004). Major molecular responses were also more frequent with dasatinib (16% versus 4%; P = 0.038). Treatment failure (hazard ratio [HR], 0.16; P <.001) and progression-free survival (HR, 0.14; P <.001) both favored dasatinib. Superficial edema (42% versus 15%) and fluid retention (45% versus 30%) were more prevalent with imatinib; pleural effusion was more common with dasatinib (17% versus 0%). Grade 3 to 4 nonhematologic toxicity was minimal. Cytopenias were more frequent and severe with dasatinib. Dasatinib represents a safe and effective therapy for CP-CML resistant to conventional imatinib doses with improved cytogenetic and molecular response rates and progression-free survival relative to high-dose imatinib.</EA>
<CC>002B19B</CC>
<FD>Imatinib; Anticancéreux; Dose forte; Protein-tyrosine kinase; Inhibiteur enzyme; Essai clinique phase II; Essai clinique; Randomisation; Hématologie; Dasatinib; Leucémie myéloïde chronique; Traitement première intention</FD>
<FG>Transferases; Enzyme; Hémopathie maligne; Myéloprolifératif syndrome; Inhibiteur de la tyrosine kinase; Inhibiteur multikinase</FG>
<ED>Imatinib; Antineoplastic agent; High dose; Protein-tyrosine kinase; Enzyme inhibitor; Phase II trial; Clinical trial; Randomization; Hematology; Chronic myelocytic leukemia; First line treatment</ED>
<EG>Transferases; Enzyme; Malignant hemopathy; Myeloproliferative syndrome</EG>
<SD>Imatinib; Anticanceroso; Dosis fuerte; Protein-tyrosine kinase; Inhibidor enzima; Ensayo clínico fase II; Ensayo clínico; Aleatorización; Hematología; Leucemia mieloidea; Tratamiento primer línea</SD>
<LO>INIST-3178.354000162838230090</LO>
<ID>07-0397572</ID>
</server>
</inist>
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Dasatinib or high-dose imatinib for chronic-phase chronic myeloid leukemia after failure of first-line imatinib : a randomized phase 2 trial. Commentary

Dasatinib or high-dose imatinib for chronic-phase chronic myeloid leukemia after failure of first-line imatinib : a randomized phase 2 trial. Commentary

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