AustralieFrV1, PascalFrancis, Corpus, bibRecord, 002B79

Dasatinib-associated major molecular responses in patients with chronic myeloid leukemia in chronic phase following imatinib failure: response dynamics and predictive value

Identifieur interne : 002B79 ( PascalFrancis/Corpus ); précédent : 002B78; suivant : 002B80

Dasatinib-associated major molecular responses in patients with chronic myeloid leukemia in chronic phase following imatinib failure: response dynamics and predictive value

Auteurs : A. Hochhaus ; M. C. Müller ; J. Radich ; S. Branford ; H. M. Kantarjiaw ; B. Hanfstetein ; P. Rousselot ; D.-W. Kim ; J. H. Lipton ; E. Bleickardt ; A. Lambert ; T. P. Hughes

Source :

Leukemia [ 0887-6924 ] ; 2009.

RBID : Pascal:09-0397947

Descripteurs français

Pascal (Inist)
- Dasatinib, Anticancéreux, Homme, Imatinib, Leucémie myéloïde chronique, Protein-tyrosine kinase, Inhibiteur enzyme, Dynamique, Valeur prédictive, Gène hybride, Translocation chromosomique, Chromosome C9 anormal, Chromosome G22 anormal, Chromosome Ph1, Non-specific serine/threonine protein kinase, Gène onc cellulaire, Traitement, Pronostic, Hématologie, Gène abl, Gène bcr, Survie sans progression.

English descriptors

KwdEn :
- Abnormal chromosome C9, Abnormal chromosome G22, Antineoplastic agent, C-Onc gene, Chromosome translocation, Chronic myelogenous leukemia, Dasatinib, Dynamics, Enzyme inhibitor, Hematology, Human, Hybrid gene, Imatinib, Non-specific serine/threonine protein kinase, Philadelphia chromosome, Predictive value, Prognosis, Progression free survival, Protein-tyrosine kinase, Treatment, bcr gene.

Abstract

Dasatinib is a highly potent BCR-ABL inhibitor that has shown durable efficacy in patients with chronic phase (CP) chronic myeloid leukemia (CML) after resistance, suboptimal response, or intolerance to prior imatinib. In patients with CML, BCR-ABL transcript measurement is the most sensitive method for assessing minimal residual disease. Here, molecular responses were analyzed in 1067 patients with CML-CP treated with dasatinib during phase II/III trials. After 3, 6, 12, and 24 months of follow-up, a major molecular response (MMR) was achieved by 12, 22, 35, and 40% of patients, respectively. The 24-month MMR rate was 34% in patients with resistance or suboptimal response to imatinib (n=829) and 63% in imatinib-intolerant patients (n=238). Among patients who had achieved a complete cytogenetic response (CCyR), 72% also achieved MMR. Responses with dasatinib 100 mg once daily were similar to other doses. In landmark analyses, 24-month progression-free survival was higher in patients who had achieved MMR or CCyR at 12 months than in those without MMR or CCyR at 12 months. MMR at 12 months was associated with a longer duration of CCyR. Overall, this analysis shows that dasatinib treatment results in high MMR rates in patients with CML-CP after imatinib failure.

Notice en format standard (ISO 2709)

Pour connaître la documentation sur le format Inist Standard.

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N21				`@1 292`
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Format Inist (serveur)

NO :	PASCAL 09-0397947 INIST
ET :	Dasatinib-associated major molecular responses in patients with chronic myeloid leukemia in chronic phase following imatinib failure: response dynamics and predictive value
AU :	HOCHHAUS (A.); MÜLLER (M. C.); RADICH (J.); BRANFORD (S.); KANTARJIAW (H. M.); HANFSTETEIN (B.); ROUSSELOT (P.); KIM (D.-W.); LIPTON (J. H.); BLEICKARDT (E.); LAMBERT (A.); HUGHES (T. P.)
AF :	III. Medizinische Klinik, Universitätsmedizin Mannheim, Universität Heidelberg/Mannheim/Allemagne (1 aut., 2 aut., 6 aut.); Department Hematology/Oncology, Universitätsklinikum Jena/Jena/Allemagne (1 aut.); Clinical Research Division, Fred Hutchinson Cancer Research Center/Seattle, WA/Etats-Unis (3 aut.); Division of Haematology, Institute of Medical and Veterinary Science/Adelaide, South Australia/Australie (4 aut., 12 aut.); Department of Leukemia, The University of Texas MD Anderson Cancer Center/Houston, TX/Etats-Unis (5 aut.); Service d'Hématologie et d'Oncologie, Hôpital André Mignot, Université de Versailles et CIC9504/France (7 aut.); St Mary's Hospital, The Catholic University of Korea/Seoul/Corée, République de (8 aut.); Department of Hematology/Medical Oncology, Princess Margaret Hospital, University of Toronto/Toronto, Ontario/Canada (9 aut.); Bristol-Myers Squibb/Wallingford, CT/Etats-Unis (10 aut., 11 aut.)
DT :	Publication en série; Niveau analytique
SO :	Leukemia; ISSN 0887-6924; Coden LEUKED; Royaume-Uni; Da. 2009; Vol. 23; No. 9; Pp. 1628-1633; Bibl. 28 ref.
LA :	Anglais
EA :	Dasatinib is a highly potent BCR-ABL inhibitor that has shown durable efficacy in patients with chronic phase (CP) chronic myeloid leukemia (CML) after resistance, suboptimal response, or intolerance to prior imatinib. In patients with CML, BCR-ABL transcript measurement is the most sensitive method for assessing minimal residual disease. Here, molecular responses were analyzed in 1067 patients with CML-CP treated with dasatinib during phase II/III trials. After 3, 6, 12, and 24 months of follow-up, a major molecular response (MMR) was achieved by 12, 22, 35, and 40% of patients, respectively. The 24-month MMR rate was 34% in patients with resistance or suboptimal response to imatinib (n=829) and 63% in imatinib-intolerant patients (n=238). Among patients who had achieved a complete cytogenetic response (CCyR), 72% also achieved MMR. Responses with dasatinib 100 mg once daily were similar to other doses. In landmark analyses, 24-month progression-free survival was higher in patients who had achieved MMR or CCyR at 12 months than in those without MMR or CCyR at 12 months. MMR at 12 months was associated with a longer duration of CCyR. Overall, this analysis shows that dasatinib treatment results in high MMR rates in patients with CML-CP after imatinib failure.
CC :	002B19B; 002B23B
FD :	Dasatinib; Anticancéreux; Homme; Imatinib; Leucémie myéloïde chronique; Protein-tyrosine kinase; Inhibiteur enzyme; Dynamique; Valeur prédictive; Gène hybride; Translocation chromosomique; Chromosome C9 anormal; Chromosome G22 anormal; Chromosome Ph1; Non-specific serine/threonine protein kinase; Gène onc cellulaire; Traitement; Pronostic; Hématologie; Gène abl; Gène bcr; Survie sans progression
FG :	Transferases; Enzyme; Chromosome anormal; Aberration chromosomique; Inhibiteur de la tyrosine kinase; Inhibiteur multikinase; Hémopathie maligne; Cancer; Syndrome myéloprolifératif
ED :	Dasatinib; Antineoplastic agent; Human; Imatinib; Chronic myelogenous leukemia; Protein-tyrosine kinase; Enzyme inhibitor; Dynamics; Predictive value; Hybrid gene; Chromosome translocation; Abnormal chromosome C9; Abnormal chromosome G22; Philadelphia chromosome; Non-specific serine/threonine protein kinase; C-Onc gene; Treatment; Prognosis; Hematology; bcr gene; Progression free survival
EG :	Transferases; Enzyme; Abnormal chromosome; Chromosomal aberration; Tyrosine kinase inhibitor; Multikinase inhibitor; Malignant hemopathy; Cancer; Myeloproliferative syndrome
SD :	Dasatinib; Anticanceroso; Hombre; Imatinib; Leucemia mieloidea crónica; Protein-tyrosine kinase; Inhibidor enzima; Dinámica; Valor predictivo; Gen híbrido; Translocación cromosómica; Cromosoma C9 anormal; Cromosoma G22 anormal; Cromosoma Ph1; Non-specific serine/threonine protein kinase; Gen onc celular; Tratamiento; Pronóstico; Hematología; Supervivencia sin progresión
LO :	INIST-21129.354000171930390120
ID :	09-0397947

Links to Exploration step

Pascal:09-0397947

Le document en format XML

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<author><name sortKey="Bleickardt, E" sort="Bleickardt, E" uniqKey="Bleickardt E" first="E." last="Bleickardt">E. Bleickardt</name>
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<affiliation><inist:fA14 i1="04"><s1>Division of Haematology, Institute of Medical and Veterinary Science</s1>
<s2>Adelaide, South Australia</s2>
<s3>AUS</s3>
<sZ>4 aut.</sZ>
<sZ>12 aut.</sZ>
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<sourceDesc><biblStruct><analytic><title xml:lang="en" level="a">Dasatinib-associated major molecular responses in patients with chronic myeloid leukemia in chronic phase following imatinib failure: response dynamics and predictive value</title>
<author><name sortKey="Hochhaus, A" sort="Hochhaus, A" uniqKey="Hochhaus A" first="A." last="Hochhaus">A. Hochhaus</name>
<affiliation><inist:fA14 i1="01"><s1>III. Medizinische Klinik, Universitätsmedizin Mannheim, Universität Heidelberg</s1>
<s2>Mannheim</s2>
<s3>DEU</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>6 aut.</sZ>
</inist:fA14>
</affiliation>
<affiliation><inist:fA14 i1="02"><s1>Department Hematology/Oncology, Universitätsklinikum Jena</s1>
<s2>Jena</s2>
<s3>DEU</s3>
<sZ>1 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Muller, M C" sort="Muller, M C" uniqKey="Muller M" first="M. C." last="Müller">M. C. Müller</name>
<affiliation><inist:fA14 i1="01"><s1>III. Medizinische Klinik, Universitätsmedizin Mannheim, Universität Heidelberg</s1>
<s2>Mannheim</s2>
<s3>DEU</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>6 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Radich, J" sort="Radich, J" uniqKey="Radich J" first="J." last="Radich">J. Radich</name>
<affiliation><inist:fA14 i1="03"><s1>Clinical Research Division, Fred Hutchinson Cancer Research Center</s1>
<s2>Seattle, WA</s2>
<s3>USA</s3>
<sZ>3 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Branford, S" sort="Branford, S" uniqKey="Branford S" first="S." last="Branford">S. Branford</name>
<affiliation><inist:fA14 i1="04"><s1>Division of Haematology, Institute of Medical and Veterinary Science</s1>
<s2>Adelaide, South Australia</s2>
<s3>AUS</s3>
<sZ>4 aut.</sZ>
<sZ>12 aut.</sZ>
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</affiliation>
</author>
<author><name sortKey="Kantarjiaw, H M" sort="Kantarjiaw, H M" uniqKey="Kantarjiaw H" first="H. M." last="Kantarjiaw">H. M. Kantarjiaw</name>
<affiliation><inist:fA14 i1="05"><s1>Department of Leukemia, The University of Texas MD Anderson Cancer Center</s1>
<s2>Houston, TX</s2>
<s3>USA</s3>
<sZ>5 aut.</sZ>
</inist:fA14>
</affiliation>
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<author><name sortKey="Hanfstetein, B" sort="Hanfstetein, B" uniqKey="Hanfstetein B" first="B." last="Hanfstetein">B. Hanfstetein</name>
<affiliation><inist:fA14 i1="01"><s1>III. Medizinische Klinik, Universitätsmedizin Mannheim, Universität Heidelberg</s1>
<s2>Mannheim</s2>
<s3>DEU</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>6 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Rousselot, P" sort="Rousselot, P" uniqKey="Rousselot P" first="P." last="Rousselot">P. Rousselot</name>
<affiliation><inist:fA14 i1="06"><s1>Service d'Hématologie et d'Oncologie, Hôpital André Mignot, Université de Versailles et CIC9504</s1>
<s3>FRA</s3>
<sZ>7 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Kim, D W" sort="Kim, D W" uniqKey="Kim D" first="D.-W." last="Kim">D.-W. Kim</name>
<affiliation><inist:fA14 i1="07"><s1>St Mary's Hospital, The Catholic University of Korea</s1>
<s2>Seoul</s2>
<s3>KOR</s3>
<sZ>8 aut.</sZ>
</inist:fA14>
</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><inist:fA14 i1="08"><s1>Department of Hematology/Medical Oncology, Princess Margaret Hospital, University of Toronto</s1>
<s2>Toronto, Ontario</s2>
<s3>CAN</s3>
<sZ>9 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Bleickardt, E" sort="Bleickardt, E" uniqKey="Bleickardt E" first="E." last="Bleickardt">E. Bleickardt</name>
<affiliation><inist:fA14 i1="09"><s1>Bristol-Myers Squibb</s1>
<s2>Wallingford, CT</s2>
<s3>USA</s3>
<sZ>10 aut.</sZ>
<sZ>11 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Lambert, A" sort="Lambert, A" uniqKey="Lambert A" first="A." last="Lambert">A. Lambert</name>
<affiliation><inist:fA14 i1="09"><s1>Bristol-Myers Squibb</s1>
<s2>Wallingford, CT</s2>
<s3>USA</s3>
<sZ>10 aut.</sZ>
<sZ>11 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Hughes, T P" sort="Hughes, T P" uniqKey="Hughes T" first="T. P." last="Hughes">T. P. Hughes</name>
<affiliation><inist:fA14 i1="04"><s1>Division of Haematology, Institute of Medical and Veterinary Science</s1>
<s2>Adelaide, South Australia</s2>
<s3>AUS</s3>
<sZ>4 aut.</sZ>
<sZ>12 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
</analytic>
<series><title level="j" type="main">Leukemia</title>
<title level="j" type="abbreviated">Leukemia</title>
<idno type="ISSN">0887-6924</idno>
<imprint><date when="2009">2009</date>
</imprint>
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<seriesStmt><title level="j" type="main">Leukemia</title>
<title level="j" type="abbreviated">Leukemia</title>
<idno type="ISSN">0887-6924</idno>
</seriesStmt>
</fileDesc>
<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Abnormal chromosome C9</term>
<term>Abnormal chromosome G22</term>
<term>Antineoplastic agent</term>
<term>C-Onc gene</term>
<term>Chromosome translocation</term>
<term>Chronic myelogenous leukemia</term>
<term>Dasatinib</term>
<term>Dynamics</term>
<term>Enzyme inhibitor</term>
<term>Hematology</term>
<term>Human</term>
<term>Hybrid gene</term>
<term>Imatinib</term>
<term>Non-specific serine/threonine protein kinase</term>
<term>Philadelphia chromosome</term>
<term>Predictive value</term>
<term>Prognosis</term>
<term>Progression free survival</term>
<term>Protein-tyrosine kinase</term>
<term>Treatment</term>
<term>bcr gene</term>
</keywords>
<keywords scheme="Pascal" xml:lang="fr"><term>Dasatinib</term>
<term>Anticancéreux</term>
<term>Homme</term>
<term>Imatinib</term>
<term>Leucémie myéloïde chronique</term>
<term>Protein-tyrosine kinase</term>
<term>Inhibiteur enzyme</term>
<term>Dynamique</term>
<term>Valeur prédictive</term>
<term>Gène hybride</term>
<term>Translocation chromosomique</term>
<term>Chromosome C9 anormal</term>
<term>Chromosome G22 anormal</term>
<term>Chromosome Ph1</term>
<term>Non-specific serine/threonine protein kinase</term>
<term>Gène onc cellulaire</term>
<term>Traitement</term>
<term>Pronostic</term>
<term>Hématologie</term>
<term>Gène abl</term>
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<front><div type="abstract" xml:lang="en">Dasatinib is a highly potent BCR-ABL inhibitor that has shown durable efficacy in patients with chronic phase (CP) chronic myeloid leukemia (CML) after resistance, suboptimal response, or intolerance to prior imatinib. In patients with CML, BCR-ABL transcript measurement is the most sensitive method for assessing minimal residual disease. Here, molecular responses were analyzed in 1067 patients with CML-CP treated with dasatinib during phase II/III trials. After 3, 6, 12, and 24 months of follow-up, a major molecular response (MMR) was achieved by 12, 22, 35, and 40% of patients, respectively. The 24-month MMR rate was 34% in patients with resistance or suboptimal response to imatinib (n=829) and 63% in imatinib-intolerant patients (n=238). Among patients who had achieved a complete cytogenetic response (CCyR), 72% also achieved MMR. Responses with dasatinib 100 mg once daily were similar to other doses. In landmark analyses, 24-month progression-free survival was higher in patients who had achieved MMR or CCyR at 12 months than in those without MMR or CCyR at 12 months. MMR at 12 months was associated with a longer duration of CCyR. Overall, this analysis shows that dasatinib treatment results in high MMR rates in patients with CML-CP after imatinib failure.</div>
</front>
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<fA14 i1="01"><s1>III. Medizinische Klinik, Universitätsmedizin Mannheim, Universität Heidelberg</s1>
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<s3>DEU</s3>
<sZ>1 aut.</sZ>
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<fA14 i1="04"><s1>Division of Haematology, Institute of Medical and Veterinary Science</s1>
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<s3>AUS</s3>
<sZ>4 aut.</sZ>
<sZ>12 aut.</sZ>
</fA14>
<fA14 i1="05"><s1>Department of Leukemia, The University of Texas MD Anderson Cancer Center</s1>
<s2>Houston, TX</s2>
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<sZ>5 aut.</sZ>
</fA14>
<fA14 i1="06"><s1>Service d'Hématologie et d'Oncologie, Hôpital André Mignot, Université de Versailles et CIC9504</s1>
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<fA14 i1="07"><s1>St Mary's Hospital, The Catholic University of Korea</s1>
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<fA14 i1="08"><s1>Department of Hematology/Medical Oncology, Princess Margaret Hospital, University of Toronto</s1>
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<s3>CAN</s3>
<sZ>9 aut.</sZ>
</fA14>
<fA14 i1="09"><s1>Bristol-Myers Squibb</s1>
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<sZ>10 aut.</sZ>
<sZ>11 aut.</sZ>
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<s5>22</s5>
</fC03>
<fC03 i1="17" i2="X" l="FRE"><s0>Traitement</s0>
<s5>23</s5>
</fC03>
<fC03 i1="17" i2="X" l="ENG"><s0>Treatment</s0>
<s5>23</s5>
</fC03>
<fC03 i1="17" i2="X" l="SPA"><s0>Tratamiento</s0>
<s5>23</s5>
</fC03>
<fC03 i1="18" i2="X" l="FRE"><s0>Pronostic</s0>
<s5>24</s5>
</fC03>
<fC03 i1="18" i2="X" l="ENG"><s0>Prognosis</s0>
<s5>24</s5>
</fC03>
<fC03 i1="18" i2="X" l="SPA"><s0>Pronóstico</s0>
<s5>24</s5>
</fC03>
<fC03 i1="19" i2="X" l="FRE"><s0>Hématologie</s0>
<s5>35</s5>
</fC03>
<fC03 i1="19" i2="X" l="ENG"><s0>Hematology</s0>
<s5>35</s5>
</fC03>
<fC03 i1="19" i2="X" l="SPA"><s0>Hematología</s0>
<s5>35</s5>
</fC03>
<fC03 i1="20" i2="X" l="FRE"><s0>Gène abl</s0>
<s4>INC</s4>
<s5>86</s5>
</fC03>
<fC03 i1="21" i2="X" l="FRE"><s0>Gène bcr</s0>
<s4>CD</s4>
<s5>96</s5>
</fC03>
<fC03 i1="21" i2="X" l="ENG"><s0>bcr gene</s0>
<s4>CD</s4>
<s5>96</s5>
</fC03>
<fC03 i1="22" i2="X" l="FRE"><s0>Survie sans progression</s0>
<s4>CD</s4>
<s5>97</s5>
</fC03>
<fC03 i1="22" i2="X" l="ENG"><s0>Progression free survival</s0>
<s4>CD</s4>
<s5>97</s5>
</fC03>
<fC03 i1="22" i2="X" l="SPA"><s0>Supervivencia sin progresión</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>Chromosome anormal</s0>
</fC07>
<fC07 i1="03" i2="X" l="ENG"><s0>Abnormal chromosome</s0>
</fC07>
<fC07 i1="03" i2="X" l="SPA"><s0>Cromosoma anormal</s0>
</fC07>
<fC07 i1="04" i2="X" l="FRE"><s0>Aberration chromosomique</s0>
</fC07>
<fC07 i1="04" i2="X" l="ENG"><s0>Chromosomal aberration</s0>
</fC07>
<fC07 i1="04" i2="X" l="SPA"><s0>Aberración cromosómica</s0>
</fC07>
<fC07 i1="05" i2="X" l="FRE"><s0>Inhibiteur de la tyrosine kinase</s0>
<s5>37</s5>
</fC07>
<fC07 i1="05" i2="X" l="ENG"><s0>Tyrosine kinase inhibitor</s0>
<s5>37</s5>
</fC07>
<fC07 i1="05" i2="X" l="SPA"><s0>Inhibidor tyrosine kinase</s0>
<s5>37</s5>
</fC07>
<fC07 i1="06" i2="X" l="FRE"><s0>Inhibiteur multikinase</s0>
<s5>38</s5>
</fC07>
<fC07 i1="06" i2="X" l="ENG"><s0>Multikinase inhibitor</s0>
<s5>38</s5>
</fC07>
<fC07 i1="06" i2="X" l="SPA"><s0>inhibidor multicinasa</s0>
<s5>38</s5>
</fC07>
<fC07 i1="07" i2="X" l="FRE"><s0>Hémopathie maligne</s0>
<s2>NM</s2>
<s5>39</s5>
</fC07>
<fC07 i1="07" i2="X" l="ENG"><s0>Malignant hemopathy</s0>
<s2>NM</s2>
<s5>39</s5>
</fC07>
<fC07 i1="07" i2="X" l="SPA"><s0>Hemopatía maligna</s0>
<s2>NM</s2>
<s5>39</s5>
</fC07>
<fC07 i1="08" i2="X" l="FRE"><s0>Cancer</s0>
<s2>NM</s2>
</fC07>
<fC07 i1="08" i2="X" l="ENG"><s0>Cancer</s0>
<s2>NM</s2>
</fC07>
<fC07 i1="08" i2="X" l="SPA"><s0>Cáncer</s0>
<s2>NM</s2>
</fC07>
<fC07 i1="09" i2="X" l="FRE"><s0>Syndrome myéloprolifératif</s0>
<s5>40</s5>
</fC07>
<fC07 i1="09" i2="X" l="ENG"><s0>Myeloproliferative syndrome</s0>
<s5>40</s5>
</fC07>
<fC07 i1="09" i2="X" l="SPA"><s0>Mieloproliferativo síndrome</s0>
<s5>40</s5>
</fC07>
<fN21><s1>292</s1>
</fN21>
<fN44 i1="01"><s1>OTO</s1>
</fN44>
<fN82><s1>OTO</s1>
</fN82>
</pA>
</standard>
<server><NO>PASCAL 09-0397947 INIST</NO>
<ET>Dasatinib-associated major molecular responses in patients with chronic myeloid leukemia in chronic phase following imatinib failure: response dynamics and predictive value</ET>
<AU>HOCHHAUS (A.); MÜLLER (M. C.); RADICH (J.); BRANFORD (S.); KANTARJIAW (H. M.); HANFSTETEIN (B.); ROUSSELOT (P.); KIM (D.-W.); LIPTON (J. H.); BLEICKARDT (E.); LAMBERT (A.); HUGHES (T. P.)</AU>
<AF>III. Medizinische Klinik, Universitätsmedizin Mannheim, Universität Heidelberg/Mannheim/Allemagne (1 aut., 2 aut., 6 aut.); Department Hematology/Oncology, Universitätsklinikum Jena/Jena/Allemagne (1 aut.); Clinical Research Division, Fred Hutchinson Cancer Research Center/Seattle, WA/Etats-Unis (3 aut.); Division of Haematology, Institute of Medical and Veterinary Science/Adelaide, South Australia/Australie (4 aut., 12 aut.); Department of Leukemia, The University of Texas MD Anderson Cancer Center/Houston, TX/Etats-Unis (5 aut.); Service d'Hématologie et d'Oncologie, Hôpital André Mignot, Université de Versailles et CIC9504/France (7 aut.); St Mary's Hospital, The Catholic University of Korea/Seoul/Corée, République de (8 aut.); Department of Hematology/Medical Oncology, Princess Margaret Hospital, University of Toronto/Toronto, Ontario/Canada (9 aut.); Bristol-Myers Squibb/Wallingford, CT/Etats-Unis (10 aut., 11 aut.)</AF>
<DT>Publication en série; Niveau analytique</DT>
<SO>Leukemia; ISSN 0887-6924; Coden LEUKED; Royaume-Uni; Da. 2009; Vol. 23; No. 9; Pp. 1628-1633; Bibl. 28 ref.</SO>
<LA>Anglais</LA>
<EA>Dasatinib is a highly potent BCR-ABL inhibitor that has shown durable efficacy in patients with chronic phase (CP) chronic myeloid leukemia (CML) after resistance, suboptimal response, or intolerance to prior imatinib. In patients with CML, BCR-ABL transcript measurement is the most sensitive method for assessing minimal residual disease. Here, molecular responses were analyzed in 1067 patients with CML-CP treated with dasatinib during phase II/III trials. After 3, 6, 12, and 24 months of follow-up, a major molecular response (MMR) was achieved by 12, 22, 35, and 40% of patients, respectively. The 24-month MMR rate was 34% in patients with resistance or suboptimal response to imatinib (n=829) and 63% in imatinib-intolerant patients (n=238). Among patients who had achieved a complete cytogenetic response (CCyR), 72% also achieved MMR. Responses with dasatinib 100 mg once daily were similar to other doses. In landmark analyses, 24-month progression-free survival was higher in patients who had achieved MMR or CCyR at 12 months than in those without MMR or CCyR at 12 months. MMR at 12 months was associated with a longer duration of CCyR. Overall, this analysis shows that dasatinib treatment results in high MMR rates in patients with CML-CP after imatinib failure.</EA>
<CC>002B19B; 002B23B</CC>
<FD>Dasatinib; Anticancéreux; Homme; Imatinib; Leucémie myéloïde chronique; Protein-tyrosine kinase; Inhibiteur enzyme; Dynamique; Valeur prédictive; Gène hybride; Translocation chromosomique; Chromosome C9 anormal; Chromosome G22 anormal; Chromosome Ph1; Non-specific serine/threonine protein kinase; Gène onc cellulaire; Traitement; Pronostic; Hématologie; Gène abl; Gène bcr; Survie sans progression</FD>
<FG>Transferases; Enzyme; Chromosome anormal; Aberration chromosomique; Inhibiteur de la tyrosine kinase; Inhibiteur multikinase; Hémopathie maligne; Cancer; Syndrome myéloprolifératif</FG>
<ED>Dasatinib; Antineoplastic agent; Human; Imatinib; Chronic myelogenous leukemia; Protein-tyrosine kinase; Enzyme inhibitor; Dynamics; Predictive value; Hybrid gene; Chromosome translocation; Abnormal chromosome C9; Abnormal chromosome G22; Philadelphia chromosome; Non-specific serine/threonine protein kinase; C-Onc gene; Treatment; Prognosis; Hematology; bcr gene; Progression free survival</ED>
<EG>Transferases; Enzyme; Abnormal chromosome; Chromosomal aberration; Tyrosine kinase inhibitor; Multikinase inhibitor; Malignant hemopathy; Cancer; Myeloproliferative syndrome</EG>
<SD>Dasatinib; Anticanceroso; Hombre; Imatinib; Leucemia mieloidea crónica; Protein-tyrosine kinase; Inhibidor enzima; Dinámica; Valor predictivo; Gen híbrido; Translocación cromosómica; Cromosoma C9 anormal; Cromosoma G22 anormal; Cromosoma Ph1; Non-specific serine/threonine protein kinase; Gen onc celular; Tratamiento; Pronóstico; Hematología; Supervivencia sin progresión</SD>
<LO>INIST-21129.354000171930390120</LO>
<ID>09-0397947</ID>
</server>
</inist>
</record>

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Dasatinib-associated major molecular responses in patients with chronic myeloid leukemia in chronic phase following imatinib failure: response dynamics and predictive value

Dasatinib-associated major molecular responses in patients with chronic myeloid leukemia in chronic phase following imatinib failure: response dynamics and predictive value

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