AustralieFrV1, PascalFrancis, Corpus, bibRecord, 003C35

Dasatinib induces notable hematologic and cytogenetic responses in chronic-phase chronic myeloid leukemia after failure of imatinib therapy. Commentary

Identifieur interne : 003C35 ( PascalFrancis/Corpus ); précédent : 003C34; suivant : 003C36

Dasatinib induces notable hematologic and cytogenetic responses in chronic-phase chronic myeloid leukemia after failure of imatinib therapy. Commentary

Auteurs : Jacob M. Rowe ; Andreas Hochhaus ; Hagop M. Kantarjian ; Michele Baccarani ; Jeffrey H. Lipton ; Jane F. Apperley ; Brian J. Druker ; Thierry Facon ; Stuart L. Goldberg ; Francisco Cervantes ; Dietger Niederwieser ; Richard T. Silver ; Richard M. Stone ; Timothy P. Hughes ; Martin C. Muller ; Rana Ezzeddine ; Athena M. Countouriotis ; Neil P. Shah

Source :

Blood [ 0006-4971 ] ; 2007.

RBID : Pascal:07-0247406

Descripteurs français

Pascal (Inist)
- Imatinib, Anticancéreux, Cytogénétique, Protein-tyrosine kinase, Inhibiteur enzyme, Traitement, Dasatinib, Leucémie myéloïde chronique.

English descriptors

KwdEn :
- Antineoplastic agent, Chronic myelocytic leukemia, Cytogenetics, Enzyme inhibitor, Imatinib, Protein-tyrosine kinase, Treatment.

Abstract

Although imatinib induces marked responses in patients with chronic myeloid leukemia (CML), resistance is increasingly problematic, and treatment options for imatinib-resistant or -intolerant CML are limited. Dasatinib, a novel, highly potent, oral, multitargeted kinase inhibitor of BCR-ABL and SRC family kinases, induced cytogenetic responses in a phase 1 study in imatinib-resistant or -intolerant CML and was well tolerated. Initial results are presented from a phase 2 study of 186 patients with imatinib-resistant or -intolerant chronic-phase CML (CML-CP) designed to further establish the efficacy and safety of dasatinib (70 mg twice daily). At 8-months' follow-up, dasatinib induced notable responses, with 90% and 52% of patients achieving complete hematologic and major cytogenetic responses (MCyR), respectively. Responses were long lasting: only 2% of patients achieving MCyR progressed or died. Importantly, comparable responses were achieved by patients carrying BCR-ABL mutations conferring imatinib resistance. Dasatinib also induced molecular responses, reducing BCR-ABL/ABL transcript ratios from 66% at baseline to 2.6% at 9 months. Nonhematologic adverse events were generally mild to moderate, and most cytopenias were effectively managed with dose modifications. Cross-intolerance with imatinib was not evident. To conclude, dasatinib induces notable responses in imatinib-resistant or -intolerant CML-CP, is well tolerated, and represents a promising therapeutic option for these patients. This trial was registered at www.clinicaltrials.gov as CA180013.

Notice en format standard (ISO 2709)

Pour connaître la documentation sur le format Inist Standard.

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A08	`01`	`1`	`ENG`	`@1 Dasatinib induces notable hematologic and cytogenetic responses in chronic-phase chronic myeloid leukemia after failure of imatinib therapy. Commentary`
A11	`01`	`1`		`@1 ROWE (Jacob M.) @9 comment.`
A11	`02`	`1`		`@1 HOCHHAUS (Andreas)`
A11	`03`	`1`		`@1 KANTARJIAN (Hagop M.)`
A11	`04`	`1`		`@1 BACCARANI (Michele)`
A11	`05`	`1`		`@1 LIPTON (Jeffrey H.)`
A11	`06`	`1`		`@1 APPERLEY (Jane F.)`
A11	`07`	`1`		`@1 DRUKER (Brian J.)`
A11	`08`	`1`		`@1 FACON (Thierry)`
A11	`09`	`1`		`@1 GOLDBERG (Stuart L.)`
A11	`10`	`1`		`@1 CERVANTES (Francisco)`
A11	`11`	`1`		`@1 NIEDERWIESER (Dietger)`
A11	`12`	`1`		`@1 SILVER (Richard T.)`
A11	`13`	`1`		`@1 STONE (Richard M.)`
A11	`14`	`1`		`@1 HUGHES (Timothy P.)`
A11	`15`	`1`		`@1 MULLER (Martin C.)`
A11	`16`	`1`		`@1 EZZEDDINE (Rana)`
A11	`17`	`1`		`@1 COUNTOURIOTIS (Athena M.)`
A11	`18`	`1`		`@1 SHAH (Neil P.)`
A14	`01`			`@1 HEMATOLOGY, RAMBAM MEDICAL CENTER @3 USA @Z 1 aut.`
A14	`02`			`@1 III. Medizinische Klinik, Medizinische Fakultät Mannheim, Universität Heidelberg @2 Mannheim @3 DEU @Z 2 aut. @Z 15 aut.`
A14	`03`			`@1 Department of Leukemia, M.D. Anderson Cancer Center @2 Houston, TX @3 USA @Z 3 aut.`
A14	`04`			`@1 Department of Hematology-Oncology "Seragnoli," S Orsola-Malpighi University Hospital, University of Bologna @3 ITA @Z 4 aut.`
A14	`05`			`@1 Princess Margaret Hospital @2 Toronto, ON @3 CAN @Z 5 aut.`
A14	`06`			`@1 Department of Haematology, Hammersmith Hospital @2 London @3 GBR @Z 6 aut.`
A14	`07`			`@1 Division of Hematology and Medical Oncology, Oregon Health Science University @2 Portland @3 USA @Z 7 aut.`
A14	`08`			`@1 Hópital Claude Huriez @2 Lille @3 FRA @Z 8 aut.`
A14	`09`			`@1 Cancer Center, Hackensack University Medical Center @2 NJ @3 USA @Z 9 aut.`
A14	`10`			`@1 Department of Hematology, Hospital Clinic @2 Barcelona @3 ESP @Z 10 aut.`
A14	`11`			`@1 Medizinische Klinik und Poliklinik II, Universitätsklinikum Leipzig @3 DEU @Z 11 aut.`
A14	`12`			`@1 Weill Medical College of Cornell University, New York Presbyterian Hospital @2 New York, NY @3 USA @Z 12 aut.`
A14	`13`			`@1 Department of Adult Oncology, Dana-Farber Cancer Institute @2 Boston, MA @3 USA @Z 13 aut.`
A14	`14`			`@1 Division of Hematology, Institute of Medical and Veterinary Science @2 Adelaide @3 AUS @Z 14 aut.`
A14	`15`			`@1 Bristol-Myers Squibb @2 Wallingford, CT @3 USA @Z 16 aut. @Z 17 aut.`
A14	`16`			`@1 Division of Hematology and Oncology, University College of San Francisco School of Medicine @2 CA @3 USA @Z 18 aut.`
A20				`@2 2271,2303-2309 [8 p.]`
A21				`@1 2007`
A23	`01`			`@0 ENG`
A43	`01`			`@1 INIST @2 3178 @5 354000143549720050`
A44				`@0 0000 @1 © 2007 INIST-CNRS. All rights reserved.`
A45				`@0 32 ref.`
A47	`01`	`1`		`@0 07-0247406`
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A66	`01`			`@0 USA`
C01	`01`		`ENG`	@0 Although imatinib induces marked responses in patients with chronic myeloid leukemia (CML), resistance is increasingly problematic, and treatment options for imatinib-resistant or -intolerant CML are limited. Dasatinib, a novel, highly potent, oral, multitargeted kinase inhibitor of BCR-ABL and SRC family kinases, induced cytogenetic responses in a phase 1 study in imatinib-resistant or -intolerant CML and was well tolerated. Initial results are presented from a phase 2 study of 186 patients with imatinib-resistant or -intolerant chronic-phase CML (CML-CP) designed to further establish the efficacy and safety of dasatinib (70 mg twice daily). At 8-months' follow-up, dasatinib induced notable responses, with 90% and 52% of patients achieving complete hematologic and major cytogenetic responses (MCyR), respectively. Responses were long lasting: only 2% of patients achieving MCyR progressed or died. Importantly, comparable responses were achieved by patients carrying BCR-ABL mutations conferring imatinib resistance. Dasatinib also induced molecular responses, reducing BCR-ABL/ABL transcript ratios from 66% at baseline to 2.6% at 9 months. Nonhematologic adverse events were generally mild to moderate, and most cytopenias were effectively managed with dose modifications. Cross-intolerance with imatinib was not evident. To conclude, dasatinib induces notable responses in imatinib-resistant or -intolerant CML-CP, is well tolerated, and represents a promising therapeutic option for these patients. This trial was registered at www.clinicaltrials.gov as CA180013.
C02	`01`	`X`		`@0 002B19B`
C03	`01`	`X`	`FRE`	`@0 Imatinib @2 FR @5 01`
C03	`01`	`X`	`ENG`	`@0 Imatinib @2 FR @5 01`
C03	`01`	`X`	`SPA`	`@0 Imatinib @2 FR @5 01`
C03	`02`	`X`	`FRE`	`@0 Anticancéreux @5 02`
C03	`02`	`X`	`ENG`	`@0 Antineoplastic agent @5 02`
C03	`02`	`X`	`SPA`	`@0 Anticanceroso @5 02`
C03	`03`	`X`	`FRE`	`@0 Cytogénétique @5 03`
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C03	`03`	`X`	`SPA`	`@0 Citogenética @5 03`
C03	`04`	`X`	`FRE`	`@0 Protein-tyrosine kinase @2 FE @5 05`
C03	`04`	`X`	`ENG`	`@0 Protein-tyrosine kinase @2 FE @5 05`
C03	`04`	`X`	`SPA`	`@0 Protein-tyrosine kinase @2 FE @5 05`
C03	`05`	`X`	`FRE`	`@0 Inhibiteur enzyme @5 06`
C03	`05`	`X`	`ENG`	`@0 Enzyme inhibitor @5 06`
C03	`05`	`X`	`SPA`	`@0 Inhibidor enzima @5 06`
C03	`06`	`X`	`FRE`	`@0 Traitement @5 08`
C03	`06`	`X`	`ENG`	`@0 Treatment @5 08`
C03	`06`	`X`	`SPA`	`@0 Tratamiento @5 08`
C03	`07`	`X`	`FRE`	`@0 Dasatinib @4 INC @5 86`
C03	`08`	`X`	`FRE`	`@0 Leucémie myéloïde chronique @4 CD @5 96`
C03	`08`	`X`	`ENG`	`@0 Chronic myelocytic leukemia @4 CD @5 96`
C03	`08`	`X`	`SPA`	`@0 Leucemia mieloidea @4 CD @5 96`
C07	`01`	`X`	`FRE`	`@0 Transferases @2 FE`
C07	`01`	`X`	`ENG`	`@0 Transferases @2 FE`
C07	`01`	`X`	`SPA`	`@0 Transferases @2 FE`
C07	`02`	`X`	`FRE`	`@0 Enzyme @2 FE`
C07	`02`	`X`	`ENG`	`@0 Enzyme @2 FE`
C07	`02`	`X`	`SPA`	`@0 Enzima @2 FE`
C07	`03`	`X`	`FRE`	`@0 Hémopathie maligne @5 37`
C07	`03`	`X`	`ENG`	`@0 Malignant hemopathy @5 37`
C07	`03`	`X`	`SPA`	`@0 Hemopatía maligna @5 37`
C07	`04`	`X`	`FRE`	`@0 Inhibiteur de la tyrosine kinase @4 INC @5 87`
C07	`05`	`X`	`FRE`	`@0 Inhibiteur multikinase @4 INC @5 88`
N21				`@1 162`
N44	`01`			`@1 OTO`
N82				`@1 OTO`

Format Inist (serveur)

NO :	PASCAL 07-0247406 INIST
ET :	Dasatinib induces notable hematologic and cytogenetic responses in chronic-phase chronic myeloid leukemia after failure of imatinib therapy. Commentary
AU :	ROWE (Jacob M.); HOCHHAUS (Andreas); KANTARJIAN (Hagop M.); BACCARANI (Michele); LIPTON (Jeffrey H.); APPERLEY (Jane F.); DRUKER (Brian J.); FACON (Thierry); GOLDBERG (Stuart L.); CERVANTES (Francisco); NIEDERWIESER (Dietger); SILVER (Richard T.); STONE (Richard M.); HUGHES (Timothy P.); MULLER (Martin C.); EZZEDDINE (Rana); COUNTOURIOTIS (Athena M.); SHAH (Neil P.)
AF :	HEMATOLOGY, RAMBAM MEDICAL CENTER/Etats-Unis (1 aut.); III. Medizinische Klinik, Medizinische Fakultät Mannheim, Universität Heidelberg/Mannheim/Allemagne (2 aut., 15 aut.); Department of Leukemia, M.D. Anderson Cancer Center/Houston, TX/Etats-Unis (3 aut.); Department of Hematology-Oncology "Seragnoli," S Orsola-Malpighi University Hospital, University of Bologna/Italie (4 aut.); Princess Margaret Hospital/Toronto, ON/Canada (5 aut.); Department of Haematology, Hammersmith Hospital/London/Royaume-Uni (6 aut.); Division of Hematology and Medical Oncology, Oregon Health Science University/Portland/Etats-Unis (7 aut.); Hópital Claude Huriez/Lille/France (8 aut.); Cancer Center, Hackensack University Medical Center/NJ/Etats-Unis (9 aut.); Department of Hematology, Hospital Clinic/Barcelona/Espagne (10 aut.); Medizinische Klinik und Poliklinik II, Universitätsklinikum Leipzig/Allemagne (11 aut.); Weill Medical College of Cornell University, New York Presbyterian Hospital/New York, NY/Etats-Unis (12 aut.); Department of Adult Oncology, Dana-Farber Cancer Institute/Boston, MA/Etats-Unis (13 aut.); Division of Hematology, Institute of Medical and Veterinary Science/Adelaide/Australie (14 aut.); Bristol-Myers Squibb/Wallingford, CT/Etats-Unis (16 aut., 17 aut.); Division of Hematology and Oncology, University College of San Francisco School of Medicine/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. 6; 2271,2303-2309 [8 p.]; Bibl. 32 ref.
LA :	Anglais
EA :	Although imatinib induces marked responses in patients with chronic myeloid leukemia (CML), resistance is increasingly problematic, and treatment options for imatinib-resistant or -intolerant CML are limited. Dasatinib, a novel, highly potent, oral, multitargeted kinase inhibitor of BCR-ABL and SRC family kinases, induced cytogenetic responses in a phase 1 study in imatinib-resistant or -intolerant CML and was well tolerated. Initial results are presented from a phase 2 study of 186 patients with imatinib-resistant or -intolerant chronic-phase CML (CML-CP) designed to further establish the efficacy and safety of dasatinib (70 mg twice daily). At 8-months' follow-up, dasatinib induced notable responses, with 90% and 52% of patients achieving complete hematologic and major cytogenetic responses (MCyR), respectively. Responses were long lasting: only 2% of patients achieving MCyR progressed or died. Importantly, comparable responses were achieved by patients carrying BCR-ABL mutations conferring imatinib resistance. Dasatinib also induced molecular responses, reducing BCR-ABL/ABL transcript ratios from 66% at baseline to 2.6% at 9 months. Nonhematologic adverse events were generally mild to moderate, and most cytopenias were effectively managed with dose modifications. Cross-intolerance with imatinib was not evident. To conclude, dasatinib induces notable responses in imatinib-resistant or -intolerant CML-CP, is well tolerated, and represents a promising therapeutic option for these patients. This trial was registered at www.clinicaltrials.gov as CA180013.
CC :	002B19B
FD :	Imatinib; Anticancéreux; Cytogénétique; Protein-tyrosine kinase; Inhibiteur enzyme; Traitement; Dasatinib; Leucémie myéloïde chronique
FG :	Transferases; Enzyme; Hémopathie maligne; Inhibiteur de la tyrosine kinase; Inhibiteur multikinase
ED :	Imatinib; Antineoplastic agent; Cytogenetics; Protein-tyrosine kinase; Enzyme inhibitor; Treatment; Chronic myelocytic leukemia
EG :	Transferases; Enzyme; Malignant hemopathy
SD :	Imatinib; Anticanceroso; Citogenética; Protein-tyrosine kinase; Inhibidor enzima; Tratamiento; Leucemia mieloidea
LO :	INIST-3178.354000143549720050
ID :	07-0247406

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Pascal:07-0247406

Le document en format XML

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<author><name sortKey="Shah, Neil P" sort="Shah, Neil P" uniqKey="Shah N" first="Neil P." last="Shah">Neil P. Shah</name>
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<sourceDesc><biblStruct><analytic><title xml:lang="en" level="a">Dasatinib induces notable hematologic and cytogenetic responses in chronic-phase chronic myeloid leukemia after failure of imatinib therapy. Commentary</title>
<author><name sortKey="Rowe, Jacob M" sort="Rowe, Jacob M" uniqKey="Rowe J" first="Jacob M." last="Rowe">Jacob M. Rowe</name>
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<author><name sortKey="Hochhaus, Andreas" sort="Hochhaus, Andreas" uniqKey="Hochhaus A" first="Andreas" last="Hochhaus">Andreas Hochhaus</name>
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<s2>Mannheim</s2>
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</author>
<author><name sortKey="Kantarjian, Hagop M" sort="Kantarjian, Hagop M" uniqKey="Kantarjian H" first="Hagop M." last="Kantarjian">Hagop M. Kantarjian</name>
<affiliation><inist:fA14 i1="03"><s1>Department of Leukemia, M.D. Anderson Cancer Center</s1>
<s2>Houston, TX</s2>
<s3>USA</s3>
<sZ>3 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Baccarani, Michele" sort="Baccarani, Michele" uniqKey="Baccarani M" first="Michele" last="Baccarani">Michele Baccarani</name>
<affiliation><inist:fA14 i1="04"><s1>Department of Hematology-Oncology "Seragnoli," S Orsola-Malpighi University Hospital, University of Bologna</s1>
<s3>ITA</s3>
<sZ>4 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Lipton, Jeffrey H" sort="Lipton, Jeffrey H" uniqKey="Lipton J" first="Jeffrey H." last="Lipton">Jeffrey H. Lipton</name>
<affiliation><inist:fA14 i1="05"><s1>Princess Margaret Hospital</s1>
<s2>Toronto, ON</s2>
<s3>CAN</s3>
<sZ>5 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Apperley, Jane F" sort="Apperley, Jane F" uniqKey="Apperley J" first="Jane F." last="Apperley">Jane F. Apperley</name>
<affiliation><inist:fA14 i1="06"><s1>Department of Haematology, Hammersmith Hospital</s1>
<s2>London</s2>
<s3>GBR</s3>
<sZ>6 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Druker, Brian J" sort="Druker, Brian J" uniqKey="Druker B" first="Brian J." last="Druker">Brian J. Druker</name>
<affiliation><inist:fA14 i1="07"><s1>Division of Hematology and Medical Oncology, Oregon Health Science University</s1>
<s2>Portland</s2>
<s3>USA</s3>
<sZ>7 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Facon, Thierry" sort="Facon, Thierry" uniqKey="Facon T" first="Thierry" last="Facon">Thierry Facon</name>
<affiliation><inist:fA14 i1="08"><s1>Hópital Claude Huriez</s1>
<s2>Lille</s2>
<s3>FRA</s3>
<sZ>8 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Goldberg, Stuart L" sort="Goldberg, Stuart L" uniqKey="Goldberg S" first="Stuart L." last="Goldberg">Stuart L. Goldberg</name>
<affiliation><inist:fA14 i1="09"><s1>Cancer Center, Hackensack University Medical Center</s1>
<s2>NJ</s2>
<s3>USA</s3>
<sZ>9 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Cervantes, Francisco" sort="Cervantes, Francisco" uniqKey="Cervantes F" first="Francisco" last="Cervantes">Francisco Cervantes</name>
<affiliation><inist:fA14 i1="10"><s1>Department of Hematology, Hospital Clinic</s1>
<s2>Barcelona</s2>
<s3>ESP</s3>
<sZ>10 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Niederwieser, Dietger" sort="Niederwieser, Dietger" uniqKey="Niederwieser D" first="Dietger" last="Niederwieser">Dietger Niederwieser</name>
<affiliation><inist:fA14 i1="11"><s1>Medizinische Klinik und Poliklinik II, Universitätsklinikum Leipzig</s1>
<s3>DEU</s3>
<sZ>11 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Silver, Richard T" sort="Silver, Richard T" uniqKey="Silver R" first="Richard T." last="Silver">Richard T. Silver</name>
<affiliation><inist:fA14 i1="12"><s1>Weill Medical College of Cornell University, New York Presbyterian Hospital</s1>
<s2>New York, NY</s2>
<s3>USA</s3>
<sZ>12 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Stone, Richard M" sort="Stone, Richard M" uniqKey="Stone R" first="Richard M." last="Stone">Richard M. Stone</name>
<affiliation><inist:fA14 i1="13"><s1>Department of Adult Oncology, Dana-Farber Cancer Institute</s1>
<s2>Boston, MA</s2>
<s3>USA</s3>
<sZ>13 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Hughes, Timothy P" sort="Hughes, Timothy P" uniqKey="Hughes T" first="Timothy P." last="Hughes">Timothy P. Hughes</name>
<affiliation><inist:fA14 i1="14"><s1>Division of Hematology, Institute of Medical and Veterinary Science</s1>
<s2>Adelaide</s2>
<s3>AUS</s3>
<sZ>14 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Muller, Martin C" sort="Muller, Martin C" uniqKey="Muller M" first="Martin C." last="Muller">Martin C. Muller</name>
<affiliation><inist:fA14 i1="02"><s1>III. Medizinische Klinik, Medizinische Fakultät Mannheim, Universität Heidelberg</s1>
<s2>Mannheim</s2>
<s3>DEU</s3>
<sZ>2 aut.</sZ>
<sZ>15 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Ezzeddine, Rana" sort="Ezzeddine, Rana" uniqKey="Ezzeddine R" first="Rana" last="Ezzeddine">Rana Ezzeddine</name>
<affiliation><inist:fA14 i1="15"><s1>Bristol-Myers Squibb</s1>
<s2>Wallingford, CT</s2>
<s3>USA</s3>
<sZ>16 aut.</sZ>
<sZ>17 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Countouriotis, Athena M" sort="Countouriotis, Athena M" uniqKey="Countouriotis A" first="Athena M." last="Countouriotis">Athena M. Countouriotis</name>
<affiliation><inist:fA14 i1="15"><s1>Bristol-Myers Squibb</s1>
<s2>Wallingford, CT</s2>
<s3>USA</s3>
<sZ>16 aut.</sZ>
<sZ>17 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Shah, Neil P" sort="Shah, Neil P" uniqKey="Shah N" first="Neil P." last="Shah">Neil P. Shah</name>
<affiliation><inist:fA14 i1="16"><s1>Division of Hematology and Oncology, University College of San Francisco School of Medicine</s1>
<s2>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>Cytogenetics</term>
<term>Enzyme inhibitor</term>
<term>Imatinib</term>
<term>Protein-tyrosine kinase</term>
<term>Treatment</term>
</keywords>
<keywords scheme="Pascal" xml:lang="fr"><term>Imatinib</term>
<term>Anticancéreux</term>
<term>Cytogénétique</term>
<term>Protein-tyrosine kinase</term>
<term>Inhibiteur enzyme</term>
<term>Traitement</term>
<term>Dasatinib</term>
<term>Leucémie myéloïde chronique</term>
</keywords>
</textClass>
</profileDesc>
</teiHeader>
<front><div type="abstract" xml:lang="en">Although imatinib induces marked responses in patients with chronic myeloid leukemia (CML), resistance is increasingly problematic, and treatment options for imatinib-resistant or -intolerant CML are limited. Dasatinib, a novel, highly potent, oral, multitargeted kinase inhibitor of BCR-ABL and SRC family kinases, induced cytogenetic responses in a phase 1 study in imatinib-resistant or -intolerant CML and was well tolerated. Initial results are presented from a phase 2 study of 186 patients with imatinib-resistant or -intolerant chronic-phase CML (CML-CP) designed to further establish the efficacy and safety of dasatinib (70 mg twice daily). At 8-months' follow-up, dasatinib induced notable responses, with 90% and 52% of patients achieving complete hematologic and major cytogenetic responses (MCyR), respectively. Responses were long lasting: only 2% of patients achieving MCyR progressed or died. Importantly, comparable responses were achieved by patients carrying BCR-ABL mutations conferring imatinib resistance. Dasatinib also induced molecular responses, reducing BCR-ABL/ABL transcript ratios from 66% at baseline to 2.6% at 9 months. Nonhematologic adverse events were generally mild to moderate, and most cytopenias were effectively managed with dose modifications. Cross-intolerance with imatinib was not evident. To conclude, dasatinib induces notable responses in imatinib-resistant or -intolerant CML-CP, is well tolerated, and represents a promising therapeutic option for these patients. This trial was registered at www.clinicaltrials.gov as CA180013.</div>
</front>
</TEI>
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<fA08 i1="01" i2="1" l="ENG"><s1>Dasatinib induces notable hematologic and cytogenetic responses in chronic-phase chronic myeloid leukemia after failure of imatinib therapy. Commentary</s1>
</fA08>
<fA11 i1="01" i2="1"><s1>ROWE (Jacob M.)</s1>
<s9>comment.</s9>
</fA11>
<fA11 i1="02" i2="1"><s1>HOCHHAUS (Andreas)</s1>
</fA11>
<fA11 i1="03" i2="1"><s1>KANTARJIAN (Hagop M.)</s1>
</fA11>
<fA11 i1="04" i2="1"><s1>BACCARANI (Michele)</s1>
</fA11>
<fA11 i1="05" i2="1"><s1>LIPTON (Jeffrey H.)</s1>
</fA11>
<fA11 i1="06" i2="1"><s1>APPERLEY (Jane F.)</s1>
</fA11>
<fA11 i1="07" i2="1"><s1>DRUKER (Brian J.)</s1>
</fA11>
<fA11 i1="08" i2="1"><s1>FACON (Thierry)</s1>
</fA11>
<fA11 i1="09" i2="1"><s1>GOLDBERG (Stuart L.)</s1>
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<fA11 i1="10" i2="1"><s1>CERVANTES (Francisco)</s1>
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<fA11 i1="11" i2="1"><s1>NIEDERWIESER (Dietger)</s1>
</fA11>
<fA11 i1="12" i2="1"><s1>SILVER (Richard T.)</s1>
</fA11>
<fA11 i1="13" i2="1"><s1>STONE (Richard M.)</s1>
</fA11>
<fA11 i1="14" i2="1"><s1>HUGHES (Timothy P.)</s1>
</fA11>
<fA11 i1="15" i2="1"><s1>MULLER (Martin C.)</s1>
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<fA11 i1="16" i2="1"><s1>EZZEDDINE (Rana)</s1>
</fA11>
<fA11 i1="17" i2="1"><s1>COUNTOURIOTIS (Athena M.)</s1>
</fA11>
<fA11 i1="18" i2="1"><s1>SHAH (Neil P.)</s1>
</fA11>
<fA14 i1="01"><s1>HEMATOLOGY, RAMBAM MEDICAL CENTER</s1>
<s3>USA</s3>
<sZ>1 aut.</sZ>
</fA14>
<fA14 i1="02"><s1>III. Medizinische Klinik, Medizinische Fakultät Mannheim, Universität Heidelberg</s1>
<s2>Mannheim</s2>
<s3>DEU</s3>
<sZ>2 aut.</sZ>
<sZ>15 aut.</sZ>
</fA14>
<fA14 i1="03"><s1>Department of Leukemia, M.D. Anderson Cancer Center</s1>
<s2>Houston, TX</s2>
<s3>USA</s3>
<sZ>3 aut.</sZ>
</fA14>
<fA14 i1="04"><s1>Department of Hematology-Oncology "Seragnoli," S Orsola-Malpighi University Hospital, University of Bologna</s1>
<s3>ITA</s3>
<sZ>4 aut.</sZ>
</fA14>
<fA14 i1="05"><s1>Princess Margaret Hospital</s1>
<s2>Toronto, ON</s2>
<s3>CAN</s3>
<sZ>5 aut.</sZ>
</fA14>
<fA14 i1="06"><s1>Department of Haematology, Hammersmith Hospital</s1>
<s2>London</s2>
<s3>GBR</s3>
<sZ>6 aut.</sZ>
</fA14>
<fA14 i1="07"><s1>Division of Hematology and Medical Oncology, Oregon Health Science University</s1>
<s2>Portland</s2>
<s3>USA</s3>
<sZ>7 aut.</sZ>
</fA14>
<fA14 i1="08"><s1>Hópital Claude Huriez</s1>
<s2>Lille</s2>
<s3>FRA</s3>
<sZ>8 aut.</sZ>
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<fA14 i1="09"><s1>Cancer Center, Hackensack University Medical Center</s1>
<s2>NJ</s2>
<s3>USA</s3>
<sZ>9 aut.</sZ>
</fA14>
<fA14 i1="10"><s1>Department of Hematology, Hospital Clinic</s1>
<s2>Barcelona</s2>
<s3>ESP</s3>
<sZ>10 aut.</sZ>
</fA14>
<fA14 i1="11"><s1>Medizinische Klinik und Poliklinik II, Universitätsklinikum Leipzig</s1>
<s3>DEU</s3>
<sZ>11 aut.</sZ>
</fA14>
<fA14 i1="12"><s1>Weill Medical College of Cornell University, New York Presbyterian Hospital</s1>
<s2>New York, NY</s2>
<s3>USA</s3>
<sZ>12 aut.</sZ>
</fA14>
<fA14 i1="13"><s1>Department of Adult Oncology, Dana-Farber Cancer Institute</s1>
<s2>Boston, MA</s2>
<s3>USA</s3>
<sZ>13 aut.</sZ>
</fA14>
<fA14 i1="14"><s1>Division of Hematology, Institute of Medical and Veterinary Science</s1>
<s2>Adelaide</s2>
<s3>AUS</s3>
<sZ>14 aut.</sZ>
</fA14>
<fA14 i1="15"><s1>Bristol-Myers Squibb</s1>
<s2>Wallingford, CT</s2>
<s3>USA</s3>
<sZ>16 aut.</sZ>
<sZ>17 aut.</sZ>
</fA14>
<fA14 i1="16"><s1>Division of Hematology and Oncology, University College of San Francisco School of Medicine</s1>
<s2>CA</s2>
<s3>USA</s3>
<sZ>18 aut.</sZ>
</fA14>
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</fA21>
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<s5>354000143549720050</s5>
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<fA44><s0>0000</s0>
<s1>© 2007 INIST-CNRS. All rights reserved.</s1>
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<fA45><s0>32 ref.</s0>
</fA45>
<fA47 i1="01" i2="1"><s0>07-0247406</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>Although imatinib induces marked responses in patients with chronic myeloid leukemia (CML), resistance is increasingly problematic, and treatment options for imatinib-resistant or -intolerant CML are limited. Dasatinib, a novel, highly potent, oral, multitargeted kinase inhibitor of BCR-ABL and SRC family kinases, induced cytogenetic responses in a phase 1 study in imatinib-resistant or -intolerant CML and was well tolerated. Initial results are presented from a phase 2 study of 186 patients with imatinib-resistant or -intolerant chronic-phase CML (CML-CP) designed to further establish the efficacy and safety of dasatinib (70 mg twice daily). At 8-months' follow-up, dasatinib induced notable responses, with 90% and 52% of patients achieving complete hematologic and major cytogenetic responses (MCyR), respectively. Responses were long lasting: only 2% of patients achieving MCyR progressed or died. Importantly, comparable responses were achieved by patients carrying BCR-ABL mutations conferring imatinib resistance. Dasatinib also induced molecular responses, reducing BCR-ABL/ABL transcript ratios from 66% at baseline to 2.6% at 9 months. Nonhematologic adverse events were generally mild to moderate, and most cytopenias were effectively managed with dose modifications. Cross-intolerance with imatinib was not evident. To conclude, dasatinib induces notable responses in imatinib-resistant or -intolerant CML-CP, is well tolerated, and represents a promising therapeutic option for these patients. This trial was registered at www.clinicaltrials.gov as CA180013.</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>
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<s5>01</s5>
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<s5>01</s5>
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<s5>02</s5>
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<s5>02</s5>
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<fC03 i1="02" i2="X" l="SPA"><s0>Anticanceroso</s0>
<s5>02</s5>
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<s5>03</s5>
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<s5>03</s5>
</fC03>
<fC03 i1="03" i2="X" l="SPA"><s0>Citogenética</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>Traitement</s0>
<s5>08</s5>
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<s5>08</s5>
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<s5>08</s5>
</fC03>
<fC03 i1="07" i2="X" l="FRE"><s0>Dasatinib</s0>
<s4>INC</s4>
<s5>86</s5>
</fC03>
<fC03 i1="08" i2="X" l="FRE"><s0>Leucémie myéloïde chronique</s0>
<s4>CD</s4>
<s5>96</s5>
</fC03>
<fC03 i1="08" i2="X" l="ENG"><s0>Chronic myelocytic leukemia</s0>
<s4>CD</s4>
<s5>96</s5>
</fC03>
<fC03 i1="08" i2="X" l="SPA"><s0>Leucemia mieloidea</s0>
<s4>CD</s4>
<s5>96</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>
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<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>Inhibiteur de la tyrosine kinase</s0>
<s4>INC</s4>
<s5>87</s5>
</fC07>
<fC07 i1="05" i2="X" l="FRE"><s0>Inhibiteur multikinase</s0>
<s4>INC</s4>
<s5>88</s5>
</fC07>
<fN21><s1>162</s1>
</fN21>
<fN44 i1="01"><s1>OTO</s1>
</fN44>
<fN82><s1>OTO</s1>
</fN82>
</pA>
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<server><NO>PASCAL 07-0247406 INIST</NO>
<ET>Dasatinib induces notable hematologic and cytogenetic responses in chronic-phase chronic myeloid leukemia after failure of imatinib therapy. Commentary</ET>
<AU>ROWE (Jacob M.); HOCHHAUS (Andreas); KANTARJIAN (Hagop M.); BACCARANI (Michele); LIPTON (Jeffrey H.); APPERLEY (Jane F.); DRUKER (Brian J.); FACON (Thierry); GOLDBERG (Stuart L.); CERVANTES (Francisco); NIEDERWIESER (Dietger); SILVER (Richard T.); STONE (Richard M.); HUGHES (Timothy P.); MULLER (Martin C.); EZZEDDINE (Rana); COUNTOURIOTIS (Athena M.); SHAH (Neil P.)</AU>
<AF>HEMATOLOGY, RAMBAM MEDICAL CENTER/Etats-Unis (1 aut.); III. Medizinische Klinik, Medizinische Fakultät Mannheim, Universität Heidelberg/Mannheim/Allemagne (2 aut., 15 aut.); Department of Leukemia, M.D. Anderson Cancer Center/Houston, TX/Etats-Unis (3 aut.); Department of Hematology-Oncology "Seragnoli," S Orsola-Malpighi University Hospital, University of Bologna/Italie (4 aut.); Princess Margaret Hospital/Toronto, ON/Canada (5 aut.); Department of Haematology, Hammersmith Hospital/London/Royaume-Uni (6 aut.); Division of Hematology and Medical Oncology, Oregon Health Science University/Portland/Etats-Unis (7 aut.); Hópital Claude Huriez/Lille/France (8 aut.); Cancer Center, Hackensack University Medical Center/NJ/Etats-Unis (9 aut.); Department of Hematology, Hospital Clinic/Barcelona/Espagne (10 aut.); Medizinische Klinik und Poliklinik II, Universitätsklinikum Leipzig/Allemagne (11 aut.); Weill Medical College of Cornell University, New York Presbyterian Hospital/New York, NY/Etats-Unis (12 aut.); Department of Adult Oncology, Dana-Farber Cancer Institute/Boston, MA/Etats-Unis (13 aut.); Division of Hematology, Institute of Medical and Veterinary Science/Adelaide/Australie (14 aut.); Bristol-Myers Squibb/Wallingford, CT/Etats-Unis (16 aut., 17 aut.); Division of Hematology and Oncology, University College of San Francisco School of Medicine/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. 6; 2271,2303-2309 [8 p.]; Bibl. 32 ref.</SO>
<LA>Anglais</LA>
<EA>Although imatinib induces marked responses in patients with chronic myeloid leukemia (CML), resistance is increasingly problematic, and treatment options for imatinib-resistant or -intolerant CML are limited. Dasatinib, a novel, highly potent, oral, multitargeted kinase inhibitor of BCR-ABL and SRC family kinases, induced cytogenetic responses in a phase 1 study in imatinib-resistant or -intolerant CML and was well tolerated. Initial results are presented from a phase 2 study of 186 patients with imatinib-resistant or -intolerant chronic-phase CML (CML-CP) designed to further establish the efficacy and safety of dasatinib (70 mg twice daily). At 8-months' follow-up, dasatinib induced notable responses, with 90% and 52% of patients achieving complete hematologic and major cytogenetic responses (MCyR), respectively. Responses were long lasting: only 2% of patients achieving MCyR progressed or died. Importantly, comparable responses were achieved by patients carrying BCR-ABL mutations conferring imatinib resistance. Dasatinib also induced molecular responses, reducing BCR-ABL/ABL transcript ratios from 66% at baseline to 2.6% at 9 months. Nonhematologic adverse events were generally mild to moderate, and most cytopenias were effectively managed with dose modifications. Cross-intolerance with imatinib was not evident. To conclude, dasatinib induces notable responses in imatinib-resistant or -intolerant CML-CP, is well tolerated, and represents a promising therapeutic option for these patients. This trial was registered at www.clinicaltrials.gov as CA180013.</EA>
<CC>002B19B</CC>
<FD>Imatinib; Anticancéreux; Cytogénétique; Protein-tyrosine kinase; Inhibiteur enzyme; Traitement; Dasatinib; Leucémie myéloïde chronique</FD>
<FG>Transferases; Enzyme; Hémopathie maligne; Inhibiteur de la tyrosine kinase; Inhibiteur multikinase</FG>
<ED>Imatinib; Antineoplastic agent; Cytogenetics; Protein-tyrosine kinase; Enzyme inhibitor; Treatment; Chronic myelocytic leukemia</ED>
<EG>Transferases; Enzyme; Malignant hemopathy</EG>
<SD>Imatinib; Anticanceroso; Citogenética; Protein-tyrosine kinase; Inhibidor enzima; Tratamiento; Leucemia mieloidea</SD>
<LO>INIST-3178.354000143549720050</LO>
<ID>07-0247406</ID>
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Dasatinib induces notable hematologic and cytogenetic responses in chronic-phase chronic myeloid leukemia after failure of imatinib therapy. Commentary

Dasatinib induces notable hematologic and cytogenetic responses in chronic-phase chronic myeloid leukemia after failure of imatinib therapy. Commentary

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