Imatinib Compared with Interferon and Low-Dose Cytarabine for Newly Diagnosed Chronic-Phase Chronic Myeloid Leukemia
Imatinib, an inhibitor of the mutant tyrosine kinase that causes chronic myeloid leukemia (CML), is effective in patients with chronic-phase CML who have no response to the standard treatment, interferon alfa. In this study of 1106 patients with previously untreated chronic-phase CML, imatinib was s...
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| Veröffentlicht in: | NEW ENGLAND JOURNAL OF MEDICINE 2003-03, Vol.348 (11), p.994-1004 |
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| creator | O'Brien, Stephen G Guilhot, François Larson, Richard A Gathmann, Insa Baccarani, Michele Cervantes, Francisco Cornelissen, Jan J Fischer, Thomas Hochhaus, Andreas Hughes, Timothy Lechner, Klaus Nielsen, Johan L Rousselot, Philippe Reiffers, Josy Saglio, Giuseppe Shepherd, John Simonsson, Bengt Gratwohl, Alois Goldman, John M Kantarjian, Hagop Taylor, Kerry Verhoef, Gregor Bolton, Ann E Capdeville, Renaud Druker, Brian J |
| description | Imatinib, an inhibitor of the mutant tyrosine kinase that causes chronic myeloid leukemia (CML), is effective in patients with chronic-phase CML who have no response to the standard treatment, interferon alfa. In this study of 1106 patients with previously untreated chronic-phase CML, imatinib was superior to a combination of interferon alfa and cytarabine as initial therapy.
In a study of 1106 patients, imatinib was superior to interferon alfa plus cytarabine as initial therapy.
The Philadelphia chromosome (Ph),
1
the result of a t(9;22) reciprocal translocation,
2
is present in over 90 percent of patients with chronic myeloid leukemia (CML) and results in the juxtaposition of DNA sequences from the
BCR
and
ABL
genes.
3
–
6
BCR-ABL
encodes a protein, p210BCR-ABL, with dysregulated tyrosine kinase activity,
7
which is necessary and sufficient for leukemogenesis.
8
–
11
Imatinib mesylate (Gleevec, Novartis), a potent competitive inhibitor of the tyrosine kinases associated with ABL,
12
,
13
C-KIT,
14
,
15
platelet-derived growth factor receptor,
13
,
14
,
16
and ARG,
17
impedes the interaction of ATP with these proteins
18
and thereby inhibits their ability to phosphorylate and activate . . . |
| doi_str_mv | 10.1056/NEJMoa022457 |
| format | Article |
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In a study of 1106 patients, imatinib was superior to interferon alfa plus cytarabine as initial therapy.
The Philadelphia chromosome (Ph),
1
the result of a t(9;22) reciprocal translocation,
2
is present in over 90 percent of patients with chronic myeloid leukemia (CML) and results in the juxtaposition of DNA sequences from the
BCR
and
ABL
genes.
3
–
6
BCR-ABL
encodes a protein, p210BCR-ABL, with dysregulated tyrosine kinase activity,
7
which is necessary and sufficient for leukemogenesis.
8
–
11
Imatinib mesylate (Gleevec, Novartis), a potent competitive inhibitor of the tyrosine kinases associated with ABL,
12
,
13
C-KIT,
14
,
15
platelet-derived growth factor receptor,
13
,
14
,
16
and ARG,
17
impedes the interaction of ATP with these proteins
18
and thereby inhibits their ability to phosphorylate and activate . . .</description><identifier>ISSN: 0028-4793</identifier><identifier>EISSN: 1533-4406</identifier><identifier>DOI: 10.1056/NEJMoa022457</identifier><identifier>PMID: 12637609</identifier><identifier>CODEN: NEJMAG</identifier><language>eng</language><publisher>Boston, MA: Massachusetts Medical Society</publisher><subject>Adolescent ; Adult ; Aged ; Antineoplastic Agents - administration & dosage ; Antineoplastic Agents - therapeutic use ; Antineoplastic Combined Chemotherapy Protocols - therapeutic use ; Benzamides ; Biological and medical sciences ; Blood. Blood coagulation. Reticuloendothelial system ; Clinical trials ; Cytarabine - administration & dosage ; Disease Progression ; Drug therapy ; Female ; Humans ; Imatinib Mesylate ; Interferon-alpha - administration & dosage ; Leukemia ; Leukemia, Myeloid, Chronic-Phase - drug therapy ; Leukemia, Myeloid, Chronic-Phase - mortality ; Male ; Medical sciences ; Middle Aged ; Pharmacology. Drug treatments ; Piperazines - therapeutic use ; Prospective Studies ; Pyrimidines - therapeutic use ; Survival Rate</subject><ispartof>NEW ENGLAND JOURNAL OF MEDICINE, 2003-03, Vol.348 (11), p.994-1004</ispartof><rights>Copyright © 2003 Massachusetts Medical Society. All rights reserved.</rights><rights>2003 INIST-CNRS</rights><rights>Copyright 2003 Massachusetts Medical Society</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c583t-944dd8ad41a72f8305e239b89c77cf1666ad3b1dc9948ef2bbf360b5a2a7b8493</citedby><cites>FETCH-LOGICAL-c583t-944dd8ad41a72f8305e239b89c77cf1666ad3b1dc9948ef2bbf360b5a2a7b8493</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.nejm.org/doi/pdf/10.1056/NEJMoa022457$$EPDF$$P50$$Gmms$$H</linktopdf><linktohtml>$$Uhttps://www.nejm.org/doi/full/10.1056/NEJMoa022457$$EHTML$$P50$$Gmms$$H</linktohtml><link.rule.ids>314,776,780,881,2746,2747,26080,27901,27902,52357,54039</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=14591747$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/12637609$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink><backlink>$$Uhttp://kipublications.ki.se/Default.aspx?queryparsed=id:19069105$$DView record from Swedish Publication Index$$Hfree_for_read</backlink></links><search><creatorcontrib>O'Brien, Stephen G</creatorcontrib><creatorcontrib>Guilhot, François</creatorcontrib><creatorcontrib>Larson, Richard A</creatorcontrib><creatorcontrib>Gathmann, Insa</creatorcontrib><creatorcontrib>Baccarani, Michele</creatorcontrib><creatorcontrib>Cervantes, Francisco</creatorcontrib><creatorcontrib>Cornelissen, Jan J</creatorcontrib><creatorcontrib>Fischer, Thomas</creatorcontrib><creatorcontrib>Hochhaus, Andreas</creatorcontrib><creatorcontrib>Hughes, Timothy</creatorcontrib><creatorcontrib>Lechner, Klaus</creatorcontrib><creatorcontrib>Nielsen, Johan L</creatorcontrib><creatorcontrib>Rousselot, Philippe</creatorcontrib><creatorcontrib>Reiffers, Josy</creatorcontrib><creatorcontrib>Saglio, Giuseppe</creatorcontrib><creatorcontrib>Shepherd, John</creatorcontrib><creatorcontrib>Simonsson, Bengt</creatorcontrib><creatorcontrib>Gratwohl, Alois</creatorcontrib><creatorcontrib>Goldman, John M</creatorcontrib><creatorcontrib>Kantarjian, Hagop</creatorcontrib><creatorcontrib>Taylor, Kerry</creatorcontrib><creatorcontrib>Verhoef, Gregor</creatorcontrib><creatorcontrib>Bolton, Ann E</creatorcontrib><creatorcontrib>Capdeville, Renaud</creatorcontrib><creatorcontrib>Druker, Brian J</creatorcontrib><creatorcontrib>IRIS Investigators</creatorcontrib><title>Imatinib Compared with Interferon and Low-Dose Cytarabine for Newly Diagnosed Chronic-Phase Chronic Myeloid Leukemia</title><title>NEW ENGLAND JOURNAL OF MEDICINE</title><addtitle>N Engl J Med</addtitle><description>Imatinib, an inhibitor of the mutant tyrosine kinase that causes chronic myeloid leukemia (CML), is effective in patients with chronic-phase CML who have no response to the standard treatment, interferon alfa. In this study of 1106 patients with previously untreated chronic-phase CML, imatinib was superior to a combination of interferon alfa and cytarabine as initial therapy.
In a study of 1106 patients, imatinib was superior to interferon alfa plus cytarabine as initial therapy.
The Philadelphia chromosome (Ph),
1
the result of a t(9;22) reciprocal translocation,
2
is present in over 90 percent of patients with chronic myeloid leukemia (CML) and results in the juxtaposition of DNA sequences from the
BCR
and
ABL
genes.
3
–
6
BCR-ABL
encodes a protein, p210BCR-ABL, with dysregulated tyrosine kinase activity,
7
which is necessary and sufficient for leukemogenesis.
8
–
11
Imatinib mesylate (Gleevec, Novartis), a potent competitive inhibitor of the tyrosine kinases associated with ABL,
12
,
13
C-KIT,
14
,
15
platelet-derived growth factor receptor,
13
,
14
,
16
and ARG,
17
impedes the interaction of ATP with these proteins
18
and thereby inhibits their ability to phosphorylate and activate . . .</description><subject>Adolescent</subject><subject>Adult</subject><subject>Aged</subject><subject>Antineoplastic Agents - administration & dosage</subject><subject>Antineoplastic Agents - therapeutic use</subject><subject>Antineoplastic Combined Chemotherapy Protocols - therapeutic use</subject><subject>Benzamides</subject><subject>Biological and medical sciences</subject><subject>Blood. Blood coagulation. Reticuloendothelial system</subject><subject>Clinical trials</subject><subject>Cytarabine - administration & dosage</subject><subject>Disease Progression</subject><subject>Drug therapy</subject><subject>Female</subject><subject>Humans</subject><subject>Imatinib Mesylate</subject><subject>Interferon-alpha - administration & dosage</subject><subject>Leukemia</subject><subject>Leukemia, Myeloid, Chronic-Phase - drug therapy</subject><subject>Leukemia, Myeloid, Chronic-Phase - mortality</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>Pharmacology. Drug treatments</subject><subject>Piperazines - therapeutic use</subject><subject>Prospective Studies</subject><subject>Pyrimidines - therapeutic use</subject><subject>Survival Rate</subject><issn>0028-4793</issn><issn>1533-4406</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2003</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BEC</sourceid><sourceid>BENPR</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNpt0c1v0zAYB2ALgVgZ3DgjC8FtAX8nPqJsjKJucICz9TpxqLsmLnaiqv89rhIxDvjir8e_19KL0GtKPlAi1cf7m693AQhjQpZP0IpKzgshiHqKVoSwqhCl5hfoRUo7kgcV-jm6oEzxUhG9QuO6h9EP3uI69AeIrsVHP27xehhd7FwMA4ahxZtwLK5Dcrg-jRDB-sHhLkR87477E7728GvIty2ut_mFb4rvWzjjeYfvTm4ffE5x04PrPbxEzzrYJ_dqmS_Rz883P-ovxebb7br-tCkaWfGx0EK0bQWtoFCyruJEOsa1rXRTlk1HlVLQckvbRmtRuY5Z23FFrAQGpa2E5peomHPT0R0maw7R9xBPJoA3y9FDXjkjNVGkzP7t7A8x_J5cGs0uTHHIXzQsV-ZcSZHR1YyaGFKKrvsbS4k5d8T825HM3yyZk-1d-4iXFmTwfgGQGth3EYbGp0cnpKalOAe9m13fJzO4Xf__en8ATICffA</recordid><startdate>20030313</startdate><enddate>20030313</enddate><creator>O'Brien, Stephen G</creator><creator>Guilhot, François</creator><creator>Larson, Richard A</creator><creator>Gathmann, Insa</creator><creator>Baccarani, Michele</creator><creator>Cervantes, Francisco</creator><creator>Cornelissen, Jan J</creator><creator>Fischer, Thomas</creator><creator>Hochhaus, Andreas</creator><creator>Hughes, Timothy</creator><creator>Lechner, Klaus</creator><creator>Nielsen, Johan L</creator><creator>Rousselot, Philippe</creator><creator>Reiffers, Josy</creator><creator>Saglio, Giuseppe</creator><creator>Shepherd, John</creator><creator>Simonsson, Bengt</creator><creator>Gratwohl, Alois</creator><creator>Goldman, John M</creator><creator>Kantarjian, Hagop</creator><creator>Taylor, Kerry</creator><creator>Verhoef, Gregor</creator><creator>Bolton, Ann E</creator><creator>Capdeville, Renaud</creator><creator>Druker, Brian J</creator><general>Massachusetts Medical Society</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>0TZ</scope><scope>7RV</scope><scope>7X7</scope><scope>7XB</scope><scope>8AO</scope><scope>8C1</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AN0</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BEC</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>HCIFZ</scope><scope>K0Y</scope><scope>LK8</scope><scope>M0R</scope><scope>M0T</scope><scope>M1P</scope><scope>M2M</scope><scope>M2O</scope><scope>M2P</scope><scope>M7P</scope><scope>MBDVC</scope><scope>NAPCQ</scope><scope>PHGZM</scope><scope>PHGZT</scope><scope>PJZUB</scope><scope>PKEHL</scope><scope>PPXIY</scope><scope>PQEST</scope><scope>PQGLB</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PSYQQ</scope><scope>Q9U</scope><scope>ADTPV</scope><scope>AOWAS</scope></search><sort><creationdate>20030313</creationdate><title>Imatinib Compared with Interferon and Low-Dose Cytarabine for Newly Diagnosed Chronic-Phase Chronic Myeloid Leukemia</title><author>O'Brien, Stephen G ; Guilhot, François ; Larson, Richard A ; Gathmann, Insa ; Baccarani, Michele ; Cervantes, Francisco ; Cornelissen, Jan J ; Fischer, Thomas ; Hochhaus, Andreas ; Hughes, Timothy ; Lechner, Klaus ; Nielsen, Johan L ; Rousselot, Philippe ; Reiffers, Josy ; Saglio, Giuseppe ; Shepherd, John ; Simonsson, Bengt ; Gratwohl, Alois ; Goldman, John M ; Kantarjian, Hagop ; Taylor, Kerry ; Verhoef, Gregor ; Bolton, Ann E ; Capdeville, Renaud ; Druker, Brian J</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c583t-944dd8ad41a72f8305e239b89c77cf1666ad3b1dc9948ef2bbf360b5a2a7b8493</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2003</creationdate><topic>Adolescent</topic><topic>Adult</topic><topic>Aged</topic><topic>Antineoplastic Agents - administration & dosage</topic><topic>Antineoplastic Agents - therapeutic use</topic><topic>Antineoplastic Combined Chemotherapy Protocols - therapeutic use</topic><topic>Benzamides</topic><topic>Biological and medical sciences</topic><topic>Blood. Blood coagulation. Reticuloendothelial system</topic><topic>Clinical trials</topic><topic>Cytarabine - administration & dosage</topic><topic>Disease Progression</topic><topic>Drug therapy</topic><topic>Female</topic><topic>Humans</topic><topic>Imatinib Mesylate</topic><topic>Interferon-alpha - administration & dosage</topic><topic>Leukemia</topic><topic>Leukemia, Myeloid, Chronic-Phase - drug therapy</topic><topic>Leukemia, Myeloid, Chronic-Phase - mortality</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Middle Aged</topic><topic>Pharmacology. 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Josy</au><au>Saglio, Giuseppe</au><au>Shepherd, John</au><au>Simonsson, Bengt</au><au>Gratwohl, Alois</au><au>Goldman, John M</au><au>Kantarjian, Hagop</au><au>Taylor, Kerry</au><au>Verhoef, Gregor</au><au>Bolton, Ann E</au><au>Capdeville, Renaud</au><au>Druker, Brian J</au><aucorp>IRIS Investigators</aucorp><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Imatinib Compared with Interferon and Low-Dose Cytarabine for Newly Diagnosed Chronic-Phase Chronic Myeloid Leukemia</atitle><jtitle>NEW ENGLAND JOURNAL OF MEDICINE</jtitle><addtitle>N Engl J Med</addtitle><date>2003-03-13</date><risdate>2003</risdate><volume>348</volume><issue>11</issue><spage>994</spage><epage>1004</epage><pages>994-1004</pages><issn>0028-4793</issn><eissn>1533-4406</eissn><coden>NEJMAG</coden><abstract>Imatinib, an inhibitor of the mutant tyrosine kinase that causes chronic myeloid leukemia (CML), is effective in patients with chronic-phase CML who have no response to the standard treatment, interferon alfa. In this study of 1106 patients with previously untreated chronic-phase CML, imatinib was superior to a combination of interferon alfa and cytarabine as initial therapy.
In a study of 1106 patients, imatinib was superior to interferon alfa plus cytarabine as initial therapy.
The Philadelphia chromosome (Ph),
1
the result of a t(9;22) reciprocal translocation,
2
is present in over 90 percent of patients with chronic myeloid leukemia (CML) and results in the juxtaposition of DNA sequences from the
BCR
and
ABL
genes.
3
–
6
BCR-ABL
encodes a protein, p210BCR-ABL, with dysregulated tyrosine kinase activity,
7
which is necessary and sufficient for leukemogenesis.
8
–
11
Imatinib mesylate (Gleevec, Novartis), a potent competitive inhibitor of the tyrosine kinases associated with ABL,
12
,
13
C-KIT,
14
,
15
platelet-derived growth factor receptor,
13
,
14
,
16
and ARG,
17
impedes the interaction of ATP with these proteins
18
and thereby inhibits their ability to phosphorylate and activate . . .</abstract><cop>Boston, MA</cop><pub>Massachusetts Medical Society</pub><pmid>12637609</pmid><doi>10.1056/NEJMoa022457</doi><tpages>11</tpages><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0028-4793 |
| ispartof | NEW ENGLAND JOURNAL OF MEDICINE, 2003-03, Vol.348 (11), p.994-1004 |
| issn | 0028-4793 1533-4406 |
| language | eng |
| recordid | cdi_proquest_journals_223933654 |
| source | MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; New England Journal of Medicine |
| subjects | Adolescent Adult Aged Antineoplastic Agents - administration & dosage Antineoplastic Agents - therapeutic use Antineoplastic Combined Chemotherapy Protocols - therapeutic use Benzamides Biological and medical sciences Blood. Blood coagulation. Reticuloendothelial system Clinical trials Cytarabine - administration & dosage Disease Progression Drug therapy Female Humans Imatinib Mesylate Interferon-alpha - administration & dosage Leukemia Leukemia, Myeloid, Chronic-Phase - drug therapy Leukemia, Myeloid, Chronic-Phase - mortality Male Medical sciences Middle Aged Pharmacology. Drug treatments Piperazines - therapeutic use Prospective Studies Pyrimidines - therapeutic use Survival Rate |
| title | Imatinib Compared with Interferon and Low-Dose Cytarabine for Newly Diagnosed Chronic-Phase Chronic Myeloid Leukemia |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-02-18T23%3A06%3A49IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_swepu&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Imatinib%20Compared%20with%20Interferon%20and%20Low-Dose%20Cytarabine%20for%20Newly%20Diagnosed%20Chronic-Phase%20Chronic%20Myeloid%20Leukemia&rft.jtitle=NEW%20ENGLAND%20JOURNAL%20OF%20MEDICINE&rft.au=O'Brien,%20Stephen%20G&rft.aucorp=IRIS%20Investigators&rft.date=2003-03-13&rft.volume=348&rft.issue=11&rft.spage=994&rft.epage=1004&rft.pages=994-1004&rft.issn=0028-4793&rft.eissn=1533-4406&rft.coden=NEJMAG&rft_id=info:doi/10.1056/NEJMoa022457&rft_dat=%3Cproquest_swepu%3E304326181%3C/proquest_swepu%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=223933654&rft_id=info:pmid/12637609&rfr_iscdi=true |